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Mucocutaneous Candidiasis (mucocutaneou + candidiasis)
Kinds of Mucocutaneous Candidiasis Selected AbstractsOral manifestation of chronic mucocutaneous candidiasis: seven case reportsJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2007Xiaosong Liu Background:, Chronic mucocutaneous candidiasis (CMC) is a rare disorder characterized by persistent or recurrent candidal infections of the skin, nails and mucous membranes or by a variable combination of endocrine failure as well as immunodeficiency. Oral clinicopathological features of CMC have seldom been described in detail. Methods:, Seven patients with CMC were reported in the study. The clinical and histological findings, etiological Candida species, immunological evaluation, and therapeutic pattern of oral lesions, were analyzed. Results:, Long-standing whitish hyperplastic and nodule-like lesions with exaggerated deep fissure were the typical and characteristic oral manifestations presented by all patients. The tongue was the most common site affected. Histologically, no obvious distinction was found between CMC and other forms of candidal infection. Abnormal proportions of T-lymphocyte subsets and positive titers of autoantibody were observed in three subjects (42.9%) and one patient (14.3%) respectively. Meanwhile, four subjects (57.1%) showed decreased albumin and increased globulin, three cases (42.9%) had high levels of ESR. But no iron deficiency was found. Candida albicans was the microorganism isolated from these patients. Conclusions:, Multiple and widespread candidal infectious lesions can be observed on the oral cavity of CMC patients. Hyperplastic and nodule-like lesion with irremovable whitish patches and deep fissure are the most common oral manifestations of these patients. Dentists, otolaryngologists and pediatricians should be familiar with the clinical appearances of CMC to make an accurate diagnosis. Potential systemic disorders should be concerned to avoid the reoccurrence of oral candidiasis. [source] Immunodeficiency with recurrent panlymphocytopenia, impaired maturation of B lymphocytes, impaired interaction of T and B lymphocytes, and impaired integrity of epithelial tissue: A variant of idiopathic CD4+ T lymphocytopenia?PEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2002Horst Von Bernuth Idiopathic CD4+ T lymphocytopenia (ICL) has been defined as a cause of immunodeficiency with a variable clinical course and an unknown etiology. Here we describe a now 18-year-old boy with ICL, chronic mucocutaneous candidiasis (CMC), recurrent abscesses, and relapsing aphthous and ulcerous lesions. In addition to ICL the patient frequently showed a panlymphocytopenia. An increased percentage of ,+,+ T lymphocytes and IgD+ IgM+ B lymphocytes, and a decreased percentage of CD21+ B lymphocytes, were observed. In vitro assays showed normal T-cell responses to candidin and T-cell mitogens, but impaired B-cell responses to pokeweed mitogen (PWM). B-cell maturation after stimulation with Staphylococcus aureus Cowan I (SAC) and interleukin 2 (IL-2) was nearly normal. The clinical course of the patient improved substantially on administration of constant low-dose therapy with fluconazole. [source] Chronic mucocutaneous candidiasis may cause elevated gliadin antibodiesACTA PAEDIATRICA, Issue 10 2009Florian Brinkert Abstract We present a 4-year-old boy admitted to the hospital due to the typical symptoms of celiac disease with severe dystrophy, anaemia and elevated gliadin IgG antibodies. Upper endoscopy ruled out celiac disease but showed severe Candida esophagitis. Due to an impaired T-cell function especially following Candida antigen stimulation in vitro, plus recurrent Candida infections of the skin, the diagnosis of chronic mucocutaneous candidasis (CMC) was made. Under the treatment with fluconazol, trimethoprim/sulfmethoxazole and IVIG, the child improved impressively. Gliadin antibodies declined steadily. Conclusion:, The common symptoms growth retardation, anaemia and elevated gliadin antibodies are suggestive for celiac disease but very unspecific. The rare immunodeficiency CMC may cause elevated gliadin antibodies. [source] Novel sequence variation of AIRE and detection of interferon-, antibodies in early infancyCLINICAL ENDOCRINOLOGY, Issue 5 2010Beáta Tóth Summary Objective, Autoimmune polyendocrine syndrome type I (APS I) is a rare primary immunodeficiency disorder characterized by chronic mucocutaneous candidiasis, multi-organ autoimmunity and ectodermal dysplasia. Autoantibodies to parathyroid and adrenal glands and type I interferons (IFN) are hallmarks of APS I, which results from mutations in the autoimmune regulator (AIRE) gene. We wished to study clinical, immunological and genetic features of APS I in Hungarian patients, and to correlate anti-IFN-, serum concentration with APS I and other multi-organ autoimmune diseases. Design, Detailed analysis of patients with APS I and multi-organ autoimmune diseases. Patients, Seven patients with APS I and 11 patients with multi-organ autoimmune diseases were studied. Measurements, Mutational analysis was performed by bidirectional sequencing of AIRE. Antibodies against IFN-, and endocrine organ-specific autoantigens were studied with radioimmunoassay. RFLP was performed by digestion of DNA with Hin6I restriction enzyme. Results, AIRE sequence analysis revealed homozygous c.769C>T mutations in three patients and compound heterozygous sequence variants (c.769C>T/c.44_66dup26bp; c.769C>T/c.965_977del13bp; c.769C>T/c.1344delC) in four patients with APS I. All the six live patients tested had markedly elevated IFN-, antibodies, which were not found in heterozygous siblings or parents. One of the identified patients was negative for antibodies against IFN-, at 6 weeks of age, but became positive at 7 months. At age 1, he is still without symptoms of the disease. In contrast to patients with APS I, no AIRE mutation or elevation of IFN-, antibodies were detected in patients with multi-organ autoimmune diseases. Conclusion, This is the first overview of patients diagnosed with APS I in Hungary. A novel c.1344delC mutation in AIRE was detected. Anti-IFN-, antibodies seem to appear very early in life and are helpful to differentiate APS I from other multi-organ autoimmune diseases. [source] |