Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040425 (tonsillitis)
 1,594 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe here a case of Scleredema of Buschke in a female patient aged 63 with IgA deficiency. The disorder appeared after an acute episode of tonsillitis, followed by non-pitting, woody hardness of the skin of the face, neck, shoulders and upper part of the trunk. The disorder resolved after 5 months of penicillin treatment.
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PMID:Scleredema of Buschke with IgA deficiency. 8 3

Nasal biopsy specimens from 15 adult patients with selective IgA deficiency but normal IgG-subclass levels were examined by immunohistochemistry for the presence of immunocytes producing various Ig isotypes. The mucosal samples were completely IgA-deficient except in two cases where 0.9% and 8.4% IgA cells were found, respectively (normal, 69.8%). Numerous IgG- (mainly IgG1-) producing cells were present in 10 samples; in five of these there were additional IgM- but virtually no IgD-producing cells, whereas in the other five a marked dominance of the IgD over the IgM isotype was seen. The latter category of patients had more upper airways infections (recurrent acute rhinosinusitis, otitis media, and tonsillitis) than the former, who had no recurrent upper respiratory tract infections except one patient with recurrent acute rhinosinusitis. The five remaining samples, which contained very few Ig-producing cells, were derived from patients with even more frequent infections than those showing IgD predominance. Our results indicate that IgM acts as a compensatory secretory Ig in the upper respiratory tract of some IgA-deficient subjects. However, immunoregulatory events favouring local IgD responses apparently do not support mucosal defence satisfactorily, either because local production of IgM is hampered or because IgD (which is not a secretory Ig) blocks complement-dependent reactions mediated by IgG and IgM antibodies within the mucosa.
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PMID:The clinical condition of IgA-deficient patients is related to the proportion of IgD- and IgM-producing cells in their nasal mucosa. 330 Nov 1

FIRST REPORT: male child with repeated pulmonary infections from the age of 4 months. He was diagnosed as IgA deficiency (undetectable IgA levels) at the age of 3 years, when he presented repeated bouts of pneumonia and tonsillitis. Several immunologic evaluations were made between the ages of 4 months and 8 years. At 8 years and 9 months, the diagnosis of IgA deficiency was confirmed, and associated IgG2 and IgG4 deficiency (29.0 mg/dl y 0.01 mg/dl) with normal total IgG serum level was found. With the administration of intravenous gammaglobulin, the lung infections remitted and the subsequent clinical course has been uneventful up to now. SECOND REPORT: a boy with repeated infections since the age of 2 months. IgA deficiency was diagnosed at 1 year 7 months (undetectable serum IgA levels). At age 51/2 years, his clinical course worsened and more serious infections appeared. A new immunologic study revealed IgA deficiency associated with CD4 cell deficiency (432 cells/mm3) and normal CD3, CD19, and CD8 levels. Despite intensive antibiotic treatment and care, the child died. The findings suggest an association of IgA deficiency and common variable immunodeficiency.
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PMID:Evolution of IgA deficiency to IgG subclass deficiency and common variable immunodeficiency. 1075 54