Patients with chronic renal failure suffer from secondary hyperparathyroidism and have greatly increased blood concentrations of intact parathyroid hormone (PTH) and PTH fragments. Thus PTH has been regarded in the last few years as a uraemic toxin possibly responsible for many clinical manifestations of the uraemic syndrome including a tendency to prolonged bleeding. Since PTH inhibits platelet aggregation 'in vitro', the possibility that hyperparathyroidism of uraemia plays a role in the pathogenesis of uraemic bleeding has been considered. Clinical data to support this possibility is not available so far. In this study we have correlated the skin bleeding time, the best clinical marker of uraemic bleeding tendency, with serum concentrations of intact PTH or PTH fragments in 40 patients with chronic renal failure undergoing chronic haemodialysis. Since the skin bleeding time is known to be influenced by packed cell volume (PCV), we also considered two distinct groups of uraemic patients on the basis of their PCV values. The results indicated that bleeding time does not correlate with serum concentrations of intact PTH or PTH fragments. Also, no correlation has been found between PTH values and blood concentrations of calcium, phosphorus, magnesium and hydroxyproline. It is concluded that elevated PTH values in renal-failure patients do not contribute to uraemic platelet defect, as reflected by the skin bleeding time.

To verify if exogenous prostaglandin E₂ (PGE₂) is able to release antidiuretic hormone (ADH) and if endogenous angiotensin II plays a role in this eventual PGE₂-induced stimulation of vasopressin, increasing doses of PGE₂ were infused in 6 normal volunteers before (PGE₂ study) and after the administration of 100 mg of captopril (captopril study). PGE₂, even at an infusion rate of 40 and 60 ng/kg/min, did not modify blood pressure when it was infused alone; a significant fall of blood pressure was observed, in contrast, in the captopril study. PGE₂ alone doubled the plasma levels of ADH. One hour after the subjects had been pre-treated with captopril, plasma levels of ADH fell by about 38%, then they increased by about 60% during the infusion of PGE₂. These results suggest that in normal man endogenous angiotensin II is an important non-osmotic regulator of plasma ADH and that exogenous PGE₂ can stimulate maximally the release of ADH only when the renin-angiotensin system is not impaired.

High levels of immunoreactive calcitonin (iCT) in the blood of heroin addicts were previously reported. As it is well known that multiple forms of calcitonin exist in the blood and in tissues, the purpose of the present study was to investigate the immunological nature of the CT-like immunoreactive material found in the blood of these subjects. We investigated 25 addicts, who had been using heroin for more than one year and were hospitalized for a 2 week detoxication program. Blood samples were drawn at the start of the program (when the subjects were still on heroin) and after 5 and 12 days of abstinence from heroin. Twenty-five healthy subjects served as controls. We used 2 commercial RIA kits, calibrated against the same reference material (WHO 70-234), but employing different antisera. One antiserum substantially confirmed the previous findings of increased levels of calcitonin during heroin use, but the other seemed to exclude any change in the hormone concentrations. This suggests that the "calcitonin like" material found in heroin addicts contains some epitopes similar to those found in the calcitonin standard which are detected by the first antiserum. However it lacks other epitopes which are also present in calcitonin standard and which are recognized by the second antiserum. Therefore, this substance seems to be different from the standard human calcitonin 1-32. A possible involvement of a calcitonin analogue (precursor or metabolite) in the biochemical changes occurring during chronic opiate use is suggested.

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