- Severe diabetes mellitus, often brittle,
usually of abrupt onset during the first two
decades of life but can develop at any age; characterized by polydipsia, polyuria,
increased appetite, weight loss, low plasma insulin levels, and susceptibility to
ketoacidosis; immune-mediated destruction of pancreatic B cells; insulin therapy and
dietary regulation are necessary. Term declared obsolete by American Diabetes
Association. Syn: growth-onset diabetes, juvenile- onset diabetes, type I diabetes.
- Diabetes mellitus:
- A chronic metabolic disorder in which utilization
of carbohydrate is impaired and
that of lipid and protein enhanced; it is caused by an absolute or relative deficiency
of insulin and is characterized, in more severe cases, by chronic hyperglycemia,
glycosuria, water and electrolyte loss, ketoacidosis, and coma; long-term
complications include neuropathy, retinopathy, nephropathy, generalized
degenerative changes in large and small blood vessels, and increased susceptibility
to infection.
- Diabetes mellitus affects at least 16 million
Americans, ranks seventh as a cause
of death in the United States, and costs the national economy over $100 billion
yearly. About 95% of persons with DM have type 2, in which the pancreatic beta
cells retain some insulin- producing potential, and the rest have type 1, in which
exogenous insulin is required for long- term survival. In type 1 DM, which
typically causes symptoms before age 25, an autoimmune process is responsible
for beta cell destruction. Type 2 DM is characterized by insulin resistance in
peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin
regulates carbohydrate metabolism by mediating the rapid transport of glucose
and amino acids from the circulation into muscle and other tissue cells, by
promoting the storage of glucose in liver cells as glycogen, and by inhibiting
gluconeogenesis. The normal stimulus for the release of insulin from the pancreas
is a rise in the concentration of glucose in circulating blood, which typically
occurs within a few minutes after a meal. When such a rise elicits an appropriate
insulin response, so that the blood level of glucose falls again as it is taken into
cells, glucose tolerance is said to be normal. The central fact in diabetes mellitus
is an impairment of glucose tolerance of such a degree as to threaten or impair
health. Revised diagnostic criteria for DM were published by the American
Diabetes Association in June 1997. All criteria depend on the glucose
concentration of venous plasma. The diagnosis is confirmed when any 2 tests
performed on different days yield levels at or above established thresholds: in
the fasting state, 126 mg/dL (7.0 mmol/L); 2 hours postprandially (after a 75-g
glucose load), or at random, 200 mg/dL (11.1 mmol/L). Long recognized as an
independent risk factor for cardiovascular disease, DM is often associated with
other risk factors, including disorders of lipid metabolism, obesity, hypertension,
and impairment of renal function. Current recommendations for the management
of DM emphasize education and individualization of therapy. Controlled studies
have shown that rigorous maintenance of plasma glucose levels as near to normal
as possible at all times substantially reduces the incidence and severity of long-
term complications, particularly microvascular complications (retinopathy,
neuropathy, and nephropathy). Such control involves limitation of dietary
carbohydrate and saturated fat; monitoring of blood glucose, including self-testing
by the patient and periodic determination of glycosylated hemoglobin; and
administration of insulin (particularly in type 1 DM), drugs that stimulate
endogenous insulin production (in type 2 DM), or both. Some studies suggest that
the risk of cardiovascular disease may be increased in some patients by intensive
treatment of DM because of elevation of body weight, blood pressure,
triglycerides, and total and low-density cholesterol. Pharmaceutical agents
developed during the 1990s have improved control of DM by enhancing
responsiveness of cells to insulin, counteracting insulin resistance, and reducing
postprandial carbohydrate absorption. See Also insulin resistance.
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