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<!--
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||
UID=377848
|
||
ConceptID=C1853193
|
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-->
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<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Recurrent skin infections</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>377848</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.">C1853193</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>Skin infections, recurrent</td></tr>
|
||
<tr><td><span class="bold">SNOMED CT: </span></td>
|
||
<td>Recurrent skin infection (736979001); Recurrent infection of skin (736979001)</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:0001581">HP:0001581</a></td></tr>
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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">Infections of the skin that happen multiple times. [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 Ccolor round" title="Clinical test"><a target="_blank" href="/gtr/tests/?term=C1853193[DISCUI]&test_type=Clinical" ref="ncbi_uid=377848">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=377848" ref="ncbi_uid=377848">V</a></span></span><span class="TLline">Recurrent skin infections</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/867388" ref="tree=MeSH" title="MedGen record for Abnormality of the immune system">Abnormality of the immune system</a></span><ul><li><span class="TLline"><a href="/medgen/869194" ref="tree=MeSH" title="MedGen record for Abnormality of immune system physiology">Abnormality of immune system physiology</a></span><ul><li><span class="TLline"><a href="/medgen/868411" ref="tree=MeSH" title="MedGen record for Abnormal inflammatory response">Abnormal inflammatory response</a></span><ul><li><span class="TLline"><a href="/medgen/868409" ref="tree=MeSH" title="MedGen record for Increased inflammatory response">Increased inflammatory response</a></span><ul><li><span class="TLline"><a href="/medgen/849741" ref="tree=MeSH" title="MedGen record for Inflammatory abnormality of the skin">Inflammatory abnormality of the skin</a></span><ul><li><span class="matched_ds">Recurrent skin infections</span></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></div></div></div></div>
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||
</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>
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||
<div class="portlet_content ln clinfeat">
|
||
<div class="divPopper rprt" id="rdis_66323"><div><strong>Biotinidase deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>66323</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.">C0220754</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Multiple carboxylase deficiency (MCD) is an autosomal recessive metabolic disorder characterized primarily by cutaneous and neurologic abnormalities. Symptoms result from the patient's inability to reutilize biotin, a necessary nutrient. Sweetman (1981) recognized that multiple carboxylase deficiency could be classified into early (see 253270) and late forms. The early form showed higher urinary excretion of 3-hydroxyisovaleric acid and 3-hydroxypropionic acid than the late form and was associated with normal plasma biotin concentrations. Sweetman (1981) proposed a defect in holocarboxylase synthetase and intestinal biotin absorption, respectively. Some patients with biotinidase deficiency present in infancy (Baumgartner et al., 1985; Kalayci et al., 1994), and some individuals with this deficiency are asymptomatic (Wolf et al., 1997).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/66323">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_336848"><div><strong>X-linked lymphoproliferative disease due to XIAP deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>336848</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.">C1845076</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">X-linked lymphoproliferative disease (XLP) in general is characterized by an inappropriate immune response to Epstein-Barr virus (EBV) infection leading to hemophagocytic lymphohistiocytosis (HLH) or severe mononucleosis, dysgammaglobulinemia, and lymphoproliferative disease (malignant lymphoma). The condition primarily affects males. XLP has two recognizable subtypes, XLP1 (due to pathogenic variants in SH2D1A) and XLP2 (due to pathogenic variants in XIAP). HLH / fulminant infectious mononucleosis is the most common presentation regardless of subtype. HLH is characterized as an acute illness with prolonged and high fever, bi- or trilineage cytopenias, and hepatosplenomegaly, which is often severe or fatal. Death is generally secondary to liver failure or multisystem organ dysfunction. In those with XLP1, dys- or hypogammaglobulinemia can lead to varying degrees of humoral immune dysfunction associated with bronchiectasis and recurrent respiratory infections that, if untreated, may result in death. Lymphoproliferative disease (malignant lymphoma) and other lymphoproliferative diseases are specific to XLP1 and often develop in childhood, usually following EBV exposure. Rarer findings in those with XLP1 can include aplastic anemia, vasculitis, and lymphoid granulomatosis. Males with XLP2 are more likely to have HLH without EBV infection, recurrent episodes of HLH (which is not typically seen in those with XLP1), splenomegaly, and gastrointestinal disease, including enterocolitis and perirectal abscesses or fistulae. Rarely, individuals with XLP2 and inflammatory bowel disease have been reported to develop inflammatory liver disease, which can progress to fatal liver failure. Transient hypogammaglobulinemia has been rarely observed in those with XLP2. To date, neither lymphoproliferative disease nor common variable immunodeficiency has been reported in males with XLP2. Heterozygous females rarely have symptoms. There are, however, increasing numbers of reports of affected females with unfavorable (skewed) X-chromosome inactivation favoring the X chromosome with the pathogenic variant who develop HLH, inflammatory bowel disease, and erythema nodosum.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/336848">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_383874"><div><strong>Granulocytopenia with immunoglobulin abnormality</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>383874</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.">C1856263</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Immunodeficiency-59 and hypoglycemia (IMD59) is an autosomal recessive primary immunologic disorder characterized by combined immunodeficiency and recurrent septic infections of the respiratory tract, skin, and mucous membranes, as well as disturbed glucose metabolism. Granulocytopenia and B-cell and dendritic cell deficiency are present (Haapaniemi et al., 2017).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/383874">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_350353"><div><strong>Dermatitis, atopic</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>350353</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.">C1864155</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/350353">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_356497"><div><strong>Ehlers-Danlos syndrome, musculocontractural type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>356497</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.">C1866294</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bleeding problems are common in the vascular type of Ehlers-Danlos syndrome and are caused by unpredictable tearing (rupture) of blood vessels and organs. These complications can lead to easy bruising, internal bleeding, a hole in the wall of the intestine (intestinal perforation), or stroke. During pregnancy, women with vascular Ehlers-Danlos syndrome may experience rupture of the uterus. Additional forms of Ehlers-Danlos syndrome that involve rupture of the blood vessels include the kyphoscoliotic, classical, and classical-like types.\n\nOther types of Ehlers-Danlos syndrome have additional signs and symptoms. The cardiac-valvular type causes severe problems with the valves that control the movement of blood through the heart. People with the kyphoscoliotic type experience severe curvature of the spine that worsens over time and can interfere with breathing by restricting lung expansion. A type of Ehlers-Danlos syndrome called brittle cornea syndrome is characterized by thinness of the clear covering of the eye (the cornea) and other eye abnormalities. The spondylodysplastic type features short stature and skeletal abnormalities such as abnormally curved (bowed) limbs. Abnormalities of muscles, including hypotonia and permanently bent joints (contractures), are among the characteristic signs of the musculocontractural and myopathic forms of Ehlers-Danlos syndrome. The periodontal type causes abnormalities of the teeth and gums.\n\nMany people with the Ehlers-Danlos syndromes have soft, velvety skin that is highly stretchy (elastic) and fragile. Affected individuals tend to bruise easily, and some types of the condition also cause abnormal scarring. People with the classical form of Ehlers-Danlos syndrome experience wounds that split open with little bleeding and leave scars that widen over time to create characteristic "cigarette paper" scars. The dermatosparaxis type of the disorder is characterized by loose skin that sags and wrinkles, and extra (redundant) folds of skin may be present.\n\nAn unusually large range of joint movement (hypermobility) occurs in most forms of Ehlers-Danlos syndrome, and it is a hallmark feature of the hypermobile type. Infants and children with hypermobility often have weak muscle tone (hypotonia), which can delay the development of motor skills such as sitting, standing, and walking. The loose joints are unstable and prone to dislocation and chronic pain. In the arthrochalasia type of Ehlers-Danlos syndrome, infants have hypermobility and dislocations of both hips at birth.\n\nThe various forms of Ehlers-Danlos syndrome have been classified in several different ways. Originally, 11 forms of Ehlers-Danlos syndrome were named using Roman numerals to indicate the types (type I, type II, and so on). In 1997, researchers proposed a simpler classification (the Villefranche nomenclature) that reduced the number of types to six and gave them descriptive names based on their major features. In 2017, the classification was updated to include rare forms of Ehlers-Danlos syndrome that were identified more recently. The 2017 classification describes 13 types of Ehlers-Danlos syndrome.\n\nEhlers-Danlos syndrome is a group of disorders that affect connective tissues supporting the skin, bones, blood vessels, and many other organs and tissues. Defects in connective tissues cause the signs and symptoms of these conditions, which range from mildly loose joints to life-threatening complications.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/356497">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_383023"><div><strong>Pyogenic bacterial infections due to MyD88 deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>383023</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.">C2677092</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Immunodeficiency-68 (IMD68) is an autosomal recessive primary immunodeficiency characterized by severe systemic and invasive bacterial infections beginning in infancy or early childhood. The most common organisms implicated are Streptococcus pneumoniae, Staphylococcus aureus, and Pseudomonas, although other organisms may be observed. IMD68 is life-threatening in infancy and early childhood. The first invasive infection typically occurs before 2 years of age, with meningitis and upper respiratory infections being common manifestations. The mortality rate in early childhood is high, with most deaths occurring before 8 years of age. Affected individuals have an impaired inflammatory response to infection, including lack of fever and neutropenia, although erythrocyte sedimentation rate (ESR) and C-reactive protein may be elevated. General immunologic workup tends to be normal, with normal levels of B cells, T cells, and NK cells. However, more detailed studies indicate impaired cytokine response to lipopolysaccharide (LPS) and IL1B (147720) stimulation; response to TNFA (191160) is usually normal. Patients have good antibody responses to most vaccinations. Viral, fungal, and parasitic infections are generally not observed. Early detection is critical in early childhood because prophylactic treatment with IVIg or certain antibiotics is effective; the disorder tends to improve naturally around adolescence. At the molecular level, IMD68 results from impaired function of selective Toll receptor (see TLR4, 603030)/IL1R (see IL1R1; 147810) signaling pathways that ultimately activate NFKB (164011) to produce cytokines (summary by Picard et al., 2010). See also IMD67 (607676), caused by mutation in the IRAK4 gene (602170), which shows a similar phenotype to IMD68. As the MYD88 and IRAK4 genes interact in the same intracellular signaling pathway, the clinical and cellular features are almost indistinguishable (summary by Picard et al., 2010).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/383023">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_411605"><div><strong>Leukocyte adhesion deficiency 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>411605</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.">C2748536</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Leukocyte adhesion deficiency-3 (LAD3), also known as LAD1 variant (LAD1V), is an autosomal recessive disorder characterized by LAD1 (116920)-like immune deficiency and Glanzmann thrombasthenia (GT; 273800)-like bleeding problems. LAD3 results from mutations in FERMT3, or KINDLIN3, which encodes an intracellular protein that interacts with beta-integrins in hematopoietic cells. In LAD3, the adhesive functions of integrins on both leukocytes and platelets are disrupted, most likely due to defects in activation-dependent alterations of surface integrins that enable high-avidity binding to ligands on target cells, a process termed 'inside-out signaling' (Svensson et al., 2009; Zimmerman, 2009). For a discussion of genetic heterogeneity of leukocyte adhesion deficiency, see 116920.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/411605">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_481656"><div><strong>Hermansky-Pudlak syndrome 9</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>481656</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.">C3280026</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, a bleeding diathesis, and, in some individuals, pulmonary fibrosis, granulomatous colitis, and/or immunodeficiency. Ocular findings include nystagmus, reduced iris pigment, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), and strabismus in many individuals. Hair color ranges from white to brown; skin color ranges from white to olive and is usually at least a shade lighter than that of other family members. The bleeding diathesis can result in variable degrees of bruising, epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and/or other surgeries. Pulmonary fibrosis, colitis, and/or neutropenia have been reported in individuals with pathogenic variants in some HPS-related genes. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early 30s and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects occur primarily in individuals with pathogenic variants in AP3B1 and AP3D1.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/481656">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_482216"><div><strong>Mannose-binding lectin deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>482216</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.">C3280586</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Mannose-binding lectin (MBL) deficiency, defined as MBL protein level of less than 100 ng/ml, is present in about 5% of people of European descent and in about 10% of sub-Saharan Africans. Most MBL-deficient adults appear healthy, but low levels of MBL are associated with increased risk of infection in toddlers, in cancer patients undergoing chemotherapy, and in organ-transplant patients receiving immunosuppressive drugs, particularly recipients of liver transplants (review by Degn et al., 2011). MBL is a soluble molecule that can activate the lectin pathway of the complement system; deficiency may thus lead to defects in the complement system (summary by Garcia-Laorden et al., 2008). Genetic Heterogeneity of Lectin Complement Activation Pathway Defects See also LCAPD2 (613791), caused by variation in the MASP2 gene (605102) on chromosome 1p36, and LCAPD3 (613860), caused by variation in the FCN3 gene (604973) on chromosome 1p36.</div>
|
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<div class="spaceAbove nowrap">See: <a href="/medgen/482216">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_483045"><div><strong>Factor I deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>483045</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.">C3463916</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with hematuria, proteinuria, hematuria and proteinuria, acute nephritic syndrome or nephrotic syndrome, and low levels of the complement component C3. Spontaneous remission of C3G is uncommon, and about half of affected individuals develop end-stage renal disease (ESRD) within ten years of diagnosis, occasionally developing the late comorbidity of impaired visual acuity.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/483045">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_766857"><div><strong>Combined immunodeficiency due to STK4 deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>766857</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.">C3553943</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Immunodeficiency-110 (IMD110) is an autosomal recessive primary T-cell immunodeficiency syndrome characterized by progressive loss of naive T cells, recurrent bacterial, viral, and fungal infections, warts, and abscesses, and autoimmune manifestations. Patients are at risk for developing lymphoproliferative disorders or lymphoma, particularly associated with EBV. Some patients may show cardiac malformations, including atrial septal defect (Abdollahpour et al., 2012; Nehme et al., 2012).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/766857">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_816049"><div><strong>Severe dermatitis-multiple allergies-metabolic wasting syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>816049</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.">C3809719</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 epidermal disorder with characteristics of congenital erythroderma with severe psoriasiform dermatitis, ichthyosis, severe palmoplantar keratoderma, yellow keratosis on the hands and feet, elevated immunoglobulin E, multiple food allergies, and metabolic wasting. Other variable features may include hypotrichosis, nail dystrophy, recurrent infections, mild global developmental delay, eosinophilia, nystagmus, growth impairment and cardiac defects.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/816049">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_906018"><div><strong>Immunodeficiency, common variable, 12</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>906018</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.">C4225277</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Common variable immunodeficiency-12 with autoimmunity (CVID12) is an autosomal dominant complex immunologic disorder with multisystem involvement. CVID12 is mainly a primary immunodeficiency characterized by recurrent infections and associated with hypogammaglobulinemia. Notably, about half of patients develop autoimmune features, including cytopenia, as well as generalized inflammation and lymphoproliferation manifest as lymphadenopathy or hepatosplenomegaly. A smaller percentage of affected individuals (less than 20%) develop cancer, most commonly solid tumors, including lymphoma. Age at onset and disease severity are highly variable, even within the same family. There is also incomplete penetrance, such that mutation carriers may be asymptomatic, even if they have hypogammaglobulinemia. The gene involved, NFKB1, encodes a transcription factor that regulates the expression of target genes involved in the immune system, thus defining the phenotype as a disorder of immune dysregulation (summary by Fliegauf et al., 2015; Lorenzini et al., 2020). For a general description and a discussion of genetic heterogeneity of common variable immunodeficiency, see CVID1 (607594).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/906018">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_894363"><div><strong>Congenital insensitivity to pain-hypohidrosis syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>894363</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.">C4225308</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hereditary sensory and autonomic neuropathy type VIII (HSAN8) is an autosomal recessive neurologic disorder characterized by congenital insensitivity to pain resulting in ulceration to the fingers, tongue, lips, and other distal appendages. Affected individuals may also have decreased sweating and tear production (summary by Chen et al., 2015). For a discussion of genetic heterogeneity of hereditary sensory and autonomic neuropathy, see HSAN1A (162400).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/894363">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_934770"><div><strong>Immunodeficiency 51</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>934770</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.">C4310803</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Immunodeficiency-51 (IMD51) is an autosomal recessive primary immune deficiency that is usually characterized by onset of chronic mucocutaneous candidiasis in the first years of life. Most patients also show recurrent Staphylococcal skin infections, and may show increased susceptibility to chronic bacterial respiratory infections. Patient cells show a lack of cellular responses to stimulation with certain IL17 isoforms, including IL17A (603149), IL17F (606496), IL17A/F, and IL17E (IL25; 605658) (summary by Levy et al., 2016).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/934770">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1616061"><div><strong>Immunodeficiency, developmental delay, and hypohomocysteinemia</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1616061</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.">C4540293</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">IMDDHH is a multisystem disorder characterized by immunodeficiency, mildly delayed psychomotor development, poor overall growth from infancy, and hypohomocysteinemia. Additional features, such as congenital heart defects and liver involvement, are more variable (summary by Huppke et al., 2017).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1616061">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1652857"><div><strong>Lymphatic malformation 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1652857</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.">C4747646</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Hereditary primary lymphedema is caused by anatomic or functional defects in the lymphatic system, resulting in chronic swelling of body parts. There may be accompanying nail and skin changes, such as nail dysplasia or papillomatosis. Onset is usually at birth or in early childhood but can occur later, and the severity is variable (summary by Gordon et al., 2013 and Balboa-Beltran et al., 2014). For a discussion of genetic heterogeneity of lymphatic malformation, see 153100.</div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/1652857">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1648483"><div><strong>Hyper-IgE recurrent infection syndrome 3, autosomal recessive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1648483</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.">C4748969</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Hyper-IgE syndrome-3 with recurrent infections (HIES3) is an autosomal recessive immunologic disorder characterized by childhood onset of atopic dermatitis, skin infections particularly with Staphylococcus aureus, recurrent sinopulmonary infections, and increased serum IgE and IgG. Patients are susceptible to bacterial and fungal infections, including chronic mucocutaneous candidiasis. Immunologic workup shows impaired differentiation of CD4+ T cells into T-helper 17 cells, decreased memory B cells, and often decreased NK cells (summary by Beziat et al., 2018). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1648483">Condition Record</a></div></div>
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||
<div class="divPopper rprt" id="rdis_1717128"><div><strong>Immunodeficiency 66</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1717128</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.">C5394265</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Immunodeficiency-66 (IMD66) is an autosomal recessive primary immune disorder caused by defective immune cell migration and chemotaxis resulting from defects in cytoskeletal actin dynamics. Neutrophils are primarily affected, although there may be defects in dendritic cells and T and B cells. The phenotype is characterized by onset of recurrent bacterial infections in infancy. Laboratory studies show normal levels of myeloid and lymphoid cells, but there may be mild thrombocytopenia (summary by Record et al., 2015).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1717128">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1716052"><div><strong>Hyper-IgE recurrent infection syndrome 5, autosomal recessive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1716052</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.">C5394550</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Hyper-IgE syndrome-5 with recurrent infections (HEIS5) is an autosomal recessive immunologic disorder characterized by onset of recurrent sinopulmonary and deep skin infections in early childhood. The infections are mostly caused by bacteria, including H. influenza and Staphylococcus aureus. Additional features include atopic dermatitis, impaired inflammatory responses during infection, increased serum IgE, and increased IL6 (147620) (summary by Spencer et al., 2019). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1716052">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1746744"><div><strong>IFAP syndrome 1, with or without BRESHECK syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1746744</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.">C5399971</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">The IFAP/BRESHECK syndrome is an X-linked multiple congenital anomaly disorder with variable severity. The classic triad, which defines IFAP, is ichthyosis follicularis, atrichia, and photophobia. Some patients have additional features, including mental retardation, brain anomalies, Hirschsprung disease, corneal opacifications, kidney dysplasia, cryptorchidism, cleft palate, and skeletal malformations, particularly of the vertebrae, which constitutes BRESHECK syndrome (summary by Naiki et al., 2012). Genetic Heterogeneity of IFAP Syndrome IFAP syndrome-2 (IFAP2; 619016) is caused by heterozygous mutation in the SREBF1 gene (184756) on chromosome 17p11.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1746744">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1781752"><div><strong>Immunodeficiency 82 with systemic inflammation</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1781752</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.">C5543581</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Immunodeficiency-82 with systemic inflammation (IMD82) is a complex autosomal dominant immunologic disorder characterized by recurrent infections with various organisms, as well as noninfectious inflammation manifest as lymphocytic organ infiltration with gastritis, colitis, and lung, liver, CNS, or skin disease. One of the more common features is inflammation of the stomach and bowel. Most patients develop symptoms in infancy or early childhood; the severity is variable. There may be accompanying fever, elevated white blood cell count, decreased B cells, hypogammaglobulinemia, increased C-reactive protein (CRP; 123260), and a generalized hyperinflammatory state. Immunologic workup shows variable B- and T-cell abnormalities such as skewed subgroups. Patients have a propensity for the development of lymphoma, usually in adulthood. At the molecular level, the disorder results from a gain-of-function mutation that leads to constitutive and enhanced activation of the intracellular inflammatory signaling pathway. Treatment with SYK inhibitors rescued human cell abnormalities and resulted in clinical improvement in mice (Wang et al., 2021).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1781752">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1799555"><div><strong>Combined immunodeficiency due to GINS1 deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1799555</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.">C5568132</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Immunodeficiency-55 is an autosomal recessive primary immunodeficiency characterized by intrauterine growth retardation, natural killer (NK) cell deficiency, and chronic neutropenia. Most patients also have postnatal growth retardation. Other clinical manifestations include mild facial dysmorphism, dry or eczematous skin, and recurrent infections with both viruses and bacteria. The disorder appears to result from a defect in DNA replication causing blockade of immune cell differentiation in the bone marrow, particularly affecting NK cells (summary by Cottineau et al., 2017).</div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/1799555">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1802991"><div><strong>Netherton syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1802991</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.">C5574950</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Netherton syndrome (NETH) is a rare and severe autosomal recessive skin disorder characterized by congenital erythroderma, a specific hair-shaft abnormality, and atopic manifestations with high IgE levels. Generalized scaly erythroderma is apparent at or soon after birth and usually persists. Scalp hair is sparse and brittle with a characteristic 'bamboo' shape under light microscopic examination due to invagination of the distal part of the hair shaft to its proximal part. Atopic manifestations include eczema-like rashes, atopic dermatitis, pruritus, hay fever, angioedema, urticaria, high levels of IgE in the serum, and hypereosinophilia. Life-threatening complications are frequent during the neonatal period, including hypernatremic dehydration, hypothermia, extreme weight loss, bronchopneumonia, and sepsis. During childhood, failure to thrive is common as a result of malnutrition, metabolic disorders, chronic erythroderma, persistent cutaneous infections, or enteropathy (summary by Bitoun et al., 2002).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1802991">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1812534"><div><strong>Immunodeficiency 102</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1812534</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.">C5676886</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Immunodeficiency-102 (IMD102) is an X-linked recessive immunologic disorder characterized by the onset of recurrent sinopulmonary, mucosal, and other infections in early childhood, usually accompanied by refractory autoimmune cytopenias. Affected individuals have bacterial, viral, and fungal infections, as well as hemolytic anemia, thrombocytopenia, lymphopenia, and decreased NK cells. Laboratory studies show defective T-cell proliferation and function, likely due to signaling abnormalities. The disorder may also manifest as a hyperinflammatory state with immune dysregulation (Delmonte et al., 2021).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1812534">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1809613"><div><strong>Hyper-IgE recurrent infection syndrome 4A, autosomal dominant</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1809613</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.">C5676920</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hyper-IgE syndrome-4A with recurrent infections (HIES4A) is an autosomal dominant immunologic disorder characterized by recurrent, mainly sinopulmonary infections associated with increased serum IgE. The phenotype is variable, even within families. Some patients have onset of symptoms in early childhood and develop complications, including bronchiectasis or hemoptysis, whereas others have later onset of less severe infections. Immunologic workup usually shows normal leukocyte levels, although some patients may demonstrate alterations in lymphocyte subsets, including T cells. Affected individuals also have variable skeletal abnormalities, including high-arched palate, hyperextensible joints, scoliosis, and bone fractures. The IL6ST mutations are loss-of-function, although the truncated mutant proteins are expressed and interfere with the wildtype protein in a dominant-negative manner by disrupting IL6 (147620) and IL11 (147681) signaling (summary by Beziat et al., 2020). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1809613">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1802936"><div><strong>Immunodeficiency 97 with autoinflammation</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1802936</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.">C5676946</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Immunodeficiency-97 with autoinflammation (IMD97) is an autosomal recessive complex immunologic disorder with variable features. Affected individuals present in the first decade of life with inflammatory interstitial lung disease or colitis due to abnormal tissue infiltration by activated T cells. Patients develop autoimmune cytopenias and may have lymphadenopathy; 1 reported patient had features of hemophagocytic lymphohistiocytosis (HLH; see FHL1, 267700). Some patients may have recurrent infections associated with mild lymphopenia, hypogammaglobulinemia, and NK cell dysfunction. Immunologic workup indicates signs of significant immune dysregulation with elevation of inflammatory serum markers, variable immune cell defects involving neutrophils, NK cells, and myeloid cells, and disrupted levels of T regulatory cells (Tregs). Two unrelated patients have been reported (summary by Takeda et al., 2019 and Thian et al., 2020).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1802936">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1824071"><div><strong>Neurodevelopmental disorder with dysmorphic facies and ischiopubic hypoplasia</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1824071</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.">C5774298</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Neurodevelopmental disorder with dysmorphic facies and ischiopubic hypoplasia (NEDFIH) is an autosomal recessive disorder characterized by these features and moderate to severe global developmental delay. Affected individuals show episodic regression during periods of stress, including seizures or infection, the latter of which may be associated with lymphopenia. Brain imaging shows diminished white matter volume, enlarged ventricles, and thin corpus callosum (Muffels et al., 2023).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1824071">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1851769"><div><strong>Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1851769</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.">C5848786</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Hyper-IgE syndrome-6 with recurrent infections (HIES6) is an autosomal dominant immunologic disorder characterized by early-childhood onset of severe refractory atopic dermatitis, IgE-mediated food and drug allergies, asthma, and eosinophilic esophagitis. Laboratory studies show increased serum IgE levels and eosinophilia. Affected individuals are susceptible to life-threatening anaphylaxis. Additional features may include allergic rhinitis, recurrent secondary infections (bacterial, viral, fungal), and short stature. Rare patients show intracerebral vascular abnormalities, including the Circle of Willis, increased risk of ruptured aneurysm, and B-cell lymphoma. The disorder results from immune dysregulation with inappropriate activation of inflammatory signaling pathways associated with a Th2 phenotype. Treatment with an IL4 (147780)/IL13 (147683) inhibitor (dupilumab) or JAK inhibitor results in clinical improvement. Sharma et al. (2023) classified this disease as a 'primary atopic disorder' (PAD). For a discussion of genetic heterogeneity of hyper-IgE syndrome, see HIES1 (147060).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1851769">Condition Record</a></div></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_66323" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Biotinidase deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1799555" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Combined immunodeficiency due to GINS1 deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_766857" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Combined immunodeficiency due to STK4 deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_894363" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital insensitivity to pain-hypohidrosis syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_350353" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Dermatitis, atopic</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (29)', lessText: 'Show less', nodeBefore: 0"><span id="clinMore">
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_356497" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Ehlers-Danlos syndrome, musculocontractural type</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_483045" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Factor I deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_383874" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Granulocytopenia with immunoglobulin abnormality</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_481656" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hermansky-Pudlak syndrome 9</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1648483" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyper-IgE recurrent infection syndrome 3, autosomal recessive</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1809613" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyper-IgE recurrent infection syndrome 4A, autosomal dominant</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1716052" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyper-IgE recurrent infection syndrome 5, autosomal recessive</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1851769" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1746744" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">IFAP syndrome 1, with or without BRESHECK syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1812534" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency 102</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_934770" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency 51</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1717128" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency 66</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1781752" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency 82 with systemic inflammation</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1802936" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency 97 with autoinflammation</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_906018" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency, common variable, 12</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1616061" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Immunodeficiency, developmental delay, and hypohomocysteinemia</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_411605" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Leukocyte adhesion deficiency 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1652857" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Lymphatic malformation 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_482216" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Mannose-binding lectin deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1802991" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Netherton syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1824071" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Neurodevelopmental disorder with dysmorphic facies and ischiopubic hypoplasia</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_383023" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pyogenic bacterial infections due to MyD88 deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_816049" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Severe dermatitis-multiple allergies-metabolic wasting syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_336848" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">X-linked lymphoproliferative disease due to XIAP deficiency</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/36331655">Recurrent skin infections associated with natalizumab treatment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Oliveira DS,
|
||
Castro AR,
|
||
Ruano L</span><br />
|
||
<span class="medgenPMjournal">Neurol Sci</span>
|
||
2023 Mar;44(3):1093-1095.
|
||
Epub 2022 Nov 4
|
||
doi: 10.1007/s10072-022-06481-2.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36331655" target="_blank">36331655</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34447369">Primary Immune Regulatory Disorders With an Autoimmune Lymphoproliferative Syndrome-Like Phenotype: Immunologic Evaluation, Early Diagnosis and Management.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">López-Nevado M,
|
||
González-Granado LI,
|
||
Ruiz-García R,
|
||
Pleguezuelo D,
|
||
Cabrera-Marante O,
|
||
Salmón N,
|
||
Blanco-Lobo P,
|
||
Domínguez-Pinilla N,
|
||
Rodríguez-Pena R,
|
||
Sebastián E,
|
||
Cruz-Rojo J,
|
||
Olbrich P,
|
||
Ruiz-Contreras J,
|
||
Paz-Artal E,
|
||
Neth O,
|
||
Allende LM</span><br />
|
||
<span class="medgenPMjournal">Front Immunol</span>
|
||
2021;12:671755.
|
||
Epub 2021 Aug 10
|
||
doi: 10.3389/fimmu.2021.671755.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34447369" target="_blank">34447369</a><a href="/pmc/articles/PMC8382720" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34170945">Skin infections due to Panton-Valentine leukocidin (PVL)-producing S. aureus-Cost effectiveness of outpatient treatment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Rentinck MN,
|
||
Krüger R,
|
||
Hoppe PA,
|
||
Humme D,
|
||
Niebank M,
|
||
Pokrywka A,
|
||
Stegemann M,
|
||
Kola A,
|
||
Hanitsch LG,
|
||
Leistner R</span><br />
|
||
<span class="medgenPMjournal">PLoS One</span>
|
||
2021;16(6):e0253633.
|
||
Epub 2021 Jun 25
|
||
doi: 10.1371/journal.pone.0253633.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34170945" target="_blank">34170945</a><a href="/pmc/articles/PMC8232536" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(%22recurrent%20skin%20infections%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 (7)</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/38218373">Infection prevention-how can we prevent transmission of community-onset methicillin-resistant Staphylococcus aureus?</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Kao CM,
|
||
Fritz SA</span><br />
|
||
<span class="medgenPMjournal">Clin Microbiol Infect</span>
|
||
2025 Feb;31(2):166-172.
|
||
Epub 2024 Jan 11
|
||
doi: 10.1016/j.cmi.2024.01.004.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38218373" target="_blank">38218373</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30923312">Cancer-associated secondary lymphoedema.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Rockson SG,
|
||
Keeley V,
|
||
Kilbreath S,
|
||
Szuba A,
|
||
Towers A</span><br />
|
||
<span class="medgenPMjournal">Nat Rev Dis Primers</span>
|
||
2019 Mar 28;5(1):22.
|
||
doi: 10.1038/s41572-019-0072-5.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30923312" target="_blank">30923312</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/29935493">Effect of Exercise on Breast Cancer-Related Lymphedema: What the Lymphatic Surgeon Needs to Know.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Panchik D,
|
||
Masco S,
|
||
Zinnikas P,
|
||
Hillriegel B,
|
||
Lauder T,
|
||
Suttmann E,
|
||
Chinchilli V,
|
||
McBeth M,
|
||
Hermann W</span><br />
|
||
<span class="medgenPMjournal">J Reconstr Microsurg</span>
|
||
2019 Jan;35(1):37-45.
|
||
Epub 2018 Jun 23
|
||
doi: 10.1055/s-0038-1660832.
|
||
<span class="bold">PMID: </span><a href="/pubmed/29935493" target="_blank">29935493</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/20670815">The infectious aspects of atopic dermatitis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Ong PY,
|
||
Leung DY</span><br />
|
||
<span class="medgenPMjournal">Immunol Allergy Clin North Am</span>
|
||
2010 Aug;30(3):309-21.
|
||
Epub 2010 Jul 1
|
||
doi: 10.1016/j.iac.2010.05.001.
|
||
<span class="bold">PMID: </span><a href="/pubmed/20670815" target="_blank">20670815</a><a href="/pmc/articles/PMC2913147" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/11957188">Neutropenia: causes and consequences.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Boxer L,
|
||
Dale DC</span><br />
|
||
<span class="medgenPMjournal">Semin Hematol</span>
|
||
2002 Apr;39(2):75-81.
|
||
doi: 10.1053/shem.2002.31911.
|
||
<span class="bold">PMID: </span><a href="/pubmed/11957188" target="_blank">11957188</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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 (29)</a></div><h3 class="subhead">Diagnosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38432743">Chronic Granulomatous Disease Presenting With Recurrent Skin Infections.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Khodadadi RB,
|
||
Yetmar ZA,
|
||
Montagnon CM</span><br />
|
||
<span class="medgenPMjournal">Mayo Clin Proc</span>
|
||
2024 Mar;99(3):357-358.
|
||
doi: 10.1016/j.mayocp.2023.09.002.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38432743" target="_blank">38432743</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/31338855">Autosomal recessive hyper-IgE syndrome successfully treated with hematopoietic stem cell transplantation.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lopes J,
|
||
Teixeira D,
|
||
Sousa C,
|
||
Baptista A,
|
||
Moreira D,
|
||
Ferreira EO</span><br />
|
||
<span class="medgenPMjournal">Pediatr Dermatol</span>
|
||
2019 Sep;36(5):693-696.
|
||
Epub 2019 Jul 24
|
||
doi: 10.1111/pde.13919.
|
||
<span class="bold">PMID: </span><a href="/pubmed/31338855" target="_blank">31338855</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30923312">Cancer-associated secondary lymphoedema.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Rockson SG,
|
||
Keeley V,
|
||
Kilbreath S,
|
||
Szuba A,
|
||
Towers A</span><br />
|
||
<span class="medgenPMjournal">Nat Rev Dis Primers</span>
|
||
2019 Mar 28;5(1):22.
|
||
doi: 10.1038/s41572-019-0072-5.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30923312" target="_blank">30923312</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/22403135">Sclerotherapy of lymphatic cysts of the leg with OK-432.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Clemens RK,
|
||
Meier TO,
|
||
Pfiffner R,
|
||
Hafner J,
|
||
Amann-Vesti B</span><br />
|
||
<span class="medgenPMjournal">Vasa</span>
|
||
2012 Mar;41(2):149-53.
|
||
doi: 10.1024/0301-1526/a000179.
|
||
<span class="bold">PMID: </span><a href="/pubmed/22403135" target="_blank">22403135</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/11957188">Neutropenia: causes and consequences.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Boxer L,
|
||
Dale DC</span><br />
|
||
<span class="medgenPMjournal">Semin Hematol</span>
|
||
2002 Apr;39(2):75-81.
|
||
doi: 10.1053/shem.2002.31911.
|
||
<span class="bold">PMID: </span><a href="/pubmed/11957188" target="_blank">11957188</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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 (28)</a></div><h3 class="subhead">Therapy</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38218373">Infection prevention-how can we prevent transmission of community-onset methicillin-resistant Staphylococcus aureus?</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Kao CM,
|
||
Fritz SA</span><br />
|
||
<span class="medgenPMjournal">Clin Microbiol Infect</span>
|
||
2025 Feb;31(2):166-172.
|
||
Epub 2024 Jan 11
|
||
doi: 10.1016/j.cmi.2024.01.004.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38218373" target="_blank">38218373</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30923312">Cancer-associated secondary lymphoedema.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Rockson SG,
|
||
Keeley V,
|
||
Kilbreath S,
|
||
Szuba A,
|
||
Towers A</span><br />
|
||
<span class="medgenPMjournal">Nat Rev Dis Primers</span>
|
||
2019 Mar 28;5(1):22.
|
||
doi: 10.1038/s41572-019-0072-5.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30923312" target="_blank">30923312</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25017526">Recurrent MRSA skin infections in atopic dermatitis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Ong PY</span><br />
|
||
<span class="medgenPMjournal">J Allergy Clin Immunol Pract</span>
|
||
2014 Jul-Aug;2(4):396-9.
|
||
Epub 2014 May 23
|
||
doi: 10.1016/j.jaip.2014.04.007.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25017526" target="_blank">25017526</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/22403135">Sclerotherapy of lymphatic cysts of the leg with OK-432.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Clemens RK,
|
||
Meier TO,
|
||
Pfiffner R,
|
||
Hafner J,
|
||
Amann-Vesti B</span><br />
|
||
<span class="medgenPMjournal">Vasa</span>
|
||
2012 Mar;41(2):149-53.
|
||
doi: 10.1024/0301-1526/a000179.
|
||
<span class="bold">PMID: </span><a href="/pubmed/22403135" target="_blank">22403135</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/7748967">Autoimmune neutropenia successfully treated with cyclosporine.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Schiphorst PP,
|
||
de Pauw BE</span><br />
|
||
<span class="medgenPMjournal">Ann Hematol</span>
|
||
1995 Apr;70(4):223-5.
|
||
doi: 10.1007/BF01700379.
|
||
<span class="bold">PMID: </span><a href="/pubmed/7748967" target="_blank">7748967</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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 (28)</a></div><h3 class="subhead">Prognosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/36017778">Neonatal cutaneous inflammatory syndrome associated with homozygous epidermal growth factor receptor mutation.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Labbouz S,
|
||
Keegan G,
|
||
King T</span><br />
|
||
<span class="medgenPMjournal">Pediatr Dermatol</span>
|
||
2023 Jan;40(1):171-175.
|
||
Epub 2022 Aug 26
|
||
doi: 10.1111/pde.15115.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36017778" target="_blank">36017778</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/34170945">Skin infections due to Panton-Valentine leukocidin (PVL)-producing S. aureus-Cost effectiveness of outpatient treatment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Rentinck MN,
|
||
Krüger R,
|
||
Hoppe PA,
|
||
Humme D,
|
||
Niebank M,
|
||
Pokrywka A,
|
||
Stegemann M,
|
||
Kola A,
|
||
Hanitsch LG,
|
||
Leistner R</span><br />
|
||
<span class="medgenPMjournal">PLoS One</span>
|
||
2021;16(6):e0253633.
|
||
Epub 2021 Jun 25
|
||
doi: 10.1371/journal.pone.0253633.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34170945" target="_blank">34170945</a><a href="/pmc/articles/PMC8232536" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/32250467">Fatal neonatal nephrocutaneous syndrome in 18 Roma children with EGFR deficiency.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Mazurova S,
|
||
Tesarova M,
|
||
Zeman J,
|
||
Stranecky V,
|
||
Hansikova H,
|
||
Baxova A,
|
||
Giertlova M,
|
||
Lastuvkova J,
|
||
Chovanova V,
|
||
Rusnakova S,
|
||
Knapkova M,
|
||
Minarik G,
|
||
Honzik T,
|
||
Magner M</span><br />
|
||
<span class="medgenPMjournal">J Dermatol</span>
|
||
2020 Jun;47(6):663-668.
|
||
Epub 2020 Apr 6
|
||
doi: 10.1111/1346-8138.15317.
|
||
<span class="bold">PMID: </span><a href="/pubmed/32250467" target="_blank">32250467</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/23760147">A clinicopathologic study of labia minora hypertrophy: signs of localized lymphedema were universal.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Barrett MM,
|
||
Carlson JA</span><br />
|
||
<span class="medgenPMjournal">J Low Genit Tract Dis</span>
|
||
2014 Jan;18(1):13-20.
|
||
doi: 10.1097/LGT.0b013e31828d3989.
|
||
<span class="bold">PMID: </span><a href="/pubmed/23760147" target="_blank">23760147</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/15719338">Deprivation and dialysis: pathways to kidney failure in Australian Aborigines.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Thomas M</span><br />
|
||
<span class="medgenPMjournal">Adv Chronic Kidney Dis</span>
|
||
2005 Jan;12(1):84-7.
|
||
doi: 10.1053/j.ackd.2004.10.008.
|
||
<span class="bold">PMID: </span><a href="/pubmed/15719338" target="_blank">15719338</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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 (17)</a></div><h3 class="subhead">Clinical prediction guides</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38879154">Breast Cancer-Related Lymphedema Results in Impaired Epidermal Differentiation and Tight Junction Dysfunction.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Campbell AC,
|
||
Baik JE,
|
||
Sarker A,
|
||
Brown S,
|
||
Park HJ,
|
||
Kuonqui KG,
|
||
Shin J,
|
||
Pollack BL,
|
||
Roberts A,
|
||
Ashokan G,
|
||
Rubin J,
|
||
Kataru RP,
|
||
Dayan JH,
|
||
Barrio AV,
|
||
Mehrara BJ</span><br />
|
||
<span class="medgenPMjournal">J Invest Dermatol</span>
|
||
2025 Jan;145(1):85-97.e4.
|
||
Epub 2024 Jun 13
|
||
doi: 10.1016/j.jid.2024.05.017.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38879154" target="_blank">38879154</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/32572726">Three Copies of Four Interferon Receptor Genes Underlie a Mild Type I Interferonopathy in Down Syndrome.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Kong XF,
|
||
Worley L,
|
||
Rinchai D,
|
||
Bondet V,
|
||
Jithesh PV,
|
||
Goulet M,
|
||
Nonnotte E,
|
||
Rebillat AS,
|
||
Conte M,
|
||
Mircher C,
|
||
Gürtler N,
|
||
Liu L,
|
||
Migaud M,
|
||
Elanbari M,
|
||
Habib T,
|
||
Ma CS,
|
||
Bustamante J,
|
||
Abel L,
|
||
Ravel A,
|
||
Lyonnet S,
|
||
Munnich A,
|
||
Duffy D,
|
||
Chaussabel D,
|
||
Casanova JL,
|
||
Tangye SG,
|
||
Boisson-Dupuis S,
|
||
Puel A</span><br />
|
||
<span class="medgenPMjournal">J Clin Immunol</span>
|
||
2020 Aug;40(6):807-819.
|
||
Epub 2020 Jun 22
|
||
doi: 10.1007/s10875-020-00803-9.
|
||
<span class="bold">PMID: </span><a href="/pubmed/32572726" target="_blank">32572726</a><a href="/pmc/articles/PMC7418179" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/23760147">A clinicopathologic study of labia minora hypertrophy: signs of localized lymphedema were universal.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Barrett MM,
|
||
Carlson JA</span><br />
|
||
<span class="medgenPMjournal">J Low Genit Tract Dis</span>
|
||
2014 Jan;18(1):13-20.
|
||
doi: 10.1097/LGT.0b013e31828d3989.
|
||
<span class="bold">PMID: </span><a href="/pubmed/23760147" target="_blank">23760147</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/21762972">The signal transducer and activator of transcription 6 gene (STAT6) increases the propensity of patients with atopic dermatitis toward disseminated viral skin infections.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Howell MD,
|
||
Gao P,
|
||
Kim BE,
|
||
Lesley LJ,
|
||
Streib JE,
|
||
Taylor PA,
|
||
Zaccaro DJ,
|
||
Boguniewicz M,
|
||
Beck LA,
|
||
Hanifin JM,
|
||
Schneider LC,
|
||
Hata TR,
|
||
Gallo RL,
|
||
Kaplan MH,
|
||
Barnes KC,
|
||
Leung DY</span><br />
|
||
<span class="medgenPMjournal">J Allergy Clin Immunol</span>
|
||
2011 Nov;128(5):1006-14.
|
||
Epub 2011 Jul 18
|
||
doi: 10.1016/j.jaci.2011.06.003.
|
||
<span class="bold">PMID: </span><a href="/pubmed/21762972" target="_blank">21762972</a><a href="/pmc/articles/PMC3205328" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/20569290">Clinical manifestations and outcome of skin infections caused by the community-acquired methicillin-resistant Staphylococcus aureus clone ST80-IV.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Del Giudice P,
|
||
Bes M,
|
||
Hubiche T,
|
||
Roudière L,
|
||
Blanc V,
|
||
Lina G,
|
||
Vandenesch F,
|
||
Etienne J</span><br />
|
||
<span class="medgenPMjournal">J Eur Acad Dermatol Venereol</span>
|
||
2011 Feb;25(2):164-9.
|
||
Epub 2010 Jun 21
|
||
doi: 10.1111/j.1468-3083.2010.03731.x.
|
||
<span class="bold">PMID: </span><a href="/pubmed/20569290" target="_blank">20569290</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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 (22)</a></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_104">
|
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<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>
|
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<div class="portlet_content ln">
|
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<div class="nl"><a target="_blank" href="/pubmed/29935493">Effect of Exercise on Breast Cancer-Related Lymphedema: What the Lymphatic Surgeon Needs to Know.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Panchik D,
|
||
Masco S,
|
||
Zinnikas P,
|
||
Hillriegel B,
|
||
Lauder T,
|
||
Suttmann E,
|
||
Chinchilli V,
|
||
McBeth M,
|
||
Hermann W</span><br />
|
||
<span class="medgenPMjournal">J Reconstr Microsurg</span>
|
||
2019 Jan;35(1):37-45.
|
||
Epub 2018 Jun 23
|
||
doi: 10.1055/s-0038-1660832.
|
||
<span class="bold">PMID: </span><a href="/pubmed/29935493" target="_blank">29935493</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Recurrent%20skin%20infections%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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|
||
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|
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|
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|
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|
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|
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|
||
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|
||
|
||
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|
||
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|
||
<div class="supplemental col three_col last">
|
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<h2 class="offscreen_noflow">Supplemental Content</h2>
|
||
|
||
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|
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|
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|
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<div class="portlet_content ln"><ul><li><a href="/gtr/tests?term=C1853193%5bDISCUI%5d&filter=method%3A2%5F8" target="_blank">Deletion/duplication analysis (2)</a></li>
|
||
<li><a href="/gtr/tests?term=C1853193%5bDISCUI%5d&filter=method%3A2%5F7" target="_blank">Sequence analysis of the entire coding region (2)</a></li>
|
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<li class="portletSeeAll portletSeeAllPad"><total><a href="/gtr/tests?term=C1853193%5bDISCUI%5d" target="_blank">See all (2)</a></total></li>
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<div class="portlet_content ln"><ul><li><a href="https://clinicaltrials.gov/search?cond=Recurrent%20skin%20infections" 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=(%22recurrent%20skin%20infections%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(%22Recurrent%20skin%20infections%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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<a href="/pubmed/clinical?term=Recurrent%20skin%20infections" ref="ncbi_uid=&discoId=gtr_reviews&linkpos=1&linkpostotal=2" target="_blank">PubMed Clinical Queries</a>
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