Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 60-year-old white man presented with a syndrome of fever, polyarthritis, pleurisy, and lymphopenia, and had a positive antinuclear antibody test (after 5 months of quinidine therapy). Quinidine-induced antinuclear autoantibodies were of the IgM and IgG classes and were directed mainly to nuclear histones, predominantly histones H1 and H2B. Antibodies to native DNA and nonhistone nuclear antigens were not seen during the patient's clinical course. Upon withdrawal of quinidine therapy, the patient had prompt improvement of clinical symptoms followed by a gradual resolution of serologic abnormalities.
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PMID:Quinidine-induced lupus erythematosus. 637 64

Progressive loss of CD4+ T lymphocytes, accompanied by opportunistic infections characteristic of the acquired immune deficiency syndrome, ahs been reported in the absence of any known etiology. The pathogenesis of this syndrome, a subset of idiopathic CD4+ T lymphocytopenia (ICL), is uncertain. We report that CD4+ T cells from seven of eight ICL patients underwent accelerated programmed cell death, a process facilitated by T cell receptor cross-linking. Apoptosis was associated with enhanced expression of Fas and Fas ligand in unstimulated cell populations, and partially inhibited by soluble anti-Fas mAb. In addition, apoptosis was suppressed by aurintricarboxylic acid, an inhibitor of calcium-dependent endonucleases and proteases, in cells from four of seven patients, The in vivo significance of these findings was supported by three factors: the absence of accelerated apoptosis in persons with stable, physiologic CD4 lymphopenia without clinical immune deficiency; detection of serum antihistone H2B autoantibodies, one consequence of DNA fragmentation, in some patients; and its selectivity, with apoptosis limited to the CD4 population in some, and occurring among CD8+ T cells predominantly in those individuals with marked depletion of both CD4+ T lymphocytes linked to clinical immune suppression have evidence for accelerated T cell apoptosis in vitro that may be pathophysiologic and amenable to therapy with apoptosis inhibitors.
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PMID:Apoptotic depletion of CD4+ T cells in idiopathic CD4+ T lymphocytopenia. 860 22