Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and adverse effects of prophylactic administration of Sulfamethoxazole-Trimethoprim (ST) for Pneumocystis carinii Pneumonia (PCP) were assessed in patients with connective tissue diseases (CTD). Eighty-four patients who were receiving more than 40 mg/day of prednisolone were entried in the present study. Patients with at least one of the two PCP risk factors (interstitial pulmonary fibrosis and lymphopenia), were administered either one (11 patients) or two (26 patients) ST tablets/day. The remaining 47 patients who did not receive ST served as the controls. Although PCP was detected in 4.3% of the patients in the no-ST group, none of the patients who received ST developed PCP. Five of these 26 patients who received two tablets of ST/day, experienced adverse reactions. However, no adverse reactions were detected in the patients who received one tablet of ST/day (p < 0.05). Abnormal laboratory data were obtained for 10 (38.5%) of the patients who received two tablets of ST/day and for 4 (36.4%) of the 11 patients who received one tablet of ST/day. The results of the present study suggest that the prophylactic administration of one tablets of ST in patients with CTD that have at least one of the two PCP risk factors is effective in preventing PCP.
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PMID:Efficacy of sulfamethoxazole-trimethoprim administration in the prevention of Pneumocystis carinii pneumonia in patients with connective tissue disease. 1062 92

Nicotinamide dinucleotide phosphate oxidase-deficient (p47(phox-/-)) mice are a model of human chronic granulomatous disease; these mice are prone to develop systemic infections and inflammatory diseases. The use of antibiotic (Bactrim) prophylaxis in a specific pathogen-free environment, however, impedes infection in the majority of p47(phox-/-) mice. We examined infection-free p47(phox-/-) mice between 1 and 14 months of age and found that they developed proliferative macrophage lesions containing Ym1/Ym2 protein and crystals in lung, bone marrow, lymph nodes, and spleen. Here, we show that the lung lesions progressed from single macrophages with intracellular Ym1/Ym2 protein crystals to severe diffuse crystalline macrophage pneumonia without histological evidence of either granulation tissue or pulmonary fibrosis. Ym1/Ym2 is a chitinase-like secretory protein that is transiently induced in alternatively activated macrophages during T-helper (Th)2-biased pathogenesis and during chemical and traumatic inflammation. Bronchoalveolar lavage from p47(phox-/-) mice contained significantly higher levels of Th-1 (interferon-gamma), Th-2 (interleukin-4), and Th-17 (interleukin-17)-associated cytokines than wild-type mice, as well as copious amounts of interleukin-12, indicating that Ym1-secreting p47(phox-/-) macrophages are also integrated into classically activated macrophage responses. These results suggest that p47(phox-/-) macrophages are extremely pliable, due in part to an intrinsic dysfunction of macrophage activation pathways that allows for distinct classical or alternative activation phenotypes.
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PMID:p47phox deficiency induces macrophage dysfunction resulting in progressive crystalline macrophage pneumonia. 1909 58