I was just scanning through some articles and this interesting review on MODY caught my attention because definitely some of our patients that are labelled Type 2 as insulin resistant diabetes may actually have MODY where the tissues are actually insulin sensitive. As a result the way we treat these patients will actually change.
Below is a summary of the salient features of MODY from Janet Ruhl published in Diabetes In Control online website:
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1. People with MODY are extremely sensitive to insulin. A dose of as little as two units may have a strong effect on their blood sugar.
2. People with MODY, no matter how high their blood sugars might be after meals, may have near normal fasting C-peptide levels. This is because the defects characteristic of MODY does not affect basal insulin secretion but only the ability to secrete insulin as blood sugars rise after eating.
3. People with MODY do not have GAD or islet antibodies. Though people with severe expressions of MODY genes may be misdiagnosed in their teens with Type 1 diabetes, they can be distinguished from true Type 1s by the very low doses of insulin they need and the lack of the autoimmune antibodies.
4. People with MODY may respond extremely strongly to sulfonylurea drugs. These drugs are often prescribed as the appropriate treatment for MODY. However, these drugs are most effective for people whose severe expression of these genes causes blood sugars high enough to be mistaken for Type 1 diabetes. For those whose MODY is milder, even 1/4 of a 1 mg tablet of Amaryl ( Glimipride) may cause a dramatic hypo. For these people the use of very small doses of insulin–no more than 2 to 4 units per meal–is more effective and more easily tailored to varying food intake.
5. MODY should always be suspected in a woman of normal weight who develops gestational diabetes early in a pregnancy and who tests negative for autoimmune antibodies. This is often how MODY first reveals itself.
6. The different forms of genetic diabetes that are lumped together under the heading of MODY have different complication profiles. The two most common forms are MODY-3 caused by a defect in HNF1-a and MODY-2 caused by a defect in the glucokinase gene GCK.
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The point of this post is for us doctors to be aware that this form of diabetes exists and that the way these patients respond to our medications differ from the typical insulin resistant Type 2 Diabetic.
Likewise patients should be aware that this kind of Diabetes exist and may need to inform their doctors if the features of the above fit their kind of diabetes.
I see a lot of diabetic patients and the need to be informed and updated all the time regarding new research on the pathophysiology, diagnosis and treatment of this epidemic is the main reason why I continue to study and learn in whatever mode or material either through books, journals, websites or conventions.
I guess the same is true to everyone everyday…
We Should Never Stop LEARNING!