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Genetic counselling in insulin‐dependent diabetes

Less than 10% of diabetics are under age 20 at onset of the disease, but this small fraction represents a distressingly large proportion of the total stress which this disorder imposes. Nearly all these young diabetics require regular insulin injections in addition to constant monitoring of their daily activities. For the insulin dependent child or adolescent, the prospect of a lifetime shackled to such a medical regime is a psychological trauma requiring great sensitivity on the part of those responsible for their care. Psychological distress is not confined to the patient and often shows itself in the anxiety of parents and unaffected sibs. One of its frequent manifestations is expressed in questions such as: “What are the chances that another child will develop the disease?”, or, “If I marry will my children become diabetic?”. Answers to these questions in the past have been difficult to give with any degree of assurance. There are some situations, however, where the counsellor can now be reassuring and the paper by Cox and Bourke, in the present issue, is a good example. What precipitates the onset of insulin dependent diabetes is still not fully understood, but it is certainly not entirely genetic. This is evidenced by the fact that only 50% of identical co-twins develop insulin-dependent diabetes in contrast to nearly 100% of co-twins who develop non-insulin dependent diabetes. However, there are some deterministic factors which can be discriminated readily. Studies in many parts of the world have shown that persons with certain tissue antigens or HLA types have an increased risk of developing insulin-dependent diabetes. Thus, a person with HLA B8 is 2.6 times more likely to develop the disease than is a person who is 68 negative. Similarly the relative risk for a person with 815 is 1.8 and with B18 is 2.0. When the HLA-D antigens are considered the relative risks are even higher, being 3.7 for DRw3 and 7.4 for DRw4. As shown by Serjeantson and her colleagues’ in a recent study of multiple-case juvenile diabetic families in Australia the relative risk for children, who carry both the DRw3 and DRw4 antigens, is increased to nearly 40. Of equal interest is that the HLA DRw2 antigen is associated with resistance to the disease. Indeed, the most recent reports show that persons carrying this antigen have a relative risk of less than 0.1. It is this fact which enabled Cox and Bourke to apply effective counselling in the case they report. The father and three sisters of the boy being counselled had insulin dependent diabetes. His mother was unaffected, but the boy himself showed anxiety symptoms related to his fear of developing the disease. HLA typing revealed the father and two affected sisters to be carrying the DRw31DRw4 high risk factors and, the other affected sister was homozygous for DRw4, itself a relatively high risk combination. The boy’s mother, who had not developed the disease, was carrying one DRw4, but also the low-risk factor, DRw2. The boy himself had inherited this low-risk DRw2 from his non-diabetic mother and was therefore considered to be unlikely to become diabetic. Unfortunately, not all families present the counsellor a genetic pattern which allows such a degree of assurance. However, HLA typing combined with studies of other genetic markers, particularly those in the C2, C4 and Bf complement systems, will become an increasingly important tool in genetic counselling for insulin dependent diabetes.