In 20 female patients treated for 2 to 37 years (mean :12) with anticonvulsant drugs, low serum levels of 25-hydroxy-vitamin D (25-OH-D; 6.4 +/- 3.2 ng/ml M +/- SD), relative hypocalcemia (9.2 +/- 0.4 mg/100 ml) and high levels of parathyroid hormone (PTH 277 +/- 165 pg/ml) were found compared to an age-matched control group (respectively 8.6 +/- 3.2 ng/ml, 9.6 +/- 0.3 mg/100 ml and 183 +/- 95 pg/ml) living in the same psychiatric clinic. A significant negative correlation was found between total duration of treatment and either serum 25-OH-D or serum calcium. After treatment with an oral vitamin D3 supplement (2000 IU/day) for 3 weeks, the serum 25-OH-D levels, although increased, remained lower than normal in the epileptic group and neither hypocalcemia nor their secondary hyperparathyroidism were corrected. These data confirm the occurrence of vitamin D deficiency in patients treated with anticonvulsant drugs resulting in hypocalcemia and secondary hyperparathyroidism.

The effects of subclinical vitamin D deficiency and vitamin D supplementation on oral glucose tolerance and secretion of pancreatic hormones were studied in 10 diphenylhydantoin-treated epileptic patients and 15 geriatric patients. Their mean serum concentrations of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 decreased markedly, but returned to normal within 2 weeks of oral supplementation with 25-hydroxyvitamin D3. The serum concentration of ionized calcium was within the normal range before treatment, and remained unchanged. Serum parathyroid hormone was increased during vitamin D deficiency, but decreased significantly (p less than 0.05) afterwards. In vitamin D-deficient epileptic and geriatric patients, the 2- and 3-h insulin levels after glucose ingestion were increased when compared with control values, and glucagon secretion was not suppressed by glucose. Oral glucose tolerance of both groups of patients did not change after 25-hydroxyvitamin D3 supplementation. Insulin secretion remained unchanged in geriatric patients, but was reduced to normal values in epileptic patients. Glucagon suppressibility by glucose was partly restored after vitamin D supplementation in epileptic patients but not in geriatric patients. In contrast to that observed in severely vitamin D-deficient rats or rabbits, correction of subclinical vitamin D deficiency failed to enhance insulin secretion or to improve glucose tolerance in man.

The aim of this study was to carry out a small-scale bacteriological comparison between a standard therapy with norfloxacin 400 mg twice daily, and fosfomycin trometamol (3 g) in single dose in uncomplicated urinary tract infections (UTI) in women. Only patients with UTI with cultures showing a bacterial count of 10(5) or more bacteria/ml were included in the study (n = 32; ages 16-75 years). After one week sterile cultures were obtained in 14 of 16 cases in the fosfomycin trometamol group, and in 14 of 16 cases in the norfloxacin group. After one month eradication was confirmed in 13 of 16 patients in the fosfomycin trometamol group, and in nine of 16 patients in the norfloxacin group. Recurrence was seen in one case in the fosfomycin trometamol group, and in five cases in the norfloxacin group. The reinfection and persistence rates were identical (1/16) in both groups. The main clinical symptoms disappeared very rapidly after initiating treatment, and the correlation with the bacteriological data after one week was excellent. Both drugs were well tolerated and the compliance for fosfomycin trometamol was 100%.

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Eighteen patients with mild to moderately severe hypertension were treated, after a run-in period of placebo for three weeks, with a combination of 160 mg sotalol and 25 mg hydrochlorothiazide for three months. Fifteen patients responded well and, after one month of treatment, had a sustained diastolic blood pressure of less than 100 mm Hg. Additional treatment reduced the blood pressure even further during the second month, with a significant fall in blood pressure after the first month of treatment. The degree of severity of the hypertension did not seem to have an effect on blood pressure response to treatment. Serum potassium values decreased significantly during treatment. They remained within the normal range, and no clinical symptoms of hypokalemia were observed. One patient developed hyperuricemia and had to be withdrawn from the study.