In the accounts which have been given [Dunn, McLetchie & Sheehan, 1943;Dunn, Kirkpatrick, McLetchie & Telfer, 1943] of the finding of necrosis of the pancreatic islets after intravenous injection of alloxan in rabbits, it was pointed out that this lesion came to light only because of the unexpected deaths at 12-48 hr. of certain of the animals so treated. Later it was recognized that such deaths were preceded by hypoglyeaemia and hypothermia, and sometimes by convulsions as had been observed by Jacobs [1937]. The doses which gave fatal results were usually relatively large, 200-300 mg./kg. body weight, but it was known, from experiments done prior to finding the islet lesions, that similar deaths might occur, though rarely, after a much smaller dose, in one case 25 mg./kg. On the other hand, somne rabbits had survived for more than 48 hr. doses of 300 and even 500 mg./kg., given on 1 day, without it being realized from ordinary observation that they had pfassed through a critical phase. As the pancreas was not examined in these animals the condition of the islets was not ascertained, nor was any alteration of the blood sugar suspected. Once the lesion of the islets had been found it appeared desirable that further information should be obtained as to the conditions of its occurrence and its pathogenesis, and it has been possible to carry out some experiments with this in view. These experiments have combined general observations on the animals and estimations of blood sugar with histological examination of the pancreas, and have been intended to find answers to three main questions: (1) the frequency of occurrence of islet necrosis after single intravenous doses of alloxan such as have been known to produce it; (2) the rate of development of necrosis from the earliest stages, and (3) the effects, if any, of smaller doses.
EXPERIMENTSThe rabbits used were bf various breeds. They were kept in metabolism cages and their usual daily food was 150 g. each of oats and bran, mixed with 200 c.c. water. About 150 g. cabbage was also given daily with rare lapses due PH. CIII.
The refeeding syndrome is increasingly recognised. It is a serious change in electrolytes when nutrition is reintroduced to malnourished patients. Alcohol dependence is a risk factor for the refeeding syndrome. We report a prospective cohort study of 36 alcoholics hospitalised for withdrawal management. We found no evidence of refeeding syndrome in any patient after 3 days of hospitalisation, despite hypomagnesaemia, a risk factor for the refeeding syndrome being prevalent (44% of subjects). Low thiamine levels were infrequent affecting 3/29 (10%). We recommend that in alcoholics admitted for managed withdrawal, risk of refeeding syndrome appears to be low, and routine testing of repeat electrolytes appears unnecessary.
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