Biomedical subjects
Publications and source records attributed to J Koster.
Forty-eight patients with proven hyperparathyroidism underwent parathyroidectomy. All patients were post-operatively normocalcaemic and free of symptoms due to their pre-operative hypercalcaemic state. However, 20 (42%) post-operative patients still had increased serum PTH and low serum phosphate levels.
Twelve patients were followed up for 3 months after parathyroidectomy. Serial measurements of serum parathyroid hormone (PTH), calcium, and phosphate were made. Four patients had an increased serum PTH postoperatively, which was already apparent by the third postoperative day. All patients became normocalcemic. Their hyperparathyroid-like phosphate parameters indicated that we were dealing with a biologically active PTH. Using preoperative biochemical parameters it was impossible to predict which patients would have an increased PTH postparathyroidectomy (PTX). Probably the patients with high PTH post-PTX had higher parathyroid volumes. In our opinion after PTX, a normocalcemic high PTH situation should be avoided by 3 1/2 parathyroid gland extirpation in all cases.
Subjective and objective psychophysiological responses to erotic visual stimulation were recorded for 24 women with diabetes mellitus type I and 10 control women. There were no significant differences in subjective responses (general sexual arousal and genital arousal) between the two groups. The objective response, a rise in the temperature of the labium minus, varied with the height of the initial temperature. Since this temperature was significantly higher in diabetic women, the subsequent rise during erotic visual stimulation was less in diabetic women than in controls. When samples from the two groups were matched for initial temperature, the difference in the increase in labial temperature was no longer statistically different. In both groups of women there was a significant correlation between the degree of subjective arousal and the rise in labial temperature when women with a high temperature (greater than 37 degrees C) at the start of the visual erotic stimulation were not included. The absence of a statistically significant effect of diabetes mellitus on the parameters studied may be due to a lack of serious neuropathy and angiopathy in the present sample of diabetic women. Future psychophysiological studies should include women with serious neuropathy with or without diabetes mellitus.
Blood lead (Pb) and urinary Pb before and after i.v. infusion of 1 g of Na2Ca EDTA were determined (atomic absorption) in 46 control subjects and 91 patients with various stages of renal failure (median serum creatinine 2.5 mg dl-1). Under baseline conditions, patients with renal failure had higher blood Pb levels (112 ng ml-1, range 44-272 vs. 76; 36-187 in controls; P less than 0.001) and lower urinary Pb (16.2 nmol 24 h-1 1.73 m-2, 4.86-66.8 vs. 33; 11-91 in controls; P = 0.001). The increment in urinary Pb after EDTA infusion (mobilizable Pb) was higher (795 nmol 4 days-1 1.73 m-2, range 155-5611 vs. 307; 131-1587 in controls; P = 0.001). In 12 patients with renal failure (13%) mobilizable Pb was above the highest value in controls. Mobilizable urinary Pb correlated (r = 0.68) significantly (P = 0.001) with blood Pb, but only marginally with serum creatinine (r = 0.32; P less than 0.007). Mobilizable Pb was higher in patients with renal failure and a history of smoking or occupational Pb exposure and tended to be higher in patients with alcoholism. Ten of 91 patients had gout; increased mobilizable Pb was present in three of the 10. The data confirm relatively high prevalence of elevated body Pb burden in European patients with chronic renal failure. The question is unresolved whether Pb plays a role in the progression of renal failure.
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In a double-blind crossover study in which patients received placebo or active drug for varying periods, we evaluated the ability of guanidine hydrochloride (20 to 35 mg/kg per day perorally) to improve the rate of recovery in patients with moderate or severe botulism, type A, intoxication. Among 14 patients who received conventional botulism therapy, there was no improvement in recovery rate in those who received guanidine compared with the nontreated group. Individual patients in the treated group showed neither an acceleration in their rate of improvement when they received guanidine nor a regression in their progress when the drug was stopped. Individual patients, likewise, noted no subjective improvement when they received the drug compared with the placebo. Treatment with guanidine does not enhance recovery from botulism.