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Insulin secretion after oral (100 g) and i.e. glucose (0.33 g/kg b.w.) was studied in 14 patients with 21-trisomy (Down's syndrome) and in 18 normal subjects. Plasma immunoreactive insulin (IRI), fasting and at predetermined time intervals during each glucose load, was measured by a double antibody method (Hales-Randle). Tolerance to oral glucose in Down's patients was found to be normal though a fiat, late peaked glyeacmic response was characteristic of the group. Fasting IRI and insulin levels after oral glucose in patients did not significantly differ from those in the normal group. After i.v. glucose, the patients showed a slower decline of the blood sugar, maintaining significantly higher levels than the normats at 30, 40, 50 and 60 min after the glucose load. However, the peripheral glucose uptake expressed by the K index (Conard).did not significantly differ from the normal despite the lower K'values in the patients. Insulin release aftcr i.v. glucose showed some differences between both groups.-The present study cannot support a causal relationship between D.M. and the 21trisomy through an altered insulin secretion.

Addison's disease has been studied. Tbe results showed no significant differences in fasting glycemia nor in I.R.I. levels in patients be fore and after hydrocortisone treatment. After hydrocortisone slightly higher glycemic levels after O.G.T.T. were obtained but still remaining within the adopted criteria of normality for this test. However, the insulinemic response after oral glucose load was significantly enhanced (p < 0.05) at 60 and 90 minutes. Also the insulinernie response induced by l.V. tolbutamide was significantly higher after hydrocortisone particularly in the very early insulin release phase (minute 1). However, hydrocortisone while slightly improving glucose peripherical uptake after I. V. glucose, did not significantly modify the insulin release pattern. Tbe results would favour an indirect rather than a direct action of hydrocortisone on glucose induced insulin release, perhaps by amplifying the effects of the entereinsular axis.

After reviewing the incidence of diabetes and hypertension as associated diseases, 1,000 cases of diabetes and 1,000 cases of arterial hypertension are reviewed. The statistical results permit us to affirm that there is no direct relation between the two diseases. If hypertension seems to be somewhat more frequent in diabetics than in the general population, this is due to vasculorenal or endocrine alterations which, with relative frequency associates with or are complications of the same diabetes, but this does not support the existence of a common etiopathogenic link.

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