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<meta name="keywords" content="C4073162, elevated glycated haemoglobin, elevated glycated hemoglobin, elevated glycosylated haemoglobin, elevated glycosylated hemoglobin, elevated haemoglobin a1c, elevated hba1c, elevated hemoglobin a1c, finding, hba1c increased, hemoglobin a1c increased, hgba1c increased, increased hba1c levels, autosomal dominant, autosomal recessive, birth defects, chromosomal disease, chromosome, clinical features, clinical findings, clinical genetics, clinical recommendations, clinvar, congenital chromosomal disease, consumer genetic resources, cytogenetic location, disease characteristics, disease definitions, disease descriptions, disease ontology, disease synonyms, disease vocabulary, dysmorphology, entrez, familial disease, gene, gene-disease relationship, genereviews, genetic disease, genetic disorder, genetic terminology, genetic testing registry, genetics home reference, genomic disease, gtr, hereditary disease, heritable disease, hpo, human phenotype ontology, inherited disease, management guidelines, maternal inheritance, medgen, medical genetics, medical subject headings, mesh, mitochondrial inheritance, mode of inheritance, national center for biotechnology information, national institutes of health, national library of medicine, ncbi, nih, nlm, omim, ordo, orphanet, paternal inheritance, phenome, position statements, professional practice guidelines, rare disease, reference sequence, refseq, snomed ct, syndrome, undiagnosed diseases, x-linked recessive" /><meta name="description" content="An increased concentration of hemoglobin A1c (HbA1c), which is the product of nonenzymatic attachment of a hexose molecule to the N-terminal amino acid of the hemoglobin molecule. This reaction is dependent on blood glucose concentration, and therefore reflects the mean glucose concentration over the previous 8 to 12 weeks. The HbA1c level provides a better indication of long-term glycemic control than one-time blood or urinary glucose measurements." /><meta name="robots" content="index,nofollow,noarchive" />
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<!--
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UID=892798
|
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ConceptID=C4073162
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-->
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<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Elevated hemoglobin A1c</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>892798</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.">C4073162</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Finding</dd></dl></div></div><table class="medgenTable"><tbody><tr><td>Synonyms:</td>
|
||
<td>Elevated HbA1c; Elevated hemoglobin A1C</td></tr>
|
||
<tr><td colspan="2" class="small"> </td></tr><tr><td>HPO:</td>
|
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<td><a target="_blank" title="Human Phenotype Ontology" href="https://hpo.jax.org/app/browse/term/HP:0040217">HP:0040217</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>
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||
<div class="portlet_content ln">An increased concentration of hemoglobin A1c (HbA1c), which is the product of nonenzymatic attachment of a hexose molecule to the N-terminal amino acid of the hemoglobin molecule. This reaction is dependent on blood glucose concentration, and therefore reflects the mean glucose concentration over the previous 8 to 12 weeks. The HbA1c level provides a better indication of long-term glycemic control than one-time blood or urinary glucose measurements. [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 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 unavailable round" title="Clinical test">C</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 unavailable" title="ClinVar">V</span></span><span class="TLline">Elevated hemoglobin A1c</span></li></ul></div></div></div></div></div><div id="tabMGEN"><div class="ds_tree"><ul><li><span class="TLline"><a href="/medgen/867443" ref="tree=MeSH" title="MedGen record for Phenotypic abnormality">Phenotypic abnormality</a></span><ul><li><span class="TLline"><a href="/medgen/163092" ref="tree=MeSH" title="MedGen record for Abnormality of blood and blood-forming tissues">Abnormality of blood and blood-forming tissues</a></span><ul><li><span class="TLline"><a href="/medgen/488883" ref="tree=MeSH" title="MedGen record for Abnormal erythrocyte morphology">Abnormal erythrocyte morphology</a></span><ul><li><span class="TLline"><a href="/medgen/776552" ref="tree=MeSH" title="MedGen record for Abnormal hemoglobin">Abnormal hemoglobin</a></span><ul><li><span class="matched_ds">Elevated hemoglobin A1c</span></li></ul></li></ul></li></ul></li></ul></li></ul></div></div></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_112">
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||
<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>
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<div class="portlet_content ln clinfeat">
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||
<div class="divPopper rprt" id="rdis_2685"><div><strong>Bloom syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>2685</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.">C0005859</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bloom syndrome (BSyn) is characterized by severe pre- and postnatal growth deficiency, immune abnormalities, sensitivity to sunlight, insulin resistance, and a high risk for many cancers that occur at an early age. Despite their very small head circumference, most affected individuals have normal intellectual ability. Women may be fertile but often have early menopause, and men tend to be infertile, with only one confirmed case of paternity. Serious medical complications that are more common than in the general population and that also appear at unusually early ages include cancer of a wide variety of types and anatomic sites, diabetes mellitus as a result of insulin resistance, chronic obstructive pulmonary disease, and hypothyroidism.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/2685">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_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>
|
||
<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>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/78675">Condition Record</a></div></div>
|
||
<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>
|
||
<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>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/354526">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_318593"><div><strong>Congenital generalized lipodystrophy type 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>318593</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.">C1720863</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Congenital Abnormality</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Berardinelli-Seip congenital lipodystrophy (BSCL) is usually diagnosed at birth or soon thereafter. Because of the absence of functional adipocytes, lipid is stored in other tissues, including muscle and liver. Affected individuals develop insulin resistance and approximately 25%-35% develop diabetes mellitus between ages 15 and 20 years. Hepatomegaly secondary to hepatic steatosis and skeletal muscle hypertrophy occur in all affected individuals. Hypertrophic cardiomyopathy is reported in 20%-25% of affected individuals and is a significant cause of morbidity from cardiac failure and early mortality.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/318593">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>
|
||
<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_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>
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||
<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>
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||
<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/383033">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863698"><div><strong>Polyendocrine-polyneuropathy syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863698</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.">C4015261</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">A rare genetic disease with characteristics of childhood onset of multiple endocrine manifestations in combination with central and peripheral nervous system abnormalities. Reported signs and symptoms include postnatal growth retardation, moderate intellectual disability, hypogonadotropic hypogonadism, insulin-dependent diabetes mellitus, central hypothyroidism, demyelinating sensorimotor polyneuropathy, cerebellar and pyramidal signs. Progressive hearing loss and a hypoplastic pituitary gland have also been described. Brain imaging shows moderate white matter abnormalities.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863698">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_863873"><div><strong>Juvenile-onset diabetes mellitus-central and peripheral neurodegeneration syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>863873</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.">C4015436</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Combined cerebellar and peripheral ataxia with hearing loss and diabetes mellitus (ACPHD) is an autosomal recessive multisystem disorder including defects in glucose metabolism, diffuse neurodegeneration, multiple hormone deficiencies, severe growth retardation with possible growth hormone deficiencies, and subtle osseous changes suggesting early-onset bone dysplasia (summary by Ozon et al., 2020).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/863873">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_908119"><div><strong>Maturity-onset diabetes of the young type 14</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>908119</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.">C4225299</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<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/908119">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_934614"><div><strong>Seckel syndrome 10</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>934614</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.">C4310647</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Any Seckel syndrome in which the cause of the disease is a mutation in the NSMCE2 gene.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/934614">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1704861"><div><strong>Abdominal obesity-metabolic syndrome 4</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1704861</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.">C5231430</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Abdominal obesity-metabolic syndrome-4 (AOMS4) is characterized by obesity, hypertension, and early-onset coronary artery disease. Most affected individuals meet the criteria for metabolic syndrome, including elevated triglyceride and low high-density lipoprotein levels, and type 2 diabetes (Esteghamat et al., 2019). For a discussion of the genetic heterogeneity of abdominal obesity-metabolic syndrome, see AOMS1 (605552).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1704861">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_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_1741713"><div><strong>Mandibuloacral dysplasia progeroid syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1741713</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.">C5436867</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Mandibuloacral dysplasia progeroid syndrome (MDPS) is an autosomal recessive severe laminopathy-like disorder characterized by growth retardation, bone resorption, arterial calcification, renal glomerulosclerosis, and hypertension (Elouej et al., 2020).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1741713">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1782107"><div><strong>Microcephaly, epilepsy, and diabetes syndrome 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1782107</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.">C5543294</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">MEDS2 is characterized by severe microcephaly and neonatal/early-onset epilepsy and diabetes (De Franco et al., 2020). For a discussion of genetic heterogeneity of microcephaly, epilepsy, and diabetes syndrome, see MEDS1 (614231).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1782107">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1799164"><div><strong>Combined oxidative phosphorylation defect type 26</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1799164</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.">C5567741</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
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<div class="spaceAbove">Peripheral neuropathy with variable spasticity, exercise intolerance, and developmental delay (PNSED) is an autosomal recessive multisystemic disorder with highly variable manifestations, even within the same family. Some patients present in infancy with hypotonia and global developmental delay with poor or absent motor skill acquisition and poor growth, whereas others present as young adults with exercise intolerance and muscle weakness. All patients have signs of a peripheral neuropathy, usually demyelinating, with distal muscle weakness and atrophy and distal sensory impairment; many become wheelchair-bound. Additional features include spasticity, extensor plantar responses, contractures, cerebellar signs, seizures, short stature, and rare involvement of other organ systems, including the heart, pancreas, and kidney. Biochemical analysis may show deficiencies in mitochondrial respiratory complex enzyme activities in patient tissue, although this is not always apparent. Lactate is frequently increased, suggesting mitochondrial dysfunction (Powell et al., 2015; Argente-Escrig et al., 2022). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1799164">Condition Record</a></div></div>
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<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>
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<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>
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||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1704861" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Abdominal obesity-metabolic syndrome 4</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_2685" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bloom syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1799164" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Combined oxidative phosphorylation defect type 26</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_318593" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital generalized lipodystrophy type 2</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (20)', 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_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_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_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_863873" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Juvenile-onset diabetes mellitus-central and peripheral neurodegeneration syndrome</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_1741713" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mandibuloacral dysplasia progeroid syndrome</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_908119" 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 14</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_1782107" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Microcephaly, epilepsy, and diabetes syndrome 2</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_863698" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Polyendocrine-polyneuropathy syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_934614" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Seckel syndrome 10</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/26340427">The treatment of type 1 diabetes mellitus with agents approved for type 2 diabetes mellitus.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Munir KM,
|
||
Davis SN</span><br />
|
||
<span class="medgenPMjournal">Expert Opin Pharmacother</span>
|
||
2015;16(15):2331-41.
|
||
Epub 2015 Sep 4
|
||
doi: 10.1517/14656566.2015.1084502.
|
||
<span class="bold">PMID: </span><a href="/pubmed/26340427" target="_blank">26340427</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/26307902">FASTING VERSUS POSTPRANDIAL HYPERGLYCEMIA AS A TREATMENT TARGET TO LOWER ELEVATED HEMOGLOBIN A1C.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Shaefer C,
|
||
Reid T,
|
||
Vlajnic A,
|
||
Zhou R,
|
||
DiGenio A</span><br />
|
||
<span class="medgenPMjournal">Endocr Pract</span>
|
||
2015 Dec;21(12):1323-32.
|
||
Epub 2015 Aug 26
|
||
doi: 10.4158/EP14498.OR.
|
||
<span class="bold">PMID: </span><a href="/pubmed/26307902" target="_blank">26307902</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25740817">Pilot study evaluating the feasibility and initial outcomes of a primary care weight loss intervention with peer coaches.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Dutton GR,
|
||
Phillips JM,
|
||
Kukkamalla M,
|
||
Cherrington AL,
|
||
Safford MM</span><br />
|
||
<span class="medgenPMjournal">Diabetes Educ</span>
|
||
2015 Jun;41(3):361-8.
|
||
Epub 2015 Mar 4
|
||
doi: 10.1177/0145721715575356.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25740817" target="_blank">25740817</a><a href="/pmc/articles/PMC4511264" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22elevated%20hemoglobin%20a1c%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 (4)</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/38861258">Prediabetes Prevalence by Adverse Social Determinants of Health in Adolescents.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Harrison C,
|
||
Peyyety V,
|
||
Rodriguez Gonzalez A,
|
||
Chivate R,
|
||
Qin X,
|
||
Zupa MF,
|
||
Ragavan MI,
|
||
Vajravelu ME</span><br />
|
||
<span class="medgenPMjournal">JAMA Netw Open</span>
|
||
2024 Jun 3;7(6):e2416088.
|
||
doi: 10.1001/jamanetworkopen.2024.16088.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38861258" target="_blank">38861258</a><a href="/pmc/articles/PMC11167496" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35075523">Elevated hemoglobin A1c level and bariatric surgery complications.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Nwokedi U,
|
||
Zia M,
|
||
Xu J,
|
||
Sadhu AR,
|
||
Baio FE,
|
||
Kash BS,
|
||
Sherman V,
|
||
Tariq N</span><br />
|
||
<span class="medgenPMjournal">Surg Endosc</span>
|
||
2022 Sep;36(9):6915-6923.
|
||
Epub 2022 Jan 24
|
||
doi: 10.1007/s00464-022-09030-2.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35075523" target="_blank">35075523</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34997363">Managing Patients Undergoing Orthopedic Surgery to Improve Glycemic Outcomes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Diaz R,
|
||
DeJesus J</span><br />
|
||
<span class="medgenPMjournal">Curr Diab Rep</span>
|
||
2022 Jan 6;21(12):68.
|
||
doi: 10.1007/s11892-021-01434-z.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34997363" target="_blank">34997363</a><a href="/pmc/articles/PMC8741266" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/22990344">Screening for the high-risk diabetic foot: a 60-second tool (2012).</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Sibbald RG,
|
||
Ayello EA,
|
||
Alavi A,
|
||
Ostrow B,
|
||
Lowe J,
|
||
Botros M,
|
||
Goodman L,
|
||
Woo K,
|
||
Smart H</span><br />
|
||
<span class="medgenPMjournal">Adv Skin Wound Care</span>
|
||
2012 Oct;25(10):465-76; quiz 477-8.
|
||
doi: 10.1097/01.ASW.0000421460.21773.7b.
|
||
<span class="bold">PMID: </span><a href="/pubmed/22990344" target="_blank">22990344</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/6334441">Decreased cognitive function in aging non-insulin-dependent diabetic patients.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Perlmuter LC,
|
||
Hakami MK,
|
||
Hodgson-Harrington C,
|
||
Ginsberg J,
|
||
Katz J,
|
||
Singer DE,
|
||
Nathan DM</span><br />
|
||
<span class="medgenPMjournal">Am J Med</span>
|
||
1984 Dec;77(6):1043-8.
|
||
doi: 10.1016/0002-9343(84)90186-4.
|
||
<span class="bold">PMID: </span><a href="/pubmed/6334441" target="_blank">6334441</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Elevated%20hemoglobin%20A1c%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 (106)</a></div><h3 class="subhead">Diagnosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38286224">Clinical laboratory tests and dementia incidence: A prospective cohort study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Huang YY,
|
||
Wang HF,
|
||
Wu BS,
|
||
Ou YN,
|
||
Ma LZ,
|
||
Yang L,
|
||
Cheng W,
|
||
Yu JT</span><br />
|
||
<span class="medgenPMjournal">J Affect Disord</span>
|
||
2024 Apr 15;351:1-7.
|
||
Epub 2024 Jan 28
|
||
doi: 10.1016/j.jad.2024.01.226.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38286224" target="_blank">38286224</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/38367007">Diabetic striatopathy: a case report.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Guan Y,
|
||
Yuan L,
|
||
Yuan L</span><br />
|
||
<span class="medgenPMjournal">Neurocase</span>
|
||
2023 Jun;29(3):90-91.
|
||
Epub 2024 Feb 17
|
||
doi: 10.1080/13554794.2024.2317788.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38367007" target="_blank">38367007</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/37929017">Case Report: Insulin hypersensitivity in youth with type 1 diabetes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Alkhatib EH,
|
||
Grundman JB,
|
||
Adamusiak AM,
|
||
Bellin MD,
|
||
Brooks JP,
|
||
Buckley KS,
|
||
Janssen EM,
|
||
Kitcharoensakkul M,
|
||
McNerney KP,
|
||
Pfeifer TL,
|
||
Polk BI,
|
||
Marks BE</span><br />
|
||
<span class="medgenPMjournal">Front Endocrinol (Lausanne)</span>
|
||
2023;14:1226231.
|
||
Epub 2023 Oct 20
|
||
doi: 10.3389/fendo.2023.1226231.
|
||
<span class="bold">PMID: </span><a href="/pubmed/37929017" target="_blank">37929017</a><a href="/pmc/articles/PMC10624121" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35236109">Elevated Hemoglobin A1c Is Associated With Leaky Plaque Neovasculature as Detected by Dynamic Contrast-Enhanced Magnetic Resonance Imaging.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Sun B,
|
||
Ge X,
|
||
Li X,
|
||
Zhang J,
|
||
Zhao Z,
|
||
Liu X,
|
||
Zhou Y,
|
||
Xu J,
|
||
Zhao H,
|
||
Sun J</span><br />
|
||
<span class="medgenPMjournal">Arterioscler Thromb Vasc Biol</span>
|
||
2022 Apr;42(4):504-513.
|
||
Epub 2022 Mar 3
|
||
doi: 10.1161/ATVBAHA.121.317190.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35236109" target="_blank">35236109</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/22990344">Screening for the high-risk diabetic foot: a 60-second tool (2012).</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Sibbald RG,
|
||
Ayello EA,
|
||
Alavi A,
|
||
Ostrow B,
|
||
Lowe J,
|
||
Botros M,
|
||
Goodman L,
|
||
Woo K,
|
||
Smart H</span><br />
|
||
<span class="medgenPMjournal">Adv Skin Wound Care</span>
|
||
2012 Oct;25(10):465-76; quiz 477-8.
|
||
doi: 10.1097/01.ASW.0000421460.21773.7b.
|
||
<span class="bold">PMID: </span><a href="/pubmed/22990344" target="_blank">22990344</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Elevated%20hemoglobin%20A1c%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 (67)</a></div><h3 class="subhead">Therapy</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/36701590">The National Clinical Care Commission Report to Congress: Leveraging Federal Policies and Programs to Prevent Diabetes in People With Prediabetes.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Boltri JM,
|
||
Tracer H,
|
||
Strogatz D,
|
||
Idzik S,
|
||
Schumacher P,
|
||
Fukagawa N,
|
||
Leake E,
|
||
Powell C,
|
||
Shell D,
|
||
Wu S,
|
||
Herman WH</span><br />
|
||
<span class="medgenPMjournal">Diabetes Care</span>
|
||
2023 Feb 1;46(2):e39-e50.
|
||
doi: 10.2337/dc22-0620.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36701590" target="_blank">36701590</a><a href="/pmc/articles/PMC9887613" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35075523">Elevated hemoglobin A1c level and bariatric surgery complications.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Nwokedi U,
|
||
Zia M,
|
||
Xu J,
|
||
Sadhu AR,
|
||
Baio FE,
|
||
Kash BS,
|
||
Sherman V,
|
||
Tariq N</span><br />
|
||
<span class="medgenPMjournal">Surg Endosc</span>
|
||
2022 Sep;36(9):6915-6923.
|
||
Epub 2022 Jan 24
|
||
doi: 10.1007/s00464-022-09030-2.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35075523" target="_blank">35075523</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34103256">The Association Between Hemoglobin A1c Levels and Inflatable Penile Prosthesis Infection: Analysis of US Insurance Claims Data.</a></div>
|
||
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<div class="nl"><a target="_blank" href="/pubmed/27338653">Association Between Hemoglobin A1c and Surgical Morbidity in Elective Foot and Ankle Surgery.</a></div>
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Dux K,
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<div class="nl"><a target="_blank" href="/pubmed/24887924">Elevated hemoglobin A1c is associated with readmission but not complications.</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/38286224">Clinical laboratory tests and dementia incidence: A prospective cohort study.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Huang YY,
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Wang HF,
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Wu BS,
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Ou YN,
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Ma LZ,
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Berlin KS,
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Klages KL,
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<span class="bold">PMID: </span><a href="/pubmed/30973748" target="_blank">30973748</a></div>
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2016 Jan;51(1):32-7.
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<span class="bold">PMID: </span><a href="/pubmed/26024974" target="_blank">26024974</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/22990344">Screening for the high-risk diabetic foot: a 60-second tool (2012).</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Sibbald RG,
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Alavi A,
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<span class="bold">PMID: </span><a href="/pubmed/22990344" target="_blank">22990344</a></div>
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Elevated%20hemoglobin%20A1c%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 (50)</a></div><h3 class="subhead">Clinical prediction guides</h3>
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<div class="nl"><a target="_blank" href="/pubmed/38861258">Prediabetes Prevalence by Adverse Social Determinants of Health in Adolescents.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Harrison C,
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Peyyety V,
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Chivate R,
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doi: 10.1001/jamanetworkopen.2024.16088.
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<span class="bold">PMID: </span><a href="/pubmed/38861258" target="_blank">38861258</a><a href="/pmc/articles/PMC11167496" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/38286224">Clinical laboratory tests and dementia incidence: A prospective cohort study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Huang YY,
|
||
Wang HF,
|
||
Wu BS,
|
||
Ou YN,
|
||
Ma LZ,
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||
Yang L,
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||
Cheng W,
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Yu JT</span><br />
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<span class="medgenPMjournal">J Affect Disord</span>
|
||
2024 Apr 15;351:1-7.
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||
Epub 2024 Jan 28
|
||
doi: 10.1016/j.jad.2024.01.226.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38286224" target="_blank">38286224</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35075523">Elevated hemoglobin A1c level and bariatric surgery complications.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Nwokedi U,
|
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Zia M,
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Xu J,
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Sadhu AR,
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Baio FE,
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Kash BS,
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Sherman V,
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Tariq N</span><br />
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<span class="medgenPMjournal">Surg Endosc</span>
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2022 Sep;36(9):6915-6923.
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Epub 2022 Jan 24
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||
<span class="bold">PMID: </span><a href="/pubmed/35075523" target="_blank">35075523</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34806607">Diabetes Mellitus, Elevated Hemoglobin A1c, and Glycated Albumin Are Associated with the Presence of All-Cause Dementia and Alzheimer's Disease: The JPSC-AD Study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Noguchi-Shinohara M,
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Yuki-Nozaki S,
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Abe C,
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Mori A,
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Horimoto M,
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Yokogawa M,
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Ishida N,
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Suga Y,
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Ishizaki J,
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Ishimiya M,
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Nakamura H,
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Komai K,
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Nakamura H,
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Shibata M,
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Ohara T,
|
||
Hata J,
|
||
Ninomiya T,
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||
Yamada M;
|
||
Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD) study group</span><br />
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||
<span class="medgenPMjournal">J Alzheimers Dis</span>
|
||
2022;85(1):235-247.
|
||
doi: 10.3233/JAD-215153.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34806607" target="_blank">34806607</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/27338653">Association Between Hemoglobin A1c and Surgical Morbidity in Elective Foot and Ankle Surgery.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Domek N,
|
||
Dux K,
|
||
Pinzur M,
|
||
Weaver F,
|
||
Rogers T</span><br />
|
||
<span class="medgenPMjournal">J Foot Ankle Surg</span>
|
||
2016 Sep-Oct;55(5):939-43.
|
||
Epub 2016 Jun 20
|
||
doi: 10.1053/j.jfas.2016.04.009.
|
||
<span class="bold">PMID: </span><a href="/pubmed/27338653" target="_blank">27338653</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Elevated%20hemoglobin%20A1c%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 (58)</a></div></div>
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<div class="nl"><a target="_blank" href="/pubmed/39888910">Prevalence of diabetic retinopathy and its associated factors among adults in East African countries: A systematic review and meta-analysis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Abuhay HW,
|
||
Tesfie TK,
|
||
Alemayehu MA,
|
||
Agimas MC,
|
||
Yismaw GA,
|
||
Alemu GG,
|
||
Derseh NM,
|
||
Yirsaw BG</span><br />
|
||
<span class="medgenPMjournal">PLoS One</span>
|
||
2025;20(1):e0316160.
|
||
Epub 2025 Jan 31
|
||
doi: 10.1371/journal.pone.0316160.
|
||
<span class="bold">PMID: </span><a href="/pubmed/39888910" target="_blank">39888910</a><a href="/pmc/articles/PMC11785277" target="_blank" class="PubMedFree">Free PMC Article</a></div>
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Elevated%20hemoglobin%20A1c%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 (1)</a></div></div>
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