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<!--
|
||
UID=5689
|
||
ConceptID=C0020456
|
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-->
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<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Hyperglycemia</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>5689</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0020456</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome; Finding</dd></dl></div></div><table class="medgenTable"><tbody><tr><td>Synonym:</td>
|
||
<td>Hyperglycemias</td></tr>
|
||
<tr><td><span class="bold">SNOMED CT: </span></td>
|
||
<td>Hyperglycemia (80394007); Hyperglycemic disorder (237598005)</td></tr>
|
||
<tr><td colspan="2" class="small"> </td></tr><tr><td>HPO:</td>
|
||
<td><a target="_blank" title="Human Phenotype Ontology" href="https://hpo.jax.org/app/browse/term/HP:0003074">HP:0003074</a></td></tr>
|
||
<tr><td>Monarch Initiative:</td>
|
||
<td><a href="https://monarchinitiative.org/disease/MONDO:0002909" target="_blank">MONDO:0002909</a></td></tr>
|
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</tbody></table></div><div class="rprt-body jig-ncbiinpagenav" data-jigconfig="smoothScroll: false, gotoTopLink: true, gotoTopLinkText: '', gotoTopLinkAttrs: {'title': 'Go to the top of the page'},allHeadingLevels: ['h1'], topOfPageTOC: true, tocId: 'my-toc'"><div id="rprt-tabs-1" class="rprt-tab"><div id="tb-termsProp-1"><div class="leftCol mgCol"><div>
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<div class="portlet mgSection" id="ID_100">
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Definition">Definition</h1><a sid="100" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln">An increased concentration of glucose in the blood. [from <a title="Human Phenotype Ontology" href="http://www.human-phenotype-ontology.org" class="defSource" target="_blank">HPO</a>]</div>
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</div>
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<div class="portlet mgSection" id="ID_118">
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Term_Hierarchy">Term Hierarchy</h1><a sid="118" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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<div class="portlet_content ln HierarchyGTR"><div class="jig-ncbitabs"><ul><li><a href="#tabGTR">GTR</a></li><li><a href="#tabMGEN">MeSH</a></li></ul><div id="tabGTR"><div class="search_result"><div class="rprts"><div class="chiclet_legend"><span class="chiclet_list" style="position:static;"><span title="Clinical test" class="chiclet Ccolor round">C</span><span>Clinical test, </span><span title="Research test" class="chiclet Rcolor round">R</span><span>Research test, </span><span title="OMIM" class="chiclet Ocolor ">O</span><span>OMIM, </span><span title="GeneReview" class="chiclet Gcolor">G</span><span><em>GeneReviews</em>, </span><span title="ClinVar" class="chiclet Vcolor">V</span><span>ClinVar </span></span></div><div id="hierarchy" class="margin_t1"><div class="ds_tree"><ul><li class="matched_ds"><span class="chiclet_list"><span class="chiclet Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C0020456[DISCUI]&test_type=Clinical" ref="ncbi_uid=5689">C</a></span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet unavailable" title="OMIM">O</span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet Vcolor" title="ClinVar"><a target="_blank" href="/clinvar?LinkName=medgen_clinvar&from_uid=5689" ref="ncbi_uid=5689">V</a></span></span><span class="TLline">Hyperglycemia</span></li></ul></div></div></div></div></div><div id="tabMGEN"><div class="ds_tree"><ul><li><span class="TLline"><a href="/medgen/233128" ref="tree=MeSH" title="MedGen record for Abnormal Blood Chemistry and Hematology Test Result">Abnormal Blood Chemistry and Hematology Test Result</a></span><ul><li><span class="matched_ds">Hyperglycemia</span><ul><li><span class="TLline"><a href="/medgen/75760" ref="tree=MeSH" title="MedGen record for Glucose intolerance">Glucose intolerance</a></span><ul><li><span class="TLline"><a href="/medgen/8350" ref="tree=MeSH" title="MedGen record for Diabetes mellitus">Diabetes mellitus</a></span><ul><li><span class="TLline"><a href="/medgen/417694" ref="tree=MeSH" title="MedGen record for Childhood Diabetes Mellitus">Childhood Diabetes Mellitus</a></span></li><li><span class="TLline"><a href="/medgen/137965" ref="tree=MeSH" title="MedGen record for Complication due to diabetes mellitus">Complication due to diabetes mellitus</a></span></li><li><span class="TLline"><a href="/medgen/41522" ref="tree=MeSH" title="MedGen record for Diabetes mellitus type 1">Diabetes mellitus type 1</a></span></li><li><span class="TLline"><a href="/medgen/543460" ref="tree=MeSH" title="MedGen record for Diabetes mellitus without complication">Diabetes mellitus without complication</a></span></li><li><span class="TLline"><a href="/medgen/38815" ref="tree=MeSH" title="MedGen record for Gestational diabetes">Gestational diabetes</a></span></li><li><span class="TLline"><a href="/medgen/895261" ref="tree=MeSH" title="MedGen record for Latent autoimmune diabetes in adults">Latent autoimmune diabetes in adults</a></span></li><li><span class="TLline"><a href="/medgen/82708" ref="tree=MeSH" title="MedGen record for Leprechaunism syndrome">Leprechaunism syndrome</a></span></li><li><span class="TLline"><a href="/medgen/4256" ref="tree=MeSH" title="MedGen record for Lipoatrophic diabetes">Lipoatrophic diabetes</a></span></li><li><span class="TLline"><a href="/medgen/87433" ref="tree=MeSH" title="MedGen record for Maturity onset diabetes mellitus in young">Maturity onset diabetes mellitus in young</a></span></li><li><span class="TLline"><a href="/medgen/1384794" ref="tree=MeSH" title="MedGen record for Mitochondrial Diabetes">Mitochondrial Diabetes</a></span></li><li><span class="TLline"><a href="/medgen/1392102" ref="tree=MeSH" title="MedGen record for Monogenic diabetes">Monogenic diabetes</a></span></li><li><span class="TLline"><a href="/medgen/856237" ref="tree=MeSH" title="MedGen record for New Onset Diabetes After Transplant">New Onset Diabetes After Transplant</a></span></li><li><span class="TLline"><a href="/medgen/821240" ref="tree=MeSH" title="MedGen record for Pre-Gestational Diabetes">Pre-Gestational Diabetes</a></span></li><li><span class="TLline"><a href="/medgen/83928" ref="tree=MeSH" title="MedGen record for Prediabetes syndrome">Prediabetes syndrome</a></span></li><li><span class="TLline"><a href="/medgen/41523" ref="tree=MeSH" title="MedGen record for Type 2 diabetes mellitus">Type 2 diabetes mellitus</a></span></li></ul></li><li><span class="TLline"><a href="/medgen/852424" ref="tree=MeSH" title="MedGen record for Impaired glucose tolerance">Impaired glucose tolerance</a></span><ul><li><span class="TLline"><a href="/medgen/339758" ref="tree=MeSH" title="MedGen record for Abnormal oral glucose tolerance">Abnormal oral glucose tolerance</a></span></li></ul></li></ul></li><li><span class="TLline"><a href="/medgen/695683" ref="tree=MeSH" title="MedGen record for Impaired fasting glucose">Impaired fasting glucose</a></span></li><li><span class="TLline"><a href="/medgen/634939" ref="tree=MeSH" title="MedGen record for Neonatal hyperglycemia">Neonatal hyperglycemia</a></span></li><li><span class="TLline"><a href="/medgen/383702" ref="tree=MeSH" title="MedGen record for Postprandial hyperglycemia">Postprandial hyperglycemia</a></span></li></ul></li></ul></li></ul></div></div></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_112">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Conditions_with_this_feature">Conditions with this feature</h1><a sid="112" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln clinfeat">
|
||
<div class="divPopper rprt" id="rdis_41522"><div><strong>Diabetes mellitus type 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>41522</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0011854</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Type 1 diabetes mellitus (T1D), also designated insulin-dependent diabetes mellitus (IDDM), is a disorder of glucose homeostasis characterized by susceptibility to ketoacidosis in the absence of insulin therapy. It is a genetically heterogeneous autoimmune disease affecting about 0.3% of Caucasian populations (Todd, 1990). Genetic studies of T1D have focused on the identification of loci associated with increased susceptibility to this multifactorial phenotype. The classic phenotype of diabetes mellitus is polydipsia, polyphagia, and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/41522">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_12147"><div><strong>Werner syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>12147</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0043119</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. Individuals with Werner syndrome develop normally until the end of the first decade. The first sign is the lack of a growth spurt during the early teen years. Early findings (usually observed in the 20s) include loss and graying of hair, hoarseness, and scleroderma-like skin changes, followed by bilateral ocular cataracts, type 2 diabetes mellitus, hypogonadism, skin ulcers, and osteoporosis in the 30s. Myocardial infarction and cancer are the most common causes of death; the mean age of death in individuals with Werner syndrome is 54 years.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/12147">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_120531"><div><strong>Greig cephalopolysyndactyly syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>120531</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0265306</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Congenital Abnormality</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Typical Greig cephalopolysyndactyly syndrome (GCPS) is characterized by macrocephaly, widely spaced eyes associated with increased interpupillary distance, preaxial polydactyly with or without postaxial polydactyly, and cutaneous syndactyly. Developmental delay, intellectual disability, or seizures appear to be uncommon manifestations (~<10%) of GCPS and may be more common in individuals with large (>300-kb) deletions that encompass GLI3. Approximately 20% of individuals with GCPS have hypoplasia or agenesis of the corpus callosum.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/120531">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_82708"><div><strong>Leprechaunism syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>82708</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0265344</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">INSR-related severe insulin resistance syndrome (INSR-SIRS) comprises a phenotypic spectrum that is a continuum from the severe phenotype of Donohue syndrome to the milder phenotype of Rabson-Mendenhall syndrome (RMS). Donohue syndrome is characterized by severe insulin resistance (hyperinsulinemia with associated fasting hypoglycemia and postprandial hyperglycemia), severe prenatal growth restriction, postnatal growth failure, hypotonia, developmental delay, characteristic facies (proptosis, infraorbital folds, large, low-set, posteriorly rotated ears, thick vermilion of the upper and lower lips, and gingival hypertrophy), and organomegaly involving the heart, kidneys, liver, spleen, and ovaries. Death usually occurs before age one year. RMS, at the milder end of the spectrum, is characterized by severe insulin resistance that, although not as severe as that of Donohue syndrome, is nonetheless accompanied by fluctuations in blood glucose levels, diabetic ketoacidosis, and – in the second decade – microvascular complications. Findings can range from severe growth delay and intellectual disability to normal growth and development. Facial features can be milder than those of Donohue syndrome. Complications of longstanding hyperglycemia are the most common cause of death. While death usually occurs in the second decade, some affected individuals live longer.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/82708">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_78675"><div><strong>Alstrom syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>78675</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information."><span class="highlight" style="background-color:">C0268425</span></a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Alström syndrome is characterized by cone-rod dystrophy, obesity, progressive bilateral sensorineural hearing impairment, acute infantile-onset cardiomyopathy and/or adolescent- or adult-onset restrictive cardiomyopathy, insulin resistance / type 2 diabetes mellitus (T2DM), nonalcoholic fatty liver disease (NAFLD), and chronic progressive kidney disease. Cone-rod dystrophy presents as progressive visual impairment, photophobia, and nystagmus usually starting between birth and age 15 months. Many individuals lose all perception of light by the end of the second decade, but a minority retain the ability to read large print into the third decade. Children usually have normal birth weight but develop truncal obesity during their first year. Sensorineural hearing loss presents in the first decade in as many as 70% of individuals and may progress to the severe or moderately severe range (40-70 db) by the end of the first to second decade. Insulin resistance is typically accompanied by the skin changes of acanthosis nigricans, and proceeds to T2DM in the majority by the third decade. Nearly all demonstrate hypertriglyceridemia. Other findings can include endocrine abnormalities (hypothyroidism, hypogonadotropic hypogonadism in males, and hyperandrogenism in females), urologic dysfunction / detrusor instability, progressive decrease in renal function, and hepatic disease (ranging from elevated transaminases to steatohepatitis/NAFLD). Approximately 20% of affected individuals have delay in early developmental milestones, most commonly in gross and fine motor skills. About 30% have a learning disability. Cognitive impairment (IQ <70) is very rare. Wide clinical variability is observed among affected individuals, even within the same family.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/78675">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_78783"><div><strong>Rabson-Mendenhall syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>78783</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0271695</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">INSR-related severe insulin resistance syndrome (INSR-SIRS) comprises a phenotypic spectrum that is a continuum from the severe phenotype of Donohue syndrome to the milder phenotype of Rabson-Mendenhall syndrome (RMS). Donohue syndrome is characterized by severe insulin resistance (hyperinsulinemia with associated fasting hypoglycemia and postprandial hyperglycemia), severe prenatal growth restriction, postnatal growth failure, hypotonia, developmental delay, characteristic facies (proptosis, infraorbital folds, large, low-set, posteriorly rotated ears, thick vermilion of the upper and lower lips, and gingival hypertrophy), and organomegaly involving the heart, kidneys, liver, spleen, and ovaries. Death usually occurs before age one year. RMS, at the milder end of the spectrum, is characterized by severe insulin resistance that, although not as severe as that of Donohue syndrome, is nonetheless accompanied by fluctuations in blood glucose levels, diabetic ketoacidosis, and – in the second decade – microvascular complications. Findings can range from severe growth delay and intellectual disability to normal growth and development. Facial features can be milder than those of Donohue syndrome. Complications of longstanding hyperglycemia are the most common cause of death. While death usually occurs in the second decade, some affected individuals live longer.</div>
|
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<div class="spaceAbove nowrap">See: <a href="/medgen/78783">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_137967"><div><strong>Hyperproinsulinemia</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>137967</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0342283</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Insulin (INS; 176730) is produced posttranslationally from its precursor molecule, proinsulin, by site-directed proteolysis in beta-cell granules. Conversion involves cleavage at pairs of basic residues that link both the insulin A and B chains to C-peptide. Human proinsulin conversion has a preferred sequential route, such that cleavage at the B-chain/C-peptide junction occurs first, producing des-31,32 split proinsulin as the major conversion intermediate. Under normal circumstances, proinsulin conversion is largely completed before secretion, and low plasma levels of intact proinsulin and conversion intermediates are found. Structural abnormalities in the proinsulin molecule can impair conversion, leading to the accumulation of proinsulin-like material in the circulation. Such defects show an autosomal dominant mode of inheritance and are the main cause of familial hyperproinsulinemia (summary by Warren-Perry et al., 1997).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/137967">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_90979"><div><strong>Diabetes-deafness syndrome maternally transmitted</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>90979</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0342289</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Maternally inherited diabetes-deafness syndrome (MIDD) is a mitochondrial disorder characterized by onset of sensorineural hearing loss and diabetes in adulthood. Some patients may have additional features observed in mitochondrial disorders, including pigmentary retinopathy, ptosis, cardiomyopathy, myopathy, renal problems, and neuropsychiatric symptoms (Ballinger et al., 1992; Reardon et al., 1992; Guillausseau et al., 2001). The association of diabetes and deafness is observed with Wolfram syndrome (see 222300), Rogers syndrome (249270), and Herrmann syndrome (172500), but all 3 of these disorders have other clinical manifestations.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/90979">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_164212"><div><strong>SHORT syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>164212</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0878684</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">SHORT syndrome is a mnemonic for short stature, hyperextensibility, ocular depression (deeply set eyes), Rieger anomaly, and teething delay. It is now recognized that the features most consistently observed in SHORT syndrome are mild intrauterine growth restriction (IUGR); mild to moderate short stature; partial lipodystrophy (evident in the face, and later in the chest and upper extremities, often sparing the buttocks and legs); and a characteristic facial gestalt. Insulin resistance may be evident in mid-childhood or adolescence, although diabetes mellitus typically does not develop until early adulthood. Other frequent features include Axenfeld-Rieger anomaly or related ocular anterior chamber dysgenesis, delayed dentition and other dental issues, and sensorineural hearing loss.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/164212">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_318591"><div><strong>Familial partial lipodystrophy, Kobberling type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>318591</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1720859</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Familial partial lipodystrophy type 1 (FPLD1), or Kobberling-type lipodystrophy, is characterized by loss of adipose tissue confined to the extremities, with normal or increased distribution of fat on the face, neck, and trunk (Kobberling and Dunnigan, 1986). For a general description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.</div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/318591">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_354526"><div><strong>Familial partial lipodystrophy, Dunnigan type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>354526</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1720860</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Familial partial lipodystrophy (FPLD) is a metabolic disorder characterized by abnormal subcutaneous adipose tissue distribution beginning in late childhood or early adult life. Affected individuals gradually lose fat from the upper and lower extremities and the gluteal and truncal regions, resulting in a muscular appearance with prominent superficial veins. In some patients, adipose tissue accumulates on the face and neck, causing a double chin, fat neck, or cushingoid appearance. Metabolic abnormalities include insulin-resistant diabetes mellitus with acanthosis nigricans and hypertriglyceridemia; hirsutism and menstrual abnormalities occur infrequently. Familial partial lipodystrophy may also be referred to as lipoatrophic diabetes mellitus, but the essential feature is loss of subcutaneous fat (review by Garg, 2004). The disorder may be misdiagnosed as Cushing disease (see 219080) (Kobberling and Dunnigan, 1986; Garg, 2004). Genetic Heterogeneity of Familial Partial Lipodystrophy Familial partial lipodystrophy is a clinically and genetically heterogeneous disorder. Types 1 and 2 were originally described as clinical subtypes: type 1 (FPLD1; 608600), characterized by loss of subcutaneous fat confined to the limbs (Kobberling et al., 1975), and FPLD2, characterized by loss of subcutaneous fat from the limbs and trunk (Dunnigan et al., 1974; Kobberling and Dunnigan, 1986). No genetic basis for FPLD1 has yet been delineated. FPLD3 (604367) is caused by mutation in the PPARG gene (601487) on chromosome 3p25; FPLD4 (613877) is caused by mutation in the PLIN1 gene (170290) on chromosome 15q26; FPLD5 (615238) is caused by mutation in the CIDEC gene (612120) on chromosome 3p25; FPLD6 (615980) is caused by mutation in the LIPE gene (151750) on chromosome 19q13; FPLD7 (606721) is caused by mutation in the CAV1 gene (601047) on chromosome 7q31; FPLD8 (620679), caused by mutation in the ADRA2A gene (104210) on chromosome 10q25; and FPLD9 (620683), caused by mutation in the PLAAT3 gene (613867) on chromosome 11q12.</div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/354526">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_328393"><div><strong>PPARG-related familial partial lipodystrophy</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>328393</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1720861</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial partial lipodystrophy type 3 (FPLD3) is an autosomal dominant disorder characterized by marked loss of subcutaneous fat from the extremities. Calves and lower arms appear prominently muscular. Excess subcutaneous facial, neck, suprascapular, and abdominal fat may be present. Patients have insulin resistance, dyslipidemia, and hypertension, and develop type 2 diabetes (summary by Hegele et al., 2002, Agarwal and Garg, 2002). For a general phenotypic description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/328393">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_371317"><div><strong>Diabetes mellitus, transient neonatal, 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>371317</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1832386</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">6q24-related transient neonatal diabetes mellitus (6q24-TNDM) is defined as transient neonatal diabetes mellitus caused by genetic aberrations of the imprinted locus at 6q24. The cardinal features are: severe intrauterine growth restriction, hyperglycemia that begins in the neonatal period in a term infant and resolves by age 18 months, dehydration, and absence of ketoacidosis. Macroglossia and umbilical hernia may be present. 6q24-TNDM associated with a multilocus imprinting disturbance (MLID) can be associated with marked hypotonia, congenital heart disease, deafness, neurologic features including epilepsy, and renal malformations. Diabetes mellitus usually starts within the first week of life and lasts on average three months but can last longer than a year. Although insulin is usually required initially, the need for insulin gradually declines over time. Intermittent episodes of hyperglycemia may occur in childhood, particularly during intercurrent illnesses. Diabetes mellitus may recur in adolescence or later in adulthood. Women who have had 6q24-TNDM are at risk for relapse during pregnancy.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/371317">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_332288"><div><strong>Permanent neonatal diabetes mellitus-pancreatic and cerebellar agenesis syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>332288</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1836780</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Permanent neonatal diabetes mellitus-pancreatic and cerebellar agenesis syndrome is characterized by neonatal diabetes mellitus associated with cerebellar and/or pancreatic agenesis.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/332288">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_332940"><div><strong>Mandibuloacral dysplasia with type B lipodystrophy</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>332940</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1837756</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mandibuloacral dysplasia with type B lipodystrophy (MADB) is a rare autosomal recessive disorder characterized by postnatal growth retardation, craniofacial anomalies such as mandibular hypoplasia, skeletal anomalies such as progressive osteolysis of the terminal phalanges and clavicles, and skin changes such as mottled hyperpigmentation and atrophy. The lipodystrophy is characterized by generalized loss of subcutaneous fat involving the face, trunk, and extremities. Some patients have a progeroid appearance. Metabolic complications associated with insulin resistance have been reported (Schrander-Stumpel et al., 1992; summary by Simha et al., 2003). For a general phenotypic description of lipodystrophy associated with mandibuloacral dysplasia, see MADA (248370).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/332940">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_324942"><div><strong>Maturity-onset diabetes of the young type 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>324942</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1838100</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">MODY is a form of familial noninsulin-dependent diabetes mellitus (T2D; 125853) and is characterized by an early age of onset (childhood, adolescence, or young adulthood under 25 years) and autosomal dominant inheritance. For a phenotypic description and discussion of genetic heterogeneity of MODY, see 606391.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/324942">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_334557"><div><strong>Male hypergonadotropic hypogonadism-intellectual disability-skeletal anomalies syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>334557</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1843994</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">This syndrome is characterized by hypergonadotropic hypogonadism, intellectual deficit, congenital skeletal anomalies involving the cervical spine and superior ribs, and diabetes mellitus.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/334557">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_342845"><div><strong>Maturity-onset diabetes of the young type 8</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>342845</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1853297</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Maturity-onset diabetes of the young type 8 (MODY8) is characterized by onset of diabetes before age 25 years, with slowly progressive pancreatic exocrine dysfunction, fatty replacement of pancreatic parenchyma (lipomatosis), and development of pancreatic cysts. Patients do not present clinical signs of chronic pancreatitis (summary by Johansson et al., 2018). For a phenotypic description and discussion of genetic heterogeneity of MODY, see 606391.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/342845">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_387801"><div><strong>Congenital lactic acidosis, Saguenay-Lac-Saint-Jean type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>387801</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1857355</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mitochondrial complex IV deficiency nuclear type 5 (MC4DN5) is an autosomal recessive severe metabolic multisystemic disorder with onset in infancy. Features include delayed psychomotor development, impaired intellectual development with speech delay, mild dysmorphic facial features, hypotonia, ataxia, and seizures. There is increased serum lactate and episodic hypoglycemia. Some patients may have cardiomyopathy, abnormal breathing, or liver abnormalities, reflecting systemic involvement. Brain imaging shows lesions in the brainstem and basal ganglia, consistent with a diagnosis of Leigh syndrome (see 256000). Affected individuals tend to have episodic metabolic and/or neurologic crises in early childhood, which often lead to early death (summary by Debray et al., 2011). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.</div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/387801">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_346886"><div><strong>Hereditary motor and sensory neuropathy, Okinawa type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>346886</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1858338</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Okinawa-type hereditary motor and sensory neuropathy (HMSNO) is an autosomal dominant neurodegenerative disorder characterized by young adult onset of proximal or distal muscle weakness and atrophy, muscle cramps, and fasciculations, with later onset of distal sensory impairment. The disorder is slowly progressive and clinically resembles amyotrophic lateral sclerosis (ALS; see 105400) (summary by Ishiura et al., 2012).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/346886">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_347182"><div><strong>Bardet-Biedl syndrome 9</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>347182</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1859567</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">BBS9 is an autosomal recessive disorder characterized by obesity, polydactyly, renal anomalies, retinopathy, and mental retardation (Abu-Safieh et al., 2012). For a general phenotypic description and a discussion of genetic heterogeneity of Bardet-Biedl syndrome, see BBS1 (209900).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/347182">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_351177"><div><strong>Diabetes mellitus, transient neonatal, 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>351177</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1864623</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any transient neonatal diabetes mellitus in which the cause of the disease is a mutation in the KCNJ11 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/351177">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_383033"><div><strong>Maturity-onset diabetes of the young type 9</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>383033</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2677132</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Maturity-onset diabetes of the young (MODY) is a group of several conditions characterized by abnormally high levels of blood glucose, also called blood sugar. These forms of diabetes typically begin before age 30, although they can occur later in life. In MODY, elevated blood glucose arises from reduced production of insulin, which is a hormone produced in the pancreas that helps regulate blood glucose levels. Specifically, insulin controls how much glucose (a type of sugar) is passed from the blood into cells, where it is used as an energy source.\n\nRCAD is associated with a combination of diabetes and kidney or urinary tract abnormalities (unrelated to the elevated blood glucose), most commonly fluid-filled sacs (cysts) in the kidneys. However, the signs and symptoms are variable, even within families, and not everyone with RCAD has both features. Affected individuals may have other features unrelated to diabetes, such as abnormalities of the pancreas or liver or a form of arthritis called gout.\n\nThe different types of MODY are distinguished by their genetic causes. The most common types are HNF1A-MODY (also known as MODY3), accounting for 50 to 70 percent of cases, and GCK-MODY (MODY2), accounting for 30 to 50 percent of cases. Less frequent types include HNF4A-MODY (MODY1) and renal cysts and diabetes (RCAD) syndrome (also known as HNF1B-MODY or MODY5), which each account for 5 to 10 percent of cases. At least ten other types have been identified, and these are very rare.\n\nHNF1A-MODY and HNF4A-MODY have similar signs and symptoms that develop slowly over time. Early signs and symptoms in these types are caused by high blood glucose and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, weight loss, and recurrent skin infections. Over time uncontrolled high blood glucose can damage small blood vessels in the eyes and kidneys. Damage to the light-sensitive tissue at the back of the eye (the retina) causes a condition known as diabetic retinopathy that can lead to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) can lead to kidney failure and end-stage renal disease (ESRD). While these two types of MODY are very similar, certain features are particular to each type. For example, babies with HNF4A-MODY tend to weigh more than average or have abnormally low blood glucose at birth, even though other signs of the condition do not occur until childhood or young adulthood. People with HNF1A-MODY have a higher-than-average risk of developing noncancerous (benign) liver tumors known as hepatocellular adenomas.\n\nGCK-MODY is a very mild type of the condition. People with this type have slightly elevated blood glucose levels, particularly in the morning before eating (fasting blood glucose). However, affected individuals often have no symptoms related to the disorder, and diabetes-related complications are extremely rare.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/383033">Condition Record</a></div></div>
|
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<div class="divPopper rprt" id="rdis_411637"><div><strong>Hypoplastic pancreas-intestinal atresia-hypoplastic gallbalder syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>411637</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2748662</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mitchell-Riley syndrome (MTCHRS) is characterized by neonatal diabetes, pancreatic hypoplasia, intestinal atresia, and gallbladder aplasia or hypoplasia. There is considerable phenotypic overlap between Mitchell-Riley syndrome and Martinez-Frias syndrome (601346), the latter being characterized by the features of the Mitchell-Riley syndrome except for neonatal diabetes, and including tracheoesophageal fistula in some patients (Smith et al., 2010).</div>
|
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<div class="spaceAbove nowrap">See: <a href="/medgen/411637">Condition Record</a></div></div>
|
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<div class="divPopper rprt" id="rdis_444022"><div><strong>Pancreatic hypoplasia-diabetes-congenital heart disease syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>444022</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C2931296</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">This syndrome has characteristics of partial pancreatic agenesis, diabetes mellitus, and heart anomalies (including transposition of the great vessels, ventricular or atrial septal defects, pulmonary stenosis, or patent ductus arteriosis). It has been described in one Japanese family, in which the mother and at least two of her four children were affected (another two children died shortly after birth). The syndrome appears to be inherited as an autosomal dominant trait.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/444022">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_461967"><div><strong>Maturity-onset diabetes of the young type 10</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>461967</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3150617</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">GCK-MODY is a very mild type of the condition. People with this type have slightly elevated blood glucose levels, particularly in the morning before eating (fasting blood glucose). However, affected individuals often have no symptoms related to the disorder, and diabetes-related complications are extremely rare.\n\nHNF1A-MODY and HNF4A-MODY have similar signs and symptoms that develop slowly over time. Early signs and symptoms in these types are caused by high blood glucose and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, weight loss, and recurrent skin infections. Over time uncontrolled high blood glucose can damage small blood vessels in the eyes and kidneys. Damage to the light-sensitive tissue at the back of the eye (the retina) causes a condition known as diabetic retinopathy that can lead to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) can lead to kidney failure and end-stage renal disease (ESRD). While these two types of MODY are very similar, certain features are particular to each type. For example, babies with HNF4A-MODY tend to weigh more than average or have abnormally low blood glucose at birth, even though other signs of the condition do not occur until childhood or young adulthood. People with HNF1A-MODY have a higher-than-average risk of developing noncancerous (benign) liver tumors known as hepatocellular adenomas.\n\nThe different types of MODY are distinguished by their genetic causes. The most common types are HNF1A-MODY (also known as MODY3), accounting for 50 to 70 percent of cases, and GCK-MODY (MODY2), accounting for 30 to 50 percent of cases. Less frequent types include HNF4A-MODY (MODY1) and renal cysts and diabetes (RCAD) syndrome (also known as HNF1B-MODY or MODY5), which each account for 5 to 10 percent of cases. At least ten other types have been identified, and these are very rare.\n\nRCAD is associated with a combination of diabetes and kidney or urinary tract abnormalities (unrelated to the elevated blood glucose), most commonly fluid-filled sacs (cysts) in the kidneys. However, the signs and symptoms are variable, even within families, and not everyone with RCAD has both features. Affected individuals may have other features unrelated to diabetes, such as abnormalities of the pancreas or liver or a form of arthritis called gout.\n\nMaturity-onset diabetes of the young (MODY) is a group of several conditions characterized by abnormally high levels of blood glucose, also called blood sugar. These forms of diabetes typically begin before age 30, although they can occur later in life. In MODY, elevated blood glucose arises from reduced production of insulin, which is a hormone produced in the pancreas that helps regulate blood glucose levels. Specifically, insulin controls how much glucose (a type of sugar) is passed from the blood into cells, where it is used as an energy source.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/461967">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_762097"><div><strong>Mitochondrial complex III deficiency nuclear type 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>762097</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3541471</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Autosomal recessive mitochondrial complex III deficiency is a severe multisystem disorder with onset at birth of lactic acidosis, hypotonia, hypoglycemia, failure to thrive, encephalopathy, and delayed psychomotor development. Visceral involvement, including hepatopathy and renal tubulopathy, may also occur. Many patients die in early childhood, but some may show longer survival (de Lonlay et al., 2001; De Meirleir et al., 2003). Genetic Heterogeneity of Mitochondrial Complex III Deficiency Mitochondrial complex III deficiency can be caused by mutation in several different nuclear-encoded genes. See MC3DN2 (615157), caused by mutation in the TTC19 gene (613814) on chromosome 17p12; MC3DN3 (615158), caused by mutation in the UQCRB gene (191330) on chromosome 8q; MC3DN4 (615159), caused by mutation in the UQCRQ gene (612080) on chromosome 5q31; MC3DN5 (615160), caused by mutation in the UQCRC2 gene (191329) on chromosome 16p12; MC3DN6 (615453), caused by mutation in the CYC1 gene (123980) on chromosome 8q24; MC3DN7 (615824), caused by mutation in the UQCC2 gene (614461) on chromosome 6p21; MC3DN8 (615838), caused by mutation in the LYRM7 gene (615831) on chromosome 5q23; MC3DN9 (616111), caused by mutation in the UQCC3 gene (616097) on chromosome 11q12; and MC3DN10 (618775), caused by mutation in the UQCRFS1 gene (191327) on chromosome 19q12. See also MTYCB (516020) for a discussion of a milder phenotype associated with isolated mitochondrial complex III deficiency and mutations in a mitochondrial-encoded gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/762097">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_815883"><div><strong>Mitochondrial complex III deficiency nuclear type 6</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>815883</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3809553</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mitochondrial complex III deficiency nuclear type 6 (MC3DN6) is an autosomal recessive disorder caused by mitochondrial dysfunction. It is characterized by onset in early childhood of episodic acute lactic acidosis, ketoacidosis, and insulin-responsive hyperglycemia, usually associated with infection. Laboratory studies show decreased activity of mitochondrial complex III. Psychomotor development is normal (summary by Gaignard et al., 2013). For a discussion of genetic heterogeneity of mitochondrial complex III deficiency, see MC3DN1 (124000).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/815883">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_816111"><div><strong>Hypopigmentation-punctate palmoplantar keratoderma syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>816111</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3809781</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Cole disease (COLED) is a rare autosomal dominant disorder characterized by congenital or early-onset punctate keratoderma associated with irregularly shaped hypopigmented macules, which are typically found over the arms and legs but not the trunk or acral regions. Skin biopsies of palmoplantar lesions show nonspecific changes including hyperorthokeratosis, hypergranulosis, and acanthosis. Hypopigmented areas of skin, however, reveal a reduction in melanin content in keratinocytes but not in melanocytes, as well as hyperkeratosis and a normal number of melanocytes. Ultrastructurally, melanocytes show a disproportionately large number of melanosomes in the cytoplasm and dendrites, whereas keratinocytes show a paucity of these organelles, suggestive of impaired melanosome transfer (summary by Eytan et al., 2013). Some patients also exhibit calcinosis cutis or early-onset calcific tendinopathy (Eytan et al., 2013).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/816111">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_862798"><div><strong>Abdominal obesity-metabolic syndrome 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>862798</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4014361</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Any metabolic syndrome in which the cause of the disease is a mutation in the DYRK1B gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/862798">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863240"><div><strong>ACTH-independent macronodular adrenal hyperplasia 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863240</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4014803</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">ACTH-independent macronodular adrenal hyperplasia-2 is an autosomal dominant tumor susceptibility with syndromic incomplete penetrance, as a second hit to the ARMC5 gene is required to develop macronodular hyperplasia (Assie et al., 2013).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863240">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_897640"><div><strong>Maturity-onset diabetes of the young type 13</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>897640</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4225365</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Maturity-onset diabetes of the young (MODY) is a group of several conditions characterized by abnormally high levels of blood glucose, also called blood sugar. These forms of diabetes typically begin before age 30, although they can occur later in life. In MODY, elevated blood glucose arises from reduced production of insulin, which is a hormone produced in the pancreas that helps regulate blood glucose levels. Specifically, insulin controls how much glucose (a type of sugar) is passed from the blood into cells, where it is used as an energy source.\n\nRCAD is associated with a combination of diabetes and kidney or urinary tract abnormalities (unrelated to the elevated blood glucose), most commonly fluid-filled sacs (cysts) in the kidneys. However, the signs and symptoms are variable, even within families, and not everyone with RCAD has both features. Affected individuals may have other features unrelated to diabetes, such as abnormalities of the pancreas or liver or a form of arthritis called gout.\n\nThe different types of MODY are distinguished by their genetic causes. The most common types are HNF1A-MODY (also known as MODY3), accounting for 50 to 70 percent of cases, and GCK-MODY (MODY2), accounting for 30 to 50 percent of cases. Less frequent types include HNF4A-MODY (MODY1) and renal cysts and diabetes (RCAD) syndrome (also known as HNF1B-MODY or MODY5), which each account for 5 to 10 percent of cases. At least ten other types have been identified, and these are very rare.\n\nHNF1A-MODY and HNF4A-MODY have similar signs and symptoms that develop slowly over time. Early signs and symptoms in these types are caused by high blood glucose and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, weight loss, and recurrent skin infections. Over time uncontrolled high blood glucose can damage small blood vessels in the eyes and kidneys. Damage to the light-sensitive tissue at the back of the eye (the retina) causes a condition known as diabetic retinopathy that can lead to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) can lead to kidney failure and end-stage renal disease (ESRD). While these two types of MODY are very similar, certain features are particular to each type. For example, babies with HNF4A-MODY tend to weigh more than average or have abnormally low blood glucose at birth, even though other signs of the condition do not occur until childhood or young adulthood. People with HNF1A-MODY have a higher-than-average risk of developing noncancerous (benign) liver tumors known as hepatocellular adenomas.\n\nGCK-MODY is a very mild type of the condition. People with this type have slightly elevated blood glucose levels, particularly in the morning before eating (fasting blood glucose). However, affected individuals often have no symptoms related to the disorder, and diabetes-related complications are extremely rare.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/897640">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1717586"><div><strong>Permanent neonatal diabetes mellitus 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1717586</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5393570</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Permanent neonatal diabetes mellitus (PNDM) is characterized by the onset of hyperglycemia within the first six months of life (mean age: 7 weeks; range: birth to age 26 weeks). The diabetes mellitus is associated with partial or complete insulin deficiency. Clinical manifestations at the time of diagnosis include hyperglycemia, glycosuria, osmotic polyuria, severe dehydration, and history of intrauterine growth deficiency. Therapy with insulin and/or oral hypoglycemic medications (in some molecular causes of PNDM) can correct the hyperglycemia and result in dramatic catch-up growth. The course of PNDM varies by genotype.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1717586">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1713823"><div><strong>Diabetes mellitus, permanent neonatal 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1713823</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5394296</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Permanent neonatal diabetes mellitus (PNDM) is characterized by the onset of hyperglycemia within the first six months of life (mean age: 7 weeks; range: birth to age 26 weeks). The diabetes mellitus is associated with partial or complete insulin deficiency. Clinical manifestations at the time of diagnosis include hyperglycemia, glycosuria, osmotic polyuria, severe dehydration, and history of intrauterine growth deficiency. Therapy with insulin and/or oral hypoglycemic medications (in some molecular causes of PNDM) can correct the hyperglycemia and result in dramatic catch-up growth. The course of PNDM varies by genotype.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1713823">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1717271"><div><strong>Diabetes mellitus, permanent neonatal 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1717271</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5394303</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Permanent neonatal diabetes mellitus (PNDM) is characterized by the onset of hyperglycemia within the first six months of life (mean age: 7 weeks; range: birth to age 26 weeks). The diabetes mellitus is associated with partial or complete insulin deficiency. Clinical manifestations at the time of diagnosis include hyperglycemia, glycosuria, osmotic polyuria, severe dehydration, and history of intrauterine growth deficiency. Therapy with insulin and/or oral hypoglycemic medications (in some molecular causes of PNDM) can correct the hyperglycemia and result in dramatic catch-up growth. The course of PNDM varies by genotype.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1717271">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1711191"><div><strong>Diabetes mellitus, permanent neonatal 4</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1711191</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5394307</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Permanent neonatal diabetes mellitus (PNDM) is characterized by the onset of hyperglycemia within the first six months of life (mean age: 7 weeks; range: birth to age 26 weeks). The diabetes mellitus is associated with partial or complete insulin deficiency. Clinical manifestations at the time of diagnosis include hyperglycemia, glycosuria, osmotic polyuria, severe dehydration, and history of intrauterine growth deficiency. Therapy with insulin and/or oral hypoglycemic medications (in some molecular causes of PNDM) can correct the hyperglycemia and result in dramatic catch-up growth. The course of PNDM varies by genotype.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1711191">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1757618"><div><strong>Mandibuloacral dysplasia with type A lipodystrophy</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1757618</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5399785</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mandibuloacral dysplasia with type A lipodystrophy (MADA) is an autosomal recessive disorder characterized by growth retardation, craniofacial anomalies with mandibular hypoplasia, skeletal abnormalities with progressive osteolysis of the distal phalanges and clavicles, and pigmentary skin changes. The lipodystrophy is characterized by a marked acral loss of fatty tissue with normal or increased fatty tissue in the neck and trunk. Some patients may show progeroid features. Metabolic complications can arise due to insulin resistance and diabetes (Young et al., 1971; Simha and Garg, 2002; summary by Garavelli et al., 2009). See also MAD type B (MADB; 608612), which is caused by mutation in the ZMPSTE24 gene (606480).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1757618">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1773574"><div><strong>Cone-rod synaptic disorder syndrome, congenital nonprogressive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1773574</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5436505</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Congenital nonprogressive cone-rod synaptic disorder syndrome (CRSDS) is characterized by retinal and neurodevelopmental disease as well as occasional anomalies of glucose homeostasis. Patients exhibit low vision, photophobia, and nystagmus, and show an electronegative waveform in response to bright flash under dark adaptation on electroretinography, with severely reduced and delayed light-adapted responses. Neurodevelopmental features include poor to no language and autistic behaviors (Mechaussier et al., 2020).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1773574">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1812715"><div><strong>Combined oxidative phosphorylation deficiency 54</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1812715</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5676912</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Combined oxidative phosphorylation deficiency-54 (COXPD54) is an autosomal recessive disorder with pleiotropic multisystem presentations resulting from a disruption in mitochondrial transcription and translation. The phenotype is highly variable. Many patients have early-onset sensorineural hearing loss, sometimes in isolation, and sometimes associated with global developmental delay or primary ovarian failure. Other features may include peripheral hypertonia, seizures, muscle weakness, behavioral abnormalities, and leukoencephalopathy on brain imaging. Serum lactate may or may not be elevated (summary by Hochberg et al., 2021). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1812715">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1841222"><div><strong>Multiple mitochondrial dysfunctions syndrome 7</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1841222</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5830586</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mitochondrial dysfunctions syndrome-7 (MMDS7) is an autosomal recessive disorder characterized by a clinical spectrum ranging from neonatal fatal glycine encephalopathy to an attenuated phenotype of developmental delay, behavioral problems, limited epilepsy, and variable movement problems (Arribas-Carreira et al., 2023). For a general description and a discussion of genetic heterogeneity of multiple mitochondrial dysfunctions syndrome, see MMDS1 (605711).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1841222">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1846436"><div><strong>Lipodystrophy, familial partial, type 8</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1846436</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5882744</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Familial partial lipodystrophy type 8 (FPLD8) is an autosomal dominant disorder characterized by abnormal distribution of subcutaneous adipose tissue. Affected individuals showed selective loss of subcutaneous adipose tissue from the limbs, resulting in a muscular appearance, beginning around 13 to 15 years of age. There is also abnormal accumulation of subcutaneous adipose tissue in the dorsal neck and face, as well as in the posterior thoracic and abdominal regions. The disorder is associated with metabolic abnormalities, including diabetes mellitus and hyperlipidemia (Garg et al., 2016). For a general description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1846436">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1847991"><div><strong>Lipodystrophy, congenital generalized, type 5</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1847991</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5882745</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Congenital generalized lipodystrophy type 5 (CGL5) is an autosomal recessive metabolic disorder characterized by childhood onset of lipodystrophy, severe nonalcoholic fatty liver disease, dyslipidemia, hypertriglyceridemia, low HDL, and insulin-resistant diabetes mellitus. Affected individuals also have short stature (Payne et al., 2014). For a discussion of genetic heterogeneity of congenital generalized lipodystrophy, see CGL1 (608594).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1847991">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1845936"><div><strong>Lipodystrophy, familial partial, type 9</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1845936</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C5882746</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial partial lipodystrophy type 9 (FPLD9) is an autosomal recessive metabolic disorder characterized by the loss of adipose tissue resulting in a lean appearance with muscular hypertrophy, usually most apparent in the limbs and trunk. Some patients have more generalized lipoatrophy, whereas others have abnormal fat accumulation in the face and neck regions and show cushingoid or acromegalic facial features. The disorder is associated with insulin-resistant diabetes mellitus, dyslipidemia, low HDL, and hepatic steatosis. Symptom onset is usually in the first decade. Females tend to have hirsutism and polycystic ovary syndrome, whereas males have gynecomastia. Most patients also have neurologic involvement, including demyelinating polyneuropathy (in most) and delayed development with intellectual disability (in about half) (Schuermans et al., 2023). For a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1845936">Condition Record</a></div></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_862798" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Abdominal obesity-metabolic syndrome 3</a></div>
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||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_863240" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">ACTH-independent macronodular adrenal hyperplasia 2</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_78675" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Alstrom syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_347182" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bardet-Biedl syndrome 9</a></div>
|
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1812715" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Combined oxidative phosphorylation deficiency 54</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (43)', lessText: 'Show less', nodeBefore: 0"><span id="clinMore">
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1773574" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Cone-rod synaptic disorder syndrome, congenital nonprogressive</a></div>
|
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_387801" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital lactic acidosis, Saguenay-Lac-Saint-Jean type</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_41522" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus type 1</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1713823" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus, permanent neonatal 2</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1717271" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus, permanent neonatal 3</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1711191" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus, permanent neonatal 4</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_371317" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus, transient neonatal, 1</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_351177" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes mellitus, transient neonatal, 3</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_90979" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Diabetes-deafness syndrome maternally transmitted</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_354526" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial partial lipodystrophy, Dunnigan type</a></div>
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||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_318591" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial partial lipodystrophy, Kobberling type</a></div>
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||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_120531" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Greig cephalopolysyndactyly syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_346886" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hereditary motor and sensory neuropathy, Okinawa type</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_137967" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyperproinsulinemia</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_816111" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypopigmentation-punctate palmoplantar keratoderma syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_411637" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypoplastic pancreas-intestinal atresia-hypoplastic gallbalder syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_82708" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Leprechaunism syndrome</a></div>
|
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1847991" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Lipodystrophy, congenital generalized, type 5</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1846436" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Lipodystrophy, familial partial, type 8</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1845936" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Lipodystrophy, familial partial, type 9</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_334557" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Male hypergonadotropic hypogonadism-intellectual disability-skeletal anomalies syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1757618" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mandibuloacral dysplasia with type A lipodystrophy</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_332940" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mandibuloacral dysplasia with type B lipodystrophy</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_461967" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Maturity-onset diabetes of the young type 10</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_897640" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Maturity-onset diabetes of the young type 13</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_324942" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Maturity-onset diabetes of the young type 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_342845" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Maturity-onset diabetes of the young type 8</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_383033" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Maturity-onset diabetes of the young type 9</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_762097" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mitochondrial complex III deficiency nuclear type 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_815883" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mitochondrial complex III deficiency nuclear type 6</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1841222" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Multiple mitochondrial dysfunctions syndrome 7</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_444022" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pancreatic hypoplasia-diabetes-congenital heart disease syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1717586" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Permanent neonatal diabetes mellitus 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_332288" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Permanent neonatal diabetes mellitus-pancreatic and cerebellar agenesis syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_328393" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">PPARG-related familial partial lipodystrophy</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_78783" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Rabson-Mendenhall syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_164212" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">SHORT syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_12147" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Werner syndrome</a></div></span></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_105">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Professional_guidelines">Professional guidelines</h1><a sid="105" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">PubMed<a class="help jig-ncbi-popper" data-jig="ncbipopper" href="#guidelinesHelpPM"><img class="pulldown" src="//static.pubmed.gov/portal/portal3rc.fcgi/4223267/img/4204968" /></a></h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/34307650">Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Samsu N</span><br />
|
||
<span class="medgenPMjournal">Biomed Res Int</span>
|
||
2021;2021:1497449.
|
||
Epub 2021 Jul 8
|
||
doi: 10.1155/2021/1497449.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34307650" target="_blank">34307650</a><a href="/pmc/articles/PMC8285185" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/33371325">Gestational Diabetes: Overview with Emphasis on Medical Management.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lende M,
|
||
Rijhsinghani A</span><br />
|
||
<span class="medgenPMjournal">Int J Environ Res Public Health</span>
|
||
2020 Dec 21;17(24)
|
||
doi: 10.3390/ijerph17249573.
|
||
<span class="bold">PMID: </span><a href="/pubmed/33371325" target="_blank">33371325</a><a href="/pmc/articles/PMC7767324" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/28121636">Perioperative Hyperglycemia Management: An Update.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Duggan EW,
|
||
Carlson K,
|
||
Umpierrez GE</span><br />
|
||
<span class="medgenPMjournal">Anesthesiology</span>
|
||
2017 Mar;126(3):547-560.
|
||
doi: 10.1097/ALN.0000000000001515.
|
||
<span class="bold">PMID: </span><a href="/pubmed/28121636" target="_blank">28121636</a><a href="/pmc/articles/PMC5309204" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22hyperglycemia%22%5Btiab%3A~0%5D)%20AND%20(%22english%20and%20humans%22%5BFilter%5D)%20AND%20(%20(%22practice%20guideline%22%5BFilter%5D)%20OR%20(practice*%5Btitl%5D%20AND%20(guideline%5Btitl%5D%20OR%20parameter%5Btitl%5D%20OR%20resource%5Btitl%5D%20OR%20bulletin%5Btitl%5D%20OR%20best%5Btitl%5D))%20OR%20(genetic*%5Btitl%5D%20AND%20(evaluation%5Btitl%5D%20OR%20counseling%5Btitl%5D%20OR%20screening%5Btitl%5D%20OR%20test*%5Btitl%5D))%20OR%20(clinical%5Btitl%5D%20AND%20((expert%5Btitl%5D%20AND%20consensus%5Btitl%5D)%20OR%20utility%5Btitl%5D%20OR%20guideline*%5Btitl%5D))%20OR%20(management%5Btitl%5D%20AND%20(clinical%5Btitl%5D%20OR%20diagnos*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20pain%5Btitl%5D%20OR%20surveillance%5Btitl%5D%20OR%20emergency%5Btitl%5D%20OR%20guideline*%5Btitl%5D%20OR%20therap*))%20OR%20(treatment%5Btitl%5D%20AND%20((evaluation%5Btitl%5D%20AND%20diagnosis%5Btitl%5D)%20OR%20(assessment%5Btitl%5D%20AND%20prevention%5Btitl%5D)%20OR%20therap*))%20OR%20(Diagnos*%5Btitl%5D%20AND%20(prenatal%5Btitl%5D%20OR%20treatment%5Btitl%5D%20OR%20follow-up%5Btitl%5D%20OR%20statement%5Btitl%5D%20OR%20criteria%5Btitl%5D%20OR%20newborn%5Btitl%5D%20OR%20differential%5Btitl%5D%20OR%20neonatal%5Btitl%5D%20OR%20neonate%5Btitl%5D))%20OR%20(guideline*%5Btitl%5D%20AND%20(pharmacogenetic*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20evidence-based%5Btitl%5D%20OR%20consensus%5Btitl%5D%20OR%20(technical%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20(molecular%5Btitl%5D%20AND%20testing%5Btitl%5D)))%20OR%20(risk%5Btitl%5D%20AND%20assessment%5Btitl%5D)%20OR%20(recommendation*%5Btitl%5D%20AND%20(statement%5Btitl%5D%20OR%20Evidence-based%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(care%20AND%20((Patient%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20primary%5Btitl%5D%20OR%20psychosocial%5Btitl%5D))%20OR%20(Health%5Btitl%5D%20AND%20supervision%5Btitl%5D)%20OR%20(statement%5Btitl%5D%20AND%20(policy%5Btitl%5D%20OR%20position%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(pharmacogenetics%5Btitl%5D%20AND%20(Dosing%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20genotype*%5Btitl%5D%20OR%20drug*%5Btitl%5D))%20OR%20(Chemotherapy%5Btitl%5D%20AND%20decision*%5Btitl%5D)%20OR%20(screening%5Btitl%5D%20AND%20(newborn%5Btitl%5D%20OR%20neonat*%5Btitl%5D%20OR%20detection%5Btitl%5D%20OR%20diagnos*%5Btitl%5D))%20OR%20(criteria%5Btitl%5D%20OR%20genotype*%5Btitl%5D)%20)%20NOT%20(%22Case%20reports%22%5BPublication%20type%5D%20OR%20%22clinical%20study%22%5BPublication%20Type%5D%20OR%20%22randomized%20controlled%20trial%22%5BPublication%20Type%5D)" title="PubMed search">See all (2151)</a></div></div>
|
||
</div>
|
||
<div class="display-none help-popup" id="guidelinesHelpPM">These guidelines are articles in PubMed that match specific search criteria developed by MedGen to capture the most relevant practice guidelines. This list may not be comprehensive and may include broader topics as well. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div><div class="display-none help-popup" id="guidelinesHelpCurated">These guidelines are manually curated by the MedGen team
|
||
to supplement articles available in PubMed. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div>
|
||
<div class="portlet mgSection" id="ID_103">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Recent_clinical_studies">Recent clinical studies</h1><a sid="103" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">Etiology</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/37985310">Drug-induced hyperglycemia and diabetes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Heurtebize MA,
|
||
Faillie JL</span><br />
|
||
<span class="medgenPMjournal">Therapie</span>
|
||
2024 Mar-Apr;79(2):221-238.
|
||
Epub 2023 Oct 31
|
||
doi: 10.1016/j.therap.2023.09.010.
|
||
<span class="bold">PMID: </span><a href="/pubmed/37985310" target="_blank">37985310</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30418830">Stress-induced hyperglycaemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Mifsud S,
|
||
Schembri EL,
|
||
Gruppetta M</span><br />
|
||
<span class="medgenPMjournal">Br J Hosp Med (Lond)</span>
|
||
2018 Nov 2;79(11):634-639.
|
||
doi: 10.12968/hmed.2018.79.11.634.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30418830" target="_blank">30418830</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/28836444">Optimizing the Treatment of Steroid-Induced Hyperglycemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Wallace MD,
|
||
Metzger NL</span><br />
|
||
<span class="medgenPMjournal">Ann Pharmacother</span>
|
||
2018 Jan;52(1):86-90.
|
||
Epub 2017 Aug 24
|
||
doi: 10.1177/1060028017728297.
|
||
<span class="bold">PMID: </span><a href="/pubmed/28836444" target="_blank">28836444</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25466161">Dysglycemia associated with quinolones.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">El Ghandour S,
|
||
Azar ST</span><br />
|
||
<span class="medgenPMjournal">Prim Care Diabetes</span>
|
||
2015 Jun;9(3):168-71.
|
||
Epub 2014 Nov 23
|
||
doi: 10.1016/j.pcd.2014.10.006.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25466161" target="_blank">25466161</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/19454391">Glucocorticoid-induced hyperglycemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Clore JN,
|
||
Thurby-Hay L</span><br />
|
||
<span class="medgenPMjournal">Endocr Pract</span>
|
||
2009 Jul-Aug;15(5):469-74.
|
||
doi: 10.4158/EP08331.RAR.
|
||
<span class="bold">PMID: </span><a href="/pubmed/19454391" target="_blank">19454391</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20Etiology%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (20957)</a></div><h3 class="subhead">Diagnosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/37985310">Drug-induced hyperglycemia and diabetes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Heurtebize MA,
|
||
Faillie JL</span><br />
|
||
<span class="medgenPMjournal">Therapie</span>
|
||
2024 Mar-Apr;79(2):221-238.
|
||
Epub 2023 Oct 31
|
||
doi: 10.1016/j.therap.2023.09.010.
|
||
<span class="bold">PMID: </span><a href="/pubmed/37985310" target="_blank">37985310</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/28121636">Perioperative Hyperglycemia Management: An Update.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Duggan EW,
|
||
Carlson K,
|
||
Umpierrez GE</span><br />
|
||
<span class="medgenPMjournal">Anesthesiology</span>
|
||
2017 Mar;126(3):547-560.
|
||
doi: 10.1097/ALN.0000000000001515.
|
||
<span class="bold">PMID: </span><a href="/pubmed/28121636" target="_blank">28121636</a><a href="/pmc/articles/PMC5309204" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25466161">Dysglycemia associated with quinolones.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">El Ghandour S,
|
||
Azar ST</span><br />
|
||
<span class="medgenPMjournal">Prim Care Diabetes</span>
|
||
2015 Jun;9(3):168-71.
|
||
Epub 2014 Nov 23
|
||
doi: 10.1016/j.pcd.2014.10.006.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25466161" target="_blank">25466161</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/24103089">Glucocorticoid-induced hyperglycemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Perez A,
|
||
Jansen-Chaparro S,
|
||
Saigi I,
|
||
Bernal-Lopez MR,
|
||
Miñambres I,
|
||
Gomez-Huelgas R</span><br />
|
||
<span class="medgenPMjournal">J Diabetes</span>
|
||
2014 Jan;6(1):9-20.
|
||
Epub 2013 Oct 29
|
||
doi: 10.1111/1753-0407.12090.
|
||
<span class="bold">PMID: </span><a href="/pubmed/24103089" target="_blank">24103089</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/19454391">Glucocorticoid-induced hyperglycemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Clore JN,
|
||
Thurby-Hay L</span><br />
|
||
<span class="medgenPMjournal">Endocr Pract</span>
|
||
2009 Jul-Aug;15(5):469-74.
|
||
doi: 10.4158/EP08331.RAR.
|
||
<span class="bold">PMID: </span><a href="/pubmed/19454391" target="_blank">19454391</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20Diagnosis%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (11278)</a></div><h3 class="subhead">Therapy</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/36493795">Continuous glucose monitoring and metrics for clinical trials: an international consensus statement.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Battelino T,
|
||
Alexander CM,
|
||
Amiel SA,
|
||
Arreaza-Rubin G,
|
||
Beck RW,
|
||
Bergenstal RM,
|
||
Buckingham BA,
|
||
Carroll J,
|
||
Ceriello A,
|
||
Chow E,
|
||
Choudhary P,
|
||
Close K,
|
||
Danne T,
|
||
Dutta S,
|
||
Gabbay R,
|
||
Garg S,
|
||
Heverly J,
|
||
Hirsch IB,
|
||
Kader T,
|
||
Kenney J,
|
||
Kovatchev B,
|
||
Laffel L,
|
||
Maahs D,
|
||
Mathieu C,
|
||
Mauricio D,
|
||
Nimri R,
|
||
Nishimura R,
|
||
Scharf M,
|
||
Del Prato S,
|
||
Renard E,
|
||
Rosenstock J,
|
||
Saboo B,
|
||
Ueki K,
|
||
Umpierrez GE,
|
||
Weinzimer SA,
|
||
Phillip M</span><br />
|
||
<span class="medgenPMjournal">Lancet Diabetes Endocrinol</span>
|
||
2023 Jan;11(1):42-57.
|
||
Epub 2022 Dec 6
|
||
doi: 10.1016/S2213-8587(22)00319-9.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36493795" target="_blank">36493795</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/33508907">Treatment of Diabetic Kidney Disease: Current and Future.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yamazaki T,
|
||
Mimura I,
|
||
Tanaka T,
|
||
Nangaku M</span><br />
|
||
<span class="medgenPMjournal">Diabetes Metab J</span>
|
||
2021 Jan;45(1):11-26.
|
||
Epub 2021 Jan 22
|
||
doi: 10.4093/dmj.2020.0217.
|
||
<span class="bold">PMID: </span><a href="/pubmed/33508907" target="_blank">33508907</a><a href="/pmc/articles/PMC7850867" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30817388">Glucose control in the ICU.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Gunst J,
|
||
De Bruyn A,
|
||
Van den Berghe G</span><br />
|
||
<span class="medgenPMjournal">Curr Opin Anaesthesiol</span>
|
||
2019 Apr;32(2):156-162.
|
||
doi: 10.1097/ACO.0000000000000706.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30817388" target="_blank">30817388</a><a href="/pmc/articles/PMC6774765" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30415158">Update on glucose in critical care.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lheureux O,
|
||
Prevedello D,
|
||
Preiser JC</span><br />
|
||
<span class="medgenPMjournal">Nutrition</span>
|
||
2019 Mar;59:14-20.
|
||
Epub 2018 Jul 12
|
||
doi: 10.1016/j.nut.2018.06.027.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30415158" target="_blank">30415158</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/18945920">Medical management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy: a consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Nathan DM,
|
||
Buse JB,
|
||
Davidson MB,
|
||
Ferrannini E,
|
||
Holman RR,
|
||
Sherwin R,
|
||
Zinman B;
|
||
American Diabetes Association;
|
||
European Association for Study of Diabetes</span><br />
|
||
<span class="medgenPMjournal">Diabetes Care</span>
|
||
2009 Jan;32(1):193-203.
|
||
Epub 2008 Oct 22
|
||
doi: 10.2337/dc08-9025.
|
||
<span class="bold">PMID: </span><a href="/pubmed/18945920" target="_blank">18945920</a><a href="/pmc/articles/PMC2606813" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20Therapy%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (17496)</a></div><h3 class="subhead">Prognosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38725059">Association between the stress hyperglycemia ratio and 28-day all-cause mortality in critically ill patients with sepsis: a retrospective cohort study and predictive model establishment based on machine learning.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yan F,
|
||
Chen X,
|
||
Quan X,
|
||
Wang L,
|
||
Wei X,
|
||
Zhu J</span><br />
|
||
<span class="medgenPMjournal">Cardiovasc Diabetol</span>
|
||
2024 May 9;23(1):163.
|
||
doi: 10.1186/s12933-024-02265-4.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38725059" target="_blank">38725059</a><a href="/pmc/articles/PMC11084034" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/37833697">Prognostic significance of the stress hyperglycemia ratio in critically ill patients.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Li L,
|
||
Zhao M,
|
||
Zhang Z,
|
||
Zhou L,
|
||
Zhang Z,
|
||
Xiong Y,
|
||
Hu Z,
|
||
Yao Y</span><br />
|
||
<span class="medgenPMjournal">Cardiovasc Diabetol</span>
|
||
2023 Oct 13;22(1):275.
|
||
doi: 10.1186/s12933-023-02005-0.
|
||
<span class="bold">PMID: </span><a href="/pubmed/37833697" target="_blank">37833697</a><a href="/pmc/articles/PMC10576399" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/37434784">The cause-effect relation of tuberculosis on incidence of diabetes mellitus.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Bisht MK,
|
||
Dahiya P,
|
||
Ghosh S,
|
||
Mukhopadhyay S</span><br />
|
||
<span class="medgenPMjournal">Front Cell Infect Microbiol</span>
|
||
2023;13:1134036.
|
||
Epub 2023 Jun 26
|
||
doi: 10.3389/fcimb.2023.1134036.
|
||
<span class="bold">PMID: </span><a href="/pubmed/37434784" target="_blank">37434784</a><a href="/pmc/articles/PMC10330781" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/26242743">Clinical review: intensive care unit acquired weakness.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Hermans G,
|
||
Van den Berghe G</span><br />
|
||
<span class="medgenPMjournal">Crit Care</span>
|
||
2015 Aug 5;19(1):274.
|
||
doi: 10.1186/s13054-015-0993-7.
|
||
<span class="bold">PMID: </span><a href="/pubmed/26242743" target="_blank">26242743</a><a href="/pmc/articles/PMC4526175" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/23531958">Glucocorticoid-induced hyperglycemia.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Kwon S,
|
||
Hermayer KL,
|
||
Hermayer K</span><br />
|
||
<span class="medgenPMjournal">Am J Med Sci</span>
|
||
2013 Apr;345(4):274-277.
|
||
doi: 10.1097/MAJ.0b013e31828a6a01.
|
||
<span class="bold">PMID: </span><a href="/pubmed/23531958" target="_blank">23531958</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20Prognosis%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (8364)</a></div><h3 class="subhead">Clinical prediction guides</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38725059">Association between the stress hyperglycemia ratio and 28-day all-cause mortality in critically ill patients with sepsis: a retrospective cohort study and predictive model establishment based on machine learning.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yan F,
|
||
Chen X,
|
||
Quan X,
|
||
Wang L,
|
||
Wei X,
|
||
Zhu J</span><br />
|
||
<span class="medgenPMjournal">Cardiovasc Diabetol</span>
|
||
2024 May 9;23(1):163.
|
||
doi: 10.1186/s12933-024-02265-4.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38725059" target="_blank">38725059</a><a href="/pmc/articles/PMC11084034" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/29174219">Familial diabetes of adulthood: A bin of ignorance that needs to be addressed.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Prudente S,
|
||
Ludovico O,
|
||
Trischitta V</span><br />
|
||
<span class="medgenPMjournal">Nutr Metab Cardiovasc Dis</span>
|
||
2017 Dec;27(12):1053-1059.
|
||
Epub 2017 Oct 26
|
||
doi: 10.1016/j.numecd.2017.10.017.
|
||
<span class="bold">PMID: </span><a href="/pubmed/29174219" target="_blank">29174219</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/20144385">Clinical need for continuous glucose monitoring in the hospital.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Joseph JI,
|
||
Hipszer B,
|
||
Mraovic B,
|
||
Chervoneva I,
|
||
Joseph M,
|
||
Grunwald Z</span><br />
|
||
<span class="medgenPMjournal">J Diabetes Sci Technol</span>
|
||
2009 Nov 1;3(6):1309-18.
|
||
doi: 10.1177/193229680900300611.
|
||
<span class="bold">PMID: </span><a href="/pubmed/20144385" target="_blank">20144385</a><a href="/pmc/articles/PMC2787031" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/20144381">Perioperative blood glucose monitoring in the general surgical population.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Raju TA,
|
||
Torjman MC,
|
||
Goldberg ME</span><br />
|
||
<span class="medgenPMjournal">J Diabetes Sci Technol</span>
|
||
2009 Nov 1;3(6):1282-7.
|
||
doi: 10.1177/193229680900300607.
|
||
<span class="bold">PMID: </span><a href="/pubmed/20144381" target="_blank">20144381</a><a href="/pmc/articles/PMC2787027" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/11822975">Heart rate variability and cardiovascular mortality.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Villareal RP,
|
||
Liu BC,
|
||
Massumi A</span><br />
|
||
<span class="medgenPMjournal">Curr Atheroscler Rep</span>
|
||
2002 Mar;4(2):120-7.
|
||
doi: 10.1007/s11883-002-0035-1.
|
||
<span class="bold">PMID: </span><a href="/pubmed/11822975" target="_blank">11822975</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20Clinical%20prediction%20guides%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (11354)</a></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_104">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Recent_systematic_reviews">Recent systematic reviews</h1><a sid="104" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln">
|
||
<div class="nl"><a target="_blank" href="/pubmed/38240484">Society of Critical Care Medicine Guidelines on Glycemic Control for Critically Ill Children and Adults 2024.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Honarmand K,
|
||
Sirimaturos M,
|
||
Hirshberg EL,
|
||
Bircher NG,
|
||
Agus MSD,
|
||
Carpenter DL,
|
||
Downs CR,
|
||
Farrington EA,
|
||
Freire AX,
|
||
Grow A,
|
||
Irving SY,
|
||
Krinsley JS,
|
||
Lanspa MJ,
|
||
Long MT,
|
||
Nagpal D,
|
||
Preiser JC,
|
||
Srinivasan V,
|
||
Umpierrez GE,
|
||
Jacobi J</span><br />
|
||
<span class="medgenPMjournal">Crit Care Med</span>
|
||
2024 Apr 1;52(4):e161-e181.
|
||
Epub 2024 Jan 19
|
||
doi: 10.1097/CCM.0000000000006174.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38240484" target="_blank">38240484</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/29879890">Pathophysiology of Type 2 Diabetes in Children and Adolescents.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Valaiyapathi B,
|
||
Gower B,
|
||
Ashraf AP</span><br />
|
||
<span class="medgenPMjournal">Curr Diabetes Rev</span>
|
||
2020;16(3):220-229.
|
||
doi: 10.2174/1573399814666180608074510.
|
||
<span class="bold">PMID: </span><a href="/pubmed/29879890" target="_blank">29879890</a><a href="/pmc/articles/PMC7516333" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/28809366">Oral manifestations of Diabetes Mellitus. A systematic review.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Mauri-Obradors E,
|
||
Estrugo-Devesa A,
|
||
Jané-Salas E,
|
||
Viñas M,
|
||
López-López J</span><br />
|
||
<span class="medgenPMjournal">Med Oral Patol Oral Cir Bucal</span>
|
||
2017 Sep 1;22(5):e586-e594.
|
||
doi: 10.4317/medoral.21655.
|
||
<span class="bold">PMID: </span><a href="/pubmed/28809366" target="_blank">28809366</a><a href="/pmc/articles/PMC5694181" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/28292654">Vinegar consumption can attenuate postprandial glucose and insulin responses; a systematic review and meta-analysis of clinical trials.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Shishehbor F,
|
||
Mansoori A,
|
||
Shirani F</span><br />
|
||
<span class="medgenPMjournal">Diabetes Res Clin Pract</span>
|
||
2017 May;127:1-9.
|
||
Epub 2017 Mar 2
|
||
doi: 10.1016/j.diabres.2017.01.021.
|
||
<span class="bold">PMID: </span><a href="/pubmed/28292654" target="_blank">28292654</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/27624087">Hyperglycaemia and risk of adverse perinatal outcomes: systematic review and meta-analysis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Farrar D,
|
||
Simmonds M,
|
||
Bryant M,
|
||
Sheldon TA,
|
||
Tuffnell D,
|
||
Golder S,
|
||
Dunne F,
|
||
Lawlor DA</span><br />
|
||
<span class="medgenPMjournal">BMJ</span>
|
||
2016 Sep 13;354:i4694.
|
||
doi: 10.1136/bmj.i4694.
|
||
<span class="bold">PMID: </span><a href="/pubmed/27624087" target="_blank">27624087</a><a href="/pmc/articles/PMC5021824" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Hyperglycemia%22%20AND%20systematic%5Bsb%5D%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (740)</a></div></div>
|
||
</div>
|
||
</div></div></div></div></div></div></div>
|
||
<div id="messagearea_bottom">
|
||
|
||
</div>
|
||
<div class=" bottom">
|
||
|
||
</div>
|
||
|
||
</div>
|
||
</div>
|
||
<div class="supplemental col three_col last">
|
||
<h2 class="offscreen_noflow">Supplemental Content</h2>
|
||
|
||
<div>
|
||
|
||
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|
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||
<div class="portlet_content ln"><ul><li><a href="/gtr/tests?term=C0020456%5bDISCUI%5d&filter=method%3A2%5F8" target="_blank">Deletion/duplication analysis (3)</a></li>
|
||
<li><a href="/gtr/tests?term=C0020456%5bDISCUI%5d&filter=method%3A2%5F7" target="_blank">Sequence analysis of the entire coding region (3)</a></li>
|
||
<li class="portletSeeAll portletSeeAllPad"><total><a href="/gtr/tests?term=C0020456%5bDISCUI%5d" target="_blank">See all (3)</a></total></li>
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<div class="portlet_content ln"><ul><li><a href="https://clinicaltrials.gov/search?cond=Hyperglycemia" target="_blank">ClinicalTrials.gov</a></li></ul></div>
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<div class="portlet_content ln"><ul class="a_poppers"><li><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22hyperglycemia%22%5Btiab%3A~0%5D)%20AND%20(%22english%20and%20humans%22%5BFilter%5D)%20AND%20(%20(%22practice%20guideline%22%5BFilter%5D)%20OR%20(practice*%5Btitl%5D%20AND%20(guideline%5Btitl%5D%20OR%20parameter%5Btitl%5D%20OR%20resource%5Btitl%5D%20OR%20bulletin%5Btitl%5D%20OR%20best%5Btitl%5D))%20OR%20(genetic*%5Btitl%5D%20AND%20(evaluation%5Btitl%5D%20OR%20counseling%5Btitl%5D%20OR%20screening%5Btitl%5D%20OR%20test*%5Btitl%5D))%20OR%20(clinical%5Btitl%5D%20AND%20((expert%5Btitl%5D%20AND%20consensus%5Btitl%5D)%20OR%20utility%5Btitl%5D%20OR%20guideline*%5Btitl%5D))%20OR%20(management%5Btitl%5D%20AND%20(clinical%5Btitl%5D%20OR%20diagnos*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20pain%5Btitl%5D%20OR%20surveillance%5Btitl%5D%20OR%20emergency%5Btitl%5D%20OR%20guideline*%5Btitl%5D%20OR%20therap*))%20OR%20(treatment%5Btitl%5D%20AND%20((evaluation%5Btitl%5D%20AND%20diagnosis%5Btitl%5D)%20OR%20(assessment%5Btitl%5D%20AND%20prevention%5Btitl%5D)%20OR%20therap*))%20OR%20(Diagnos*%5Btitl%5D%20AND%20(prenatal%5Btitl%5D%20OR%20treatment%5Btitl%5D%20OR%20follow-up%5Btitl%5D%20OR%20statement%5Btitl%5D%20OR%20criteria%5Btitl%5D%20OR%20newborn%5Btitl%5D%20OR%20differential%5Btitl%5D%20OR%20neonatal%5Btitl%5D%20OR%20neonate%5Btitl%5D))%20OR%20(guideline*%5Btitl%5D%20AND%20(pharmacogenetic*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20evidence-based%5Btitl%5D%20OR%20consensus%5Btitl%5D%20OR%20(technical%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20(molecular%5Btitl%5D%20AND%20testing%5Btitl%5D)))%20OR%20(risk%5Btitl%5D%20AND%20assessment%5Btitl%5D)%20OR%20(recommendation*%5Btitl%5D%20AND%20(statement%5Btitl%5D%20OR%20Evidence-based%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(care%20AND%20((Patient%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20primary%5Btitl%5D%20OR%20psychosocial%5Btitl%5D))%20OR%20(Health%5Btitl%5D%20AND%20supervision%5Btitl%5D)%20OR%20(statement%5Btitl%5D%20AND%20(policy%5Btitl%5D%20OR%20position%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(pharmacogenetics%5Btitl%5D%20AND%20(Dosing%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20genotype*%5Btitl%5D%20OR%20drug*%5Btitl%5D))%20OR%20(Chemotherapy%5Btitl%5D%20AND%20decision*%5Btitl%5D)%20OR%20(screening%5Btitl%5D%20AND%20(newborn%5Btitl%5D%20OR%20neonat*%5Btitl%5D%20OR%20detection%5Btitl%5D%20OR%20diagnos*%5Btitl%5D))%20OR%20(criteria%5Btitl%5D%20OR%20genotype*%5Btitl%5D)%20)%20NOT%20(%22Case%20reports%22%5BPublication%20type%5D%20OR%20%22clinical%20study%22%5BPublication%20Type%5D%20OR%20%22randomized%20controlled%20trial%22%5BPublication%20Type%5D)" title="PubMed search">PubMed</a><div class="help-popup">See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div></li><li><a target="_blank" href="/books/?term=((%22clinical%20guidelines%22%5BResource%20Type%5D)%20OR%20%22practice%20guideline%22%5BPublication%20Type%5D)%20AND%20(%22Hyperglycemia%22)">Bookshelf</a><div class="help-popup">See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div></li></ul></div>
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<div class="portlet_content ln"><ul><li><a href="https://vsearch.nlm.nih.gov/vivisimo/cgi-bin/query-meta?v:project=medlineplus&query=Hyperglycemia" target="_blank">MedlinePlus</a></li></ul></div>
|
||
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||
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<div class="portlet brieflink">
|
||
<div class="portlet_head">
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<h3>Reviews</h3>
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<a href="/pubmed/clinical?term=Hyperglycemia" ref="ncbi_uid=&discoId=gtr_reviews&linkpos=1&linkpostotal=2" target="_blank">PubMed Clinical Queries</a>
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<a href="/pubmed?term=Hyperglycemia%20AND%20humans[mesh]%20AND%20review[publication%20type]" ref="ncbi_uid=&discoId=gtr_reviews&linkpos=2&linkpostotal=2" target="_blank">Reviews in PubMed</a>
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<li class="brieflinkpopper">
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||
<a class="brieflinkpopperctrl" href="/clinvar?LinkName=medgen_clinvar&from_uid=5689" ref="log$=recordlinks">ClinVar</a>
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||
<div class="brieflinkpop offscreen_noflow">Related medical variations</div>
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||
</li>
|
||
<li class="brieflinkpopper">
|
||
<a class="brieflinkpopperctrl" href="/gtr/tests?term=C0020456[DISCUI]" ref="log$=recordlinks">GTR</a>
|
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<div class="brieflinkpop offscreen_noflow">Related information in GTR</div>
|
||
</li>
|
||
<li class="brieflinkpopper">
|
||
<a class="brieflinkpopperctrl" href="/gtr/tests?term=C0020456[DISCUI]&test_type=Clinical" ref="log$=recordlinks">GTR(Clinical)</a>
|
||
<div class="brieflinkpop offscreen_noflow">Clinical tests in GTR</div>
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||
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||
<a class="brieflinkpopperctrl" href="/mesh?LinkName=medgen_mesh&from_uid=5689" ref="log$=recordlinks">MeSH</a>
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<div class="brieflinkpop offscreen_noflow">Related Medical Subject Headings</div>
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<a class="brieflinkpopperctrl" href="/pmc?LinkName=medgen_pmc&from_uid=5689" ref="log$=recordlinks">PMC Articles</a>
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<div class="brieflinkpop offscreen_noflow">Related information in PubMed Central Links</div>
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<a class="brieflinkpopperctrl" href="/pubmed?LinkName=medgen_pubmed&from_uid=5689" ref="log$=recordlinks">PubMed</a>
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<div class="brieflinkpop offscreen_noflow">Related literature resources in PubMed</div>
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|
||
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||
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||
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<h3>Recent activity</h3>
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<a name="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory" sid="1" realname="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory" cmd="ClearHT" href="?cmd=ClearHT&" onclick="return false;" id="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.ClearHistory">
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Clear
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<a name="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle" sid="1" realname="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle" class="HTOn" cmd="HTOff" href="?cmd=HTOff&" onclick="return false;" id="EntrezSystem2.PEntrez.MedGen.MedGen_ResultsPanel.HistoryDisplay.HistoryToggle">
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Turn Off
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Turn On
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|
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<ul id="activity">
|
||
<li class="ra_rcd ralinkpopper two_line">
|
||
<a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=1" href="/portal/utils/pageresolver.fcgi?recordid=67d2f02967c23b31e0a1d2ee">Hyperglycemia</a>
|
||
<div class="ralinkpop offscreen_noflow">Hyperglycemia<div class="brieflinkpopdesc"></div></div>
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<div class="tertiary">MedGen</div>
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<div class="tertiary">MedGen</div>
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