Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report]. 807 26

Chemical burns are associated with significant morbidity, especially anhydrous ammonia burns. Anhydrous ammonia is a colorless, pungent gas that is stored and transported under pressure in liquid form. A 28 year-old patient suffered 45% total body surface area of second and third degree burns as well as inhalational injury from an anhydrous ammonia explosion. Along with fluid resuscitation, the patient's body was scrubbed every 6 h with sterile water for the first 48 h to decrease the skin pH from 10 to 6-8. He subsequently underwent a total of seven wound debridements; initially with allograft and then autograft. On post burn day 45, he was discharged. The injuries associated with anhydrous ammonia burns are specific to the effects of ammonium hydroxide. Severity of symptoms and tissue damage produced is directly related to the concentration of hydroxyl ions. Liquefactive necrosis results in superficial to full-thickness tissue loss. The affinity of anhydrous ammonia and its byproducts for mucous membranes can result in hemoptysis, pharyngitis, pulmonary edema, and bronchiectasis. Ocular sequelae include iritis, glaucoma, cataracts, and retinal atrophy. The desirability of treating anhydrous ammonia burns immediately cannot be overemphasized. Clothing must be removed quickly, and irrigation with water initiated at the scene and continued for the first 24 h. Resuscitative measures should be started as well as early debridement of nonviable skin. Patients with significant facial or pharyngeal burns should be intubated, and the eyes irrigated until a conjunctivae sac pH below 8.5 is achieved. Although health care professionals need to be prepared to treat chemical burns, educating the public, especially those workers in the agricultural and industrial setting, should be the first line of prevention.
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PMID:Anhydrous ammonia burns case report and review of the literature. 1081 76