Finding
Paper
Abstract
been given for a short time and then restarted after a long interval of treatment by diet alone. In this connexion it is not very uncommon for manifestations of insulin allergy to be associated with a return to insulin therapy. None of our cases showed such manifestations, but the association between allergy and resistance has been noted on a number of occasions (Berne and Wallerstein, 19O). The reason why greater amounts of antibody are not formed in response to insulin treA.ment may possibly be related to the method of its administration; in no course of prophylactic immunization is antigen given once or more daily over long periods. The restarting of insuLin might well be expected to act as a booster dose, and, on general principles, be more likely to lead to greater antibody production. The results of the P.C.A. and R.D. tests obtained in our cases support the widely held view that there are a number of different causes of insulin resistance. It can be assumed that a serum giving a positive P.C.A. test contains insulin antibodies, whereas the R.D. test is capable of de-tecting several different types of antagonist. In Case 5 the P.C.A. test was negative and the R.D. test positive, but it is significant that P.C.A. ant.5odies have not been found when the serum contained no demonstrable antagonist. At present prednisone appears to benefit a group of insulin-resistant diabetics whose daily insulin requirement is nearer 1;000 than 200 units and in whom can be found no apparent cause for the resistance. The time interval between the start of insulin treatment and the development of resistance is usually less than a year, and often between three and six months; in our experience all such cases have had demonstrable insulin antibodies.
Authors
C. Stuart-harris
Journal
British Medical Journal