Chronic autoimmune lymphocytic thyroiditis is particularly common and can result in hypothyroidism. Because symptoms can be subtle, thyroid function tests should be performed annually. Other disorders that occur with increased frequency in children with DM1 include celiac disease, IgA deficiency, Addison disease, and peptic ulcer disease.
Special Problems: Hypoglycemia
Hypoglycemia occurs commonly in patients with DM1. For patients in adequate or better control, it is expected to occur on average once or twice a week. Severe episodes of hypoglycemia, resulting in seizures or coma or requiring assistance from another person, occur in 10% to 25% of these patients per year.
Hypoglycemia in patients with DM1 results from a relative excess of insulin in relation to the serum glucose concentration. This excess can be caused by alterations in the dose, timing, or absorption of insulin; alterations of carbohydrate intake; or changes in insulin sensitivity resulting from activity. Defective counterregulatory responses also contribute to hypoglycemia. Abnormal glucagon responses to falling serum glucose concentrations develop within the first few years of the disease, and abnormalities in epinephrine release occur after a longer duration.
Lack of awareness of hypoglycemia occurs in approximately 25% of patients with diabetes. Recent episodes ofhypoglycemia may play a role in the pathophysiology ofhypoglycemia unawareness; after an episode of hypoglycemia, autonomic responses to subsequent episodes are reduced. Areturn of symptoms of hypoglycemia can be exhibited in thesepatients after 2 to 3 weeks of strict avoidance of hypoglycemicepisodes.
Symptoms of hypoglycemia include symptoms resultingfrom neuroglycopenia (headache, visual changes, confusion, irritability, or seizures) and symptoms resulting fromthe catecholamine response (tremors, tachycardia, diaphoresis, or anxiety). Mild episodes can be treated with administration of rapidly absorbed oral glucose (glucose gel ortablets or fruit juices). More severe episodes that result in seizures or loss of consciousness at home should be treated with glucagon injections. IV glucose should be given in hospital settings.
Long-term complications of DM1 include retinopathy, nephropathy, neuropathy, and macrovascular disease. Evidence of organ damage caused by hyperglycemia is rare in patients with diabetes of less than 5 to 10 years’ duration; clinically apparent disease rarely occurs before 10 to 15 years’ duration. Diabetic retinopathy is the leading cause of blindness in the United States. Nephropathy eventually occurs in 30% to 40% and accounts for approximately 30% of all new adult cases of end-stage renal disease. Neuropathy occurs in 30% to 40% of postpubertal patients with DM1 and leads to sensory, motor, or autonomic deficits. Macrovascular disease results in an increased risk of myocardial infarction and stroke among individuals with diabetes.
Intensive control of diabetes, using frequent blood glucose testing and multiple daily injections of insulin or an insulin pump, can reduce the development or progression of diabetic complications, including a 76% reduction of risk for retinopathy, a 39% reduction in microalbuminuria, and a 60% reduction in clinical neuropathy. For pubertal and adult patients, the benefits of intensive therapy likely outweigh the increased risk for hypoglycemia. For younger patients, in whom the risks for hypoglycemia are greater and the benefits of tight glucose control may be lower, a less intensive regimen may be appropriate.
DM2 can occur as the result of various pathophysiologic processes; however the most common form results from peripheral insulin resistance and compensatory hyperinsulinemia, followed by failure of the pancreas to maintain adequate insulin secretion (see Table 171-1).