From Camden, Arkansas USA:
My 15 year old son, who has been taking human growth hormone for about 21 months, started to exhibit symptoms of, and was diagnosed as type 1 diabetes 20 months ago, but no antibodies were detected. He was hospitalized with sugar levels of about 450 mg/dl [25 mmol/L] and placed on combination injections twice a day. Throughout this period, he has maintained an average blood glucose level of 100-105 mg/dl [5.6-5.8 mmol/L] with his hemoglobin A1c readings consistently at 4.9%. We noticed that diet and activity did not seem to affect his sugars radically, and in fact, his doctor is reducing the insulin by 10% per week. So fa, we have reduced it by 40% and his two blood sugar week averages remain the same.
My son's endocrinologist says he has not seen anything like this. He is mystified and that is why we have started the reduction to see where this leads us. Could the growth hormone be responsible for initial elevated sugars? Is this just the honeymoon period? Could the hormone have caused the onset of diabetes or is it possible he does not even have type 1 diabetes?
I think it is possible that the answer to your question will lie in a reevaluation of the laboratory data that led to the almost simultaneous diagnosis of hypopituitarism and type 1 diabetes.
To begin with, by far the most common type of diabetes in an adolescent from a Caucasian family in the U.S. is type 1A (autoimmune) diabetes in which case the antibody test should have been positive. It is possible though that only the immunofluorescent islet cell antibody screening test was asked for and not the more definitive test for anti-ICA512, anti-GAD, and anti-insulin IAA. Had the full arrays of testing been done, it might have shown evidence of autoimmunity:, and it might indeed be still worth doing these tests.
Had there been this evidence of autoimmunity, then the short stature would most probably have been due to hypothyroidism which is another form of autoimmunity frequently associated with type 1A diabetes in what is now recognised as the Autoimmune Polyglandular Syndrome Type II. If this was the case, then you could now be seeing the honeymoon period. However, a TSH test for hypothyroidism was probably done.
If the initial laboratory work rules out these possibilities convincingly, then it would seem that your son has some other form of diabetes and the most likely is type 1B which is common in African American and Hispanic children, but is only seen in 5% of new onset cases in Caucasians. About 50% of this latter group do in fact become insulin independent after a few months, and little is known at the moment about the underlying pathology. However, these people are uniformly antibody negative.
There is the final possibility that growth hormone did indeed exacerbate the insulin resistance that may already be present in hypopituitarism to the point of producing clinical diabetes. It is a rare event, and, if it was the case, you might not expect the slowly diminishing insulin need that you have observed.
Original posting 23 Aug 2002
Posted to Other Medications
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