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From Manila, Philippines:

  1. Why are IDDM patients undernourished while NIDDM patients are usually obese?

  2. What is the possible genetic aspect of Type 1 vs. Type 2 diabetes mellitus?

  3. Here's a case of a 14 year old girl who was admitted to a children's hospital in a coma. The girl had been in good health until approximately two weeks previously, when she developed a sore throat and moderate fever. She subsequently lost her appetite and generally did not feel well. Several days before admission, she began to complain of undue thirst and also started to get up several times during the night to urinate. On the day of admission, the girl had started to vomit, had become drowsy and difficult to arouse. On examination, she was dehydrated, her skin was cold, she was breathing in a deep sighing manner (Kussmaul's breathing), and her breath had a fruity odor. Her blood pressure was 90/60 and her pulse rate was 115 per minute. A diagnosis of severe Type 1 IDDM with ketoacidosis and coma was made. What is the significance of the sore throat which preceded the above case?


Here are brief answers to your questions.

  1. Usually, well controlled IDDM patients getting a normal diet are not malnourished, indeed obesity may be a problem (especially in teenage girls). There are a number of reasons why patients with Type 1 diabetes may seem malnourished in the Philippines. First of all you may be seeing cases of Tropical Calcific Pancreatitis (TCP) and Fibrocalculous Pancreatic Diabetes (FCPD). Also in situations where insulin may be hard to get, young diabetics lose both lean body mass and subcutaneous fat, they may also lose body water from a continuous osmotic diuresis. Another possible explanation in some cases is that there is an associated autoimmune hypothyroidism that has not yet been detected.

  2. The inheritance of Type 1 diabetes or IDDM or autoimmune diabetes is based on certain specific cell surface proteins or HLA antigens which confer susceptibility to the disorder. The autoimmune process however has to be triggered by some environmental factor(s). Peptide components of certain cows' milk proteins have attracted a lot of attention in this connection as have certain viruses; but so far no specific culprits have been identified. Type 2 Diabetes or NIDDM is increasingly getting subdivided into genetically separate; but clinically similar subgroups. Treatment is much the same for all of them and this has discouraged particular diagnosis which is anyway difficult to obtain and expensive to carry out. In consequence, genetic patterns are much less clear. It is likely though that the detection of one form of MODY diabetes, which is glucokinase deficiency, will be encouraged because it carries the assurance of a good prognosis and mild course.

  3. The destruction of islet tissue in Type 1 Diabetes normally takes place slowly over a period of several years. Near the end of the process when insulin synthesis is marginal, the stress of any severe infection will precipitate insulin dependence and clinical diabetes including ketoacidosis. This is what I think happened in the case that you describe.


Original posting 12 Dec 97


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