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In the United States, the National Institutes of Health has classified diabetes into a number of types. Type I, or insulin-dependent diabetes mellitus (IDDM), formerly termed juvenile-onset diabetes, can occur at any age of life. Affected individuals have insulin deficiency due to islet cell loss and may become comatose when exogenous insulin is withheld. Type II, or non-insulin-dependent diabetes mellitus (NIDDM), previously called maturity-onset diabetes, also can occur at any age but is most common in adults. Affected individuals are not prone to coma except in the presence of stress, although they often require insulin to control hyperglycemia. The majority are obese. Other types are a miscellaneous group, formerly called secondary diabetes, and include diseases attacking the pancreas (e.g., hemochromatosis, pancreatitis), and syndromes characterized by insulin antagonism (e.g., Cushing's disease, acromegaly). The term impaired glucose tolerance (IGT) is applied to those who have oral glucose tolerance tests (OGTT) that exceed normal levels but are not sufficiently abnormal to justify the diagnosis of diabetes mellitus. Most of these individuals do not progress to overt diabetes and do not develop the chronic complications of the disease. The term gestational diabetes mellitus (GDM) is reserved for diabetes or glucose intolerance that develops, or is first recognized, during pregnancy. Patients usually revert to normal glucose tolerance following pregnancy.
In order to diagnose diabetes mellitus in an apparently healthy adult, a physician must observe either two fasting plasma glucose values greater than 140 milligrams per decilitre or any two values greater than 200 milligrams per decilitre following a 75-gram oral glucose load. Criteria for the diagnosis of glucose intolerance include a fasting plasma glucose value between 115 and 140 milligrams per decilitre, a two-hour postprandial value between 140 and 200 milligrams per decilitre, and at least one value greater than 200 milligrams per decilitre during a standard oral glucose tolerance test.
It seems likely that there are two distinct causes for IDDM
and NIDDM. A genetic factor appears to be more important in
NIDDM, since analysis of a large series of identical twins has
shown a concordance (the appearance of the trait) in both twins
of more than 90 percent for NIDDM, while in IDDM the rate is
about 50 percent. This relatively low incidence of the disease
among the identical twins of insulin-dependent diabetics suggests
that other factors are important. One such factor may be immune-related.
Among insulin-dependent diabetics, there is a relatively high
prevalence of certain patterns of the inherited tissue compatibility
antigens (HLA), while in NIDDM the prevalence of these HLA types
is normal. In addition, there is a high prevalence of autoantibodies
to islet cells found in the sera of insulin-dependent diabetics,
along with inflammation of the islets. There is evidence that
in some cases of IDDM, viral infections may play a role.
Coxsackie virus B
has been isolated from the pancreas of a child who died accidentally
shortly after the onset of diabetes. This virus was cultured
and found to cause beta cell damage when injected into mice.
Further evidence for an infectious factor in the causation of
type I diabetes mellitus is the seasonal appearance of new cases
of the disease.
It may be that viral and autoimmune factors combine to cause diabetes, the viral infection of the pancreas leading to the release of proteins into the circulation that are recognized as foreign by the victim's immune system. In this theory, autoantibodies cause destruction of the beta cells of the pancreas. This thesis suggests the possibility of preventing the disease either by immunization against suspect viruses or early treatment with immunosuppressive drugs. Patients with NIDDM appear to suffer from resistance to insulin along with abnormal secretion of the hormone. In fact, these patients may initially have higher than normal concentrations of plasma insulin. The primary site of resistance is likely to be within the cell (i.e., a postreceptor defect), although a receptor abnormality may also be implicated. In many, but not all type II patients, resistance to insulin is linked to obesity.
A relative or absolute deficiency of insulin results in
Not all complications are directly related to vascular disease.
Early cataract formation, impaired function of the autonomic
nervous system, and peripheral nerve damage (neuropathy) cannot
be fully explained by blood vessel changes. Autonomic nervous
system dysfunction may be manifested by gastric retention, chronic
diarrhea, incomplete emptying of the bladder, impotence, and
low blood pressure when standing. Diabetic neuropathy often
affects the lower extremities, causing either loss of feeling
or disagreeable sensations of burning or itching. It is not
known if these complications are due to long-standing hyperglycemia
and insulin deficiency or are caused, at least in part, by an
unidentified factor.
There are three basic components in the treatment of IDDM:
insulin, diet, and exercise. Insulin is prepared in a number
of forms, providing short, intermediate, and long actions to
accommodate the specific needs of individual patients. Sources
of insulin traditionally have been from pork and beef pancreases,
but insulin with a structure identical to that produced by human
islets is now widely available. It is either synthesized using
recombinant DNA technology or prepared by the chemical alteration
of porcine insulin. Insulin is given by one or more injections
each day or by continuous infusion using an insulin pump, a
computerized device the size of a deck of cards, which is worn
by the patient and delivers a preset amount of hormone throughout
the day. A typical diabetic diet contains sufficient total calories
to maintain ideal body weight and consists of carbohydrate,
fat, and protein and of ample fibre. Simple sugars and alcohol
are prohibited. Compared to insulin and diet, exercise is more
difficult to measure. Ideally, the diabetic exercises a fixed
amount each day, and insulin and diet are tailored to accommodate
that amount.
The goals of treatment include maintenance of the blood sugar
near or within normal limits, freedom from hypoglycemia, and
an acceptable life-style. The blood sugar usually can be monitored
at home by the patient. Measurement of that portion of hemoglobin
complexed to glucose provides another index of the adequacy
of blood sugar control. Proteins exposed to glucose-containing
solutions undergo glycosylation (i.e.,
a certain number of glucose molecules become irreversibly fixed
to the protein molecule). The higher the glucose concentration,
the greater the degree of glycosylation. In normal humans approximately
6 percent of circulating hemoglobin is glycosylated; in poorly
controlled diabetics, the figure may be 14 percent or more.
Glycosylation of structural proteins, such as those in the basement
membranes of capillaries, may play a role in the pathogenesis
of the chronic complications of diabetes.
In the treatment of NIDDM, diet and exercise again are important.
In the obese patient, evidence of diabetes mellitus may disappear
if the patient can achieve and maintain ideal body weight. Insulin
or a blood-sugar-lowering drug, however, may be required to
control blood sugar.
Copyright (c) 1995 Encyclopaedia Britannica, Inc. All Rights Reserved