symptoms of diabetes type 1 2

Secondary hyperglycemia has been associated with various disorders of insulin target tissues (liver, muscle, and adipose tissue) (Table 27-6). Other secondary causes of carbohydrate intolerance include endocrine disorders — often specific endocrine tumors — associated with excess production of growth hormone, glucocorticoids, catecholamines, glucagon, or somatostatin. In the first four situations, peripheral responsiveness to insulin is impaired. With excess of glucocorticoids, catecholamines, or glucagon, increased hepatic output of glucose is a contributory factor; in the case of catecholamines, decreased insulin release is an additional factor in producing carbohydrate intolerance, and with excess somatostatin production it is the major factor.
A rare syndrome of extreme insulin resistance associated with acanthosis nigricans afflicts either young women with androgenic features as well as insulin receptor mutations or older people, mostly women, in whom a circulating immunoglobulin binds to insulin receptors and reduces their affinity to insulin.
Medications such as diuretics, phenytoin, niacin, and high-dose glucocorticoids can produce hyperglycemia that is reversible once the drugs are discontinued or when diuretic-induced hypokalemia is corrected. Chronic pancreatitis or subtotal pancreatectomy reduces the number of functioning B cells and can result in a metabolic derangement very similar to that of genetic type 1 diabetes except that a concomitant reduction in pancreatic A cells may reduce glucagon secretion so that relatively lower doses of insulin replacement are needed. Insulin-dependent diabetes is occasionally associated with Addison's disease and autoimmune thyroiditis (Schmidt's syndrome, or polyglandular failure syndrome). This occurs more commonly in women and represents an autoimmune disorder in which there are circulating antibodies to adrenocortical and thyroid tissue, thyroglobulin, and gastric parietal cells. (current MD&T)