Glomerular filtration rate is an independent determinant of plasma tHcy and tCys concentrations, and GFR is rate limiting for renal clearance of both homocysteine and cysteine in diabetic patients without overt nephropathy. Declining GFR explains the age-related increase in plasma tHcy, and hyperfiltration explains the lower than normal mean plasma tHcy and tCys concentrations in populations of diabetic patients.

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The well-known size-reducing effect of bromocriptine on prolactinomas was tested on five types of large, extrasellar pituitary tumors. Twenty patients were treated prospectively for up to 4.5 years with bromocriptine, 30 or 60 mg/d (two patients received 15 mg and 160 mg, respectively). The effect on the size of the pituitary tumors was quantitated by planimetry of computed tomographic scans before and during treatment. The immediate success rate was 16 of 20 tumors. Eleven nonsecreting tumors were reduced by a median of 32% (range of reduction for 50% of cases, 18%-41%) with an immediate success rate of nine of 11. Nine secreting tumors (four that secreted prolactin; three, growth hormone; one, adrenocorticotropic hormone; and one, thyroid stimulating hormone) were reduced by a median of 51% (range of reduction for 50% of cases, 25%-72%). The reduction in tumor size was significantly associated with pretreatment size (r=0.6360, p less than 0.005), but not with the serum concentration of any hormones assayed or previous radiation treatment. Bromocriptine causes a clinically significant reduction in size of nonsecreting as well as secreting pituitary tumors with the same success rate as that of conventional treatments.U

We have investigated the effect on the human pituitary-gonadal axis of the H2-receptor antagonists cimetidine 300 mg and ranitidine 50, 100, and 200 mg by i.v. bolus, or treatment for 6 months with either cimetidine (1000 mg/day for 1.5 months followed by 400 mg/day for 4.5 months) or ranitidine (200-400 mg/day for 1.5 months followed by 100-200 mg/day for 4.5 months). Administration of the H2-antagonists (i.v.) to normal men did not cause any release of LH, FSH, or testosterone. Long-term treatment with cimetidine of duodenal ulcer patients caused a significant rise in basal LH (6 weeks) and FSH secretion (11 weeks). Following reduction of the cimetidine dose LH and later FSH returned to pre-treatment values. However, despite reduction of the cimetidine dose, the LH and FSH responses to LHRH stimulation were still significantly higher after 6 months of treatment compared with pre-treatment responses. No changes were found in basal or in LHRH stimulated testosterone or dihydrotestosterone secretion. Treatment with the more potent H2-antagonist ranitidine did not cause any change in basal or in LHRH stimulated LH and FSH secretion. The effects on LH and FSH secretion observed during cimetidine treatment might therefore be caused by other mechanisms than blockade of H2-receptors. It is possible that cimetidine, having anti-androgen properties, blocks pituitary or hypothalamic androgen receptors.