Necrotizing sarcoid granulomatosis with extrapulmonary involvement. Clinical, pathologic, ultrastructural, and immunologic features.
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Biomedical subjects
Publications and source records attributed to M Conway.
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In this report we describe the characteristics of human anti-LRH antibodies detected in the serum of a male patient with isolated gonadotropin deficiency. He had received 90 days of therapy with LRH (1 mg, sc, three times daily) and was then placed on three cycles of intermittent therapy (3 weeks of LRH daily, followed by hCG every 3 days for 15 days). At the start of the fourth cycle of therapy with LRH, he developed urticaria at the site of injection, at sites of previous LRH injections, and at distant sites. Upon direct skin testing, the patient reacted positively to 0.02 ng LRH intradermally. A positive intradermal reaction was induced in a normal adult male by preparing his skin with 0.1 ml of the patient's serum and, 24 h later, injecting 0.2 microgram LRH at that site. A binding factor for LRH was detected in the patient's serum by incubation with [125I]LRH. The serum bound 33% of tracer compared to 6% in control serum. We have detected both immunoglobulin G and immunoglobulin E antibodies against LRH in the patient's serum. We have compared displacement of tracer by synthetic LRH with displacement achieved by a series of analogs. Displacements of tracer by LRH, [Lys8]LRH, [D-Trp6,Pro9-NEt]LRH, [des-Gly10]LRH, and [Phe2]LRH were similar, whereas the potencies of Ac-LRH5-10 and AcLRH2-10 were 0.1% or less.
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This study examined the effects of clofibrate therapy on basal plasma substrate and hormone concentrations in ketosis-prone insulin-dependent diabetic man. A double-blind crossover design was utilized during a 3-mo period in which clofibrate treatment (1 g b.i.d.) was compared to that of a lactose placebo (1 g b.i.d.). Our results demonstrate that clofibrate treatment resulted in a significant reduction in the concentration of plasma glucose, ketone bodies, free fatty acids, triglyceride, and cholesterol in diabetic man. These beneficial effects were observed without demonstrable changes in circulating concentrations of insulin and glucagon. These observations suggest that in ketosis-prone diabetic man, clofibrate therapy may provide an adjunct to exogenous insulin administration.
The effect of pharmacologically induced altered autonomic tone upon alanine stimulated insulin release was examined in adult norgrel dogs. In control studies, intravenous administration of alanine, 1 gm/kg body weight resulted in a mean rise in plasma insulin concentration from basal levels of 7.4 (+/- 2) MUU/ml to a maximum of 24.5 (+/- 6) muU/ml by 10 minutes after injection. In paired studies, epinephrine infusion or atropine administration had no significant effect on the insulin rise in response to the alanine stimulus. This data indicates that in contrast to a glucose stimulus, the insulin response to the amino acid alanine is not influenced by epinephrine or cholinergic blockade. These studies provide further evidence that alanine acts through alternate pathways, different from those utilized by glucose to effect insulin secretion.
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Glucagon concentration and regulation were examined in the Zucker rat, in which obesity and hyperlipemia are phenotypic expressions of an autosomal recessive gene. Using littermate animals which are phenotypically thin and normolipemic as controls, we observed reduced basal plasma glucagon levels in the obese lipemic rats. In response to fasting, obese lipemic animals inappropriately demonstrated a further reduction in plasma glucagon concentration. In response to pharmacologic glucagon stimulation (arginine), a subnormal rise in plasma glucagon concentration was observed in the obese, lipemic animals. Glucagon suppressibility with exogenous glucose remained intact. The reduced secretion of glucagon may be a consequence of the abnormal elevation in concentration of plasma insulin, free fatty acids, and glucose, which are characteristic of the obese, lipemic animal. A possible role of glucagon deficiency in the evolution or maintenance of the lipemic state is suggested.
An oxygen electrode mounted in the tip of an umbilical artery catheter was used in 36 newborn infants with severe respiratory illnesses, 28 of whom survived. Thirty-seven electrodes were used. The median age at insertion was 4 hours (range, 30 minutes to 122 hours). Three electrodes failed to work and they were removed or replaced, and two could not be properly evaluated. Thirty-two electrodes functioned satisfactorily for 10 to 190 hours (mean, 75 hours) after a one-point calibration against blood sampled through the catheter. Twenty-two did not need recalibrating before they were removed after 10 to 190 hours (mean, 88 hours. Four of the remaining ten electrodes were recalibrated once after 33 to 97 hours and then functioned until removed 15 to 55 hours later. The other six electrodes failed after 32 to 105 hours (mean, 49 hours). Complications were few. A total of 356 arterial blood samples, obtained after the initial calibration and before any recalibration was necessary, gave a correlation coefficient of 0.93 (P less than .0001) against an independent system for measuring arterial oxygen tension (Pao2) (Radiometer Type E.5046 oxygen electrode). We conclude that the catheter-tip electrode is a safe and reliable instrument for continuously recording Pao2 in newborn infants which much simplifies the management of serious respiratory illnesses.
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A double-blind crossover study comparing floctafenine 200 mg, a new analgesic drug, and dihydrocodeine 60 mg, was performed on 72 patients suffering from post-operative pain. Degree of pain relief by floctafenine was similar to that of dihydrocodeine but the relief afforded by the former was of longer duration. Side-effects associated with dihydrocodeine were statistically higher than those associated with floctafenine. Floctafenine was demonstrated to be an effective analgesic with an insignificant incidence of untoward side-effects.
Seventy-seven patients took part in a double-blind crossover trial to compare the effects of floctafenine, dextropropxyhene and aspirin in the relief of post-operative pain. Pain levels were recorded at hourly intervals and pain relief scores calculated. For Dose 1, the difference between the mean pain relief score for patients receiving floctafenin (12.8) and that for patients receiving dextropropoxyphen (6.2) was significant, (p smaller than 0.05) but the difference between the mean score for aspirin (9.2) and that for dextropropoxyphene was not significant. For Dose 2, there were no significant differences between the mean pain relief scores for floctafenine (12.5), for aspirin (10.9) and for dextropropoxyphene (13.2).
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