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Changes in blood glucose and insulin metabolism, both under basal conditions and after glucose and glucagon stimulus, were studied in 95 patients with chronic alcoholic hepatopathy. Peptide C was also determined in 19 patients. A high incidence of islet-cell insufficiency was noted. Stress is laid on the multiplicity of the pathogenetic mechanisms responsible for blood glucose and insulin changes during chronic alcoholic hepatopathy, particularly liver cell damage, hyperglucagonaemia, organic and/or functional islet-cell insufficiency, and peripheral insulin resistance. It is felt that the last two of these are of major importance, whereas liver cell damage is of secondary significance, at any rate as far as glucose and insulin turnover is concerned.

The authors have investigated the changes of kalemia and kaluria levels in 40 patients suffering from delirium tremens, and have observed during the acute stage of the illness, a swift fall of kalemia level without an increase of the kaluric excretion. The kalemic values quickly rise up again at the end of the delirium.. The authors think that an adrenergic mechanism is responsible for this quick and transient hypokalemia. The significance of this adrenergic mechanism in the alcohol withdrawal syndrome is at present widely proved.