Hypersensitivity vasculitis due to ofloxacin.
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Biomedical subjects
Publications and source records attributed to S Dux.
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Two patients with severe hypoglycemia due to inadvertent use of oral hypoglycemic agents are described. Unintentional substitution of tablets with sulfonylurea drugs was related in both cases to a similarity in shape and color of the pills. In one case glyburide was interchanged with an artificial sweetener, while in the other case chlorpropamide was dispensed by a pharmacist instead of quinidine bisulfate. To our knowledge, 20 similar cases have been reported in the medical literature. Most of them were attributed to sound-alike trade names of drugs. Inadvertent sulfonylurea-induced hypoglycemia has to be included in the differential diagnosis of severe unexplained hypoglycemia. This dangerous condition can be prevented by instructing patients to carefully identify their drugs, introducing typed prescription forms using generic names, and avoiding similar names and appearance of pills.
Erythema nodosum and IgA nephropathy are nosologic entities with an immunologic background. IgA nephropathy is a specific disease of the kidneys, while erythema nodosum may be associated with other illnesses. We report a unique case in which intermittent hematuria due to IgA nephropathy was superimposed on recurrent attacks of erythema nodosum and arthritis. A common pathophysiology is suggested.
Hyperammonemic coma developed in a 69-year-old woman with prolonged symptoms of abdominal pain, dysphagia, and fever. At laparotomy for an acute condition within the abdomen, mesenteric vein thrombosis was found and partial intestinal resection was performed. Following surgery, the patient regained consciousness and blood ammonia levels became normal. Hyperammonemia and coma complicating mesenteric vein thrombosis have not yet been described. Venous shunts are suggested as being responsible for this rare complication.
We have previously described, in insulin-dependent diabetic subjects (IDDM), a small, but significant, increase in the insulin clearance rate (ICR) during 0600-0800 h as compared with 0100-0300 h. To determine whether this increase was also seen at more physiologic levels of insulin replacement, we calculated ICR during euglycemic clamp studies in 13 patients with IDDM with a constant infusion of insulin at 20 mU/min/m2 and during insulin replacement from the Biostator GCIIS without exogenous glucose. During the euglycemic clamp study with constant insulin infusion at 20 mU/min/m2, the ICR was 16% higher at 0600-0800 h than at 0100-0300 h (264 +/- 50 ml/min/m2 versus 228 +/- 51 ml/min/m2; P less than 0.005). During insulin replacement by the Biostator, the mean insulin infusion rate increased by 92 +/- 27% (7.5 +/- 1.1 to 13.5 +/- 1.2 mU/min/m2; P less than 0.001) and ICR increased by 123 +/- 30% (130 +/- 24 to 268 +/- 51 ml/min/m2; P less than 0.01) during the prebreakfast period when compared with 0100-0300 h. There was a highly significant correlation (r = 0.97) between the increment in insulin infusion rate and the increment in ICR. Measurement of insulin concentration in saline solutions, delivered by the Biostator at a same rate and under similar conditions to those in this study, showed that insulin delivery was stable for the 8-h period of this study.(ABSTRACT TRUNCATED AT 250 WORDS)
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D-penicillamine and a variety of analogs have been tested for their ability to interfere with the various stages of bone development using a model for endochondral bone formation. At the highest dose tested (40 mg/rat/day), D-penicillamine inhibited mineralization, D-2-Amino-3-methyl-3-[(2-acetamidoethyl)dithio]butanoic acid (II), at a relatively low dose (10 mg/day), decreased the amount of insoluble collagen in skin, mesenchymal cell proliferation on Day 3, and inhibited bone formation on Day 14. Several other compounds tested, sodium 4-[(D-1, 1-dimethyl-2-amino-2-carboxyethyl)-dithio]butanesulfinate (IV), 2-acetamidoethyl-2-acetamidoethanethiolsulfonate (V), and sodium 4-mercaptobutanesulfinate trihydrate (VI), also inhibited osteogenesis on Day 14.
Undiagnosed myocardial infarction of the right ventricle presented as Dressler's syndrome. Radioisotopic diagnostic procedures including first-pass and multigated acquisition nuclear angiography ( MUGA ) and thallium-201 perfusion studies enabled a retroactive diagnosis of myocardial infarction, showed it to be in the right ventricle, and clarified the aetiology of the unexplained fever and pleuropericarditis.
Empyema of the left pleural cavity developed suddenly in a nonalcoholic cirrhotic patient. Cultures of the pleural fluid under anaerobic conditions grew Clostridium perfringens, an organism normally found in the enteric flora. The infection developed in an old pleural effusion. Since there was no evidence of trauma, necrotizing pneumonitis or subphrenic infection, spontaneous bacterial pleuritis is proposed.
Plasma renin activity, plasma aldosterone, and serum-converting enzyme activity were measured in 13 normotensive pregnant women in three sequential periods: 19-21, 29-31, and 38-40 weeks of gestation. The converting enzyme activity was also measured in a group of 6 women with hypertensive pregnancy and an age-matched control group of 35 normal nonpregnant women. Plasma renin activity and plasma aldosterone values were both significantly elevated in the three periods of pregnancy, but plasma aldosterone levels were relatively lower during the first two periods. This is suggested to be secondary to depressed aldosterone secretion by intravascular volume expansion. The serum-converting enzyme activity did not change during pregnancy, and the mean values (1.02 +/- 0.27 U) were lower than those found in the control group (1.23 +/- 0.26 U). Similar low values were found in the hypertensive pregnancy group (1.11 +/- 0.35 U). Therefore, we assume that the converting enzyme is not a limiting factor in the conversion of angiotensin nor does it contribute significantly to the pathogenesis of hypertensive pregnancy.
The serum converting enzyme activity (SCEA) was measured in 86 healthy individuals (1.44 +/- 0.82 u, mean +/- SD), 39 patients with essential hypertension (1.53 +/- 0.71 u), 7 patients with hypertension due to renal artery stenosis (1.76 +/- 0.77 u), 14 patients with chronic renal failure (2.10 +/- 0.57 u), 7 patients with renal failure and hypertension (2.62 +/- 0.35 u), 22 normotensive pregnant women (1.02 +/- 0.26 u) and 6 hypertensive pregnant women (1.1 +/- 0.3). No difference was detected between men and women or between normotensives and hypertensives. However, a significant rise in SCEA was found in patients with chromic renal failure (P less than 0.005), in whom an enlarged pulmonary vascular bed and accelerated cellular breakdown are thought to be the causes of the elevated SCEA. During pregnancy, subnormal SCEA was found (P less than 0.005), and this is thought to be due to the enzyme consumption in the kinin system, which is activated during pregnancy. We assume that converting enzyme is not a limiting factor in angiotensin conversion, and most probably it does not contribute significantly to the pathogenesis of hypertension.
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A previously healthy 65-yr-old man developed clinical signs of prepatellar bursitis. Aerobic cultures from fluid aspirated from the inflamed prepatellar bursa were negative. Direct microscopic examination of the fluid showed gram-positive cocci, and anaerobic cultures grew Streptococcus hemalyticus group A. The bacterial etiology of bursitis has recently been emphasized in the literature; in most of our cases Staphylococcus was responsible. Negative cultures were next in frequency. Other microorganisms may indeed be responsible for prepatellar bursitis and should be sought where aerobic cultures are negative.
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A percutaneous renal biopsy was performed on a 50-year-old female with rapidly progressive renal failure. The histologic specimen was characteristic of an immune complex disease, most likely systemic lupus erythematosus. Serologic tests were negative. 8 days after the biopsy, there was a spontaneous rupture of the kidney which necessitated nephrectomy. As no connection was found between the biopsy site and the rupture, it was concluded that the rupture was spontaneous in a patient with an immune complex disease.