Top Document: diabetes FAQ: treatment (part 3 of 5) Previous Document: Gastroparesis Next Document: What is pycnogenol? Where and how is it sold? See reader questions & answers on this topic! - Help others by sharing your knowledge Mayer Davidson writes several pages about insulin resistance in his book _Diabetes Mellitus: Diagnosis and Treatment_. Except for what's in [brackets], the following information is from pp 126-132 of the third edition or pp 112-119 in the fourth edition. I'd recommend finding a copy. Most university libraries will have it, even those without medical schools. It's about $65; if necessary you can order from the Rittenhouse Medical Bookstore in Philadelphia at 215-545-6072. In this context, "insulin resistance" refers to patients requiring more than the arbitrary amount of 200 units/day. Davidson uses the term "insulin antagonism" for the phenomenon which is commonly part of type 2 diabetes. Davidson cites ten major causes of insulin resistance. The first eight are obvious major medical problems that you would immediately suspect were related, so I won't bother listing those. Rarely, insulin is destroyed at the subcutaneous injection site; this form can be treated with normal amounts of insulin administered intravenously or intraperitoneally. The most common form of insulin resistance is immune-mediated. Everyone taking injected insulin develops IgG antibodies to insulin. In most, the antibody levels are low. In about 1 in 1000, the levels are much higher, from 5 to over 1000 times higher than usual. In Davidson's words: The reason for this markedly enhanced response and the subsequent decline to normal levels is completely unknown. The antibodies bind to, and neutralize, the insulin. At one time it was thought that the antibodies resulted from impurities in the insulin preparations, and that using highly purified preparations would avoid the problem. This has proven not to be the case; purified insulin helps but usually does not resolve the problem, [though it seems to be worth trying]. Also, switching to a different insulin does not help, as the antibodies bind to beef, pork and human insulin. They may bind to one more than the others, but the titers of antibody are so high as to neutralize virtually all of any of the insulins. Two treatments which are effective are not generally available in the US. First, insulin can be treated with sulfuric acid. The modified molecule retains some biological activity but has reduced affinity for binding to the IgG antibodies to insulin. This treatment was tested by a Canadian laboratory in the late 1960s but is available in the US only by special petition to the FDA. Novo Nordisk Pharmaceutical can provide information at 609-987-5800. Second, fish insulin works in humans but does not bind to the antibodies. Cod insulin, for example, differs from human insulin in 33 amino acid positions compared with 3 differences for beef insulin. But nonmammalian insulins are not available in the US at all. This leaves the two treatments that are actually used on a regular basis, and a promising new treatment. Because this condition is rare, there's been little experience treating it with lispro insulin (Humalog). That experience is promising; it appears that the structural change in lispro may inhibit the antibody binding. If this is borne out by further experience, lispro will be the treatment of choice for extreme insulin resistance. Glucorticoids such as prednisone decrease the extreme insulin resistance, possibly by inhibiting the production of IgG antibodies. As the antibodies have a half life of 3-4 weeks, the response is delayed, during which time bg control is even more difficult due to the effects of the glucocorticoids. After several weeks the dosage can be reduced to maintenance levels or eliminated, but relapse is common. Since glucocorticoids have other nasty effects in addition to the problems listed above, there are significant problems with this course of treatment. Davidson's recommendation is based on The Good News: insulin resistance is self-limited and only lasts a few months to a year. He simply uses as much insulin as is needed in the meantime. U-500 concentration is available for this purpose. The antibodies delay the action, so even though U-500 is regular insulin it acts like a lente or semilente in resistant patients. For unknown reasons, much less U-500 is needed than the equivalent amount of U-100, 50% to 75% less. Since the situation is difficult to manage and is temporary, Davidson advises not trying for good bg control, but just avoiding ketosis and the overt symptoms of hyperglycemia (thirst, excess urination, infections). When insulin sensitivity returns, it can happen quite suddenly. Davidson starts reducing the high insulin doses when fasting bg is under 200 mg/dl (11.0 mmol/L). At these times, large amounts of insulin previously bound to the antibodies may be released, so avoiding hypoglycemia is a major concern. The return to normal sensitivity will take at least several weeks due to the half-life of the antibodies, and insulin requirements may fluctuate a great deal during this time. A fast response to U-500 insulin (2-4 hours from injection to measurably lower bg) may indicate the decline of insulin resistance. [This was the movie. Now go read the book.] User Contributions:Comment about this article, ask questions, or add new information about this topic:Top Document: diabetes FAQ: treatment (part 3 of 5) Previous Document: Gastroparesis Next Document: What is pycnogenol? Where and how is it sold? 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Last Update March 27 2014 @ 02:11 PM
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between and mg/dl and mmol/l is, i came across your article and was so pleased to aquire a lot more info regarding blood glucose, how to read and convert it.