Diabetes Mellitus

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diabetes mellitus

[‚dī·ə′bēd·ēz ′mel·ə·dəs]
A metabolic disorder arising from a defect in carbohydrate utilization by the body, related to inadequate or abnormal insulin production by the pancreas.

Diabetes Mellitus


a chronic disease characterized by all kinds of metabolic disorders, chiefly carbohydrate, caused by the absolute or (more often) relative deficiency of the pancreatic hormone, insulin.

Heredity plays a major role in the origin of functional insufficiency of the islands of Langerhans of the pancreas, which produce insulin; the functional insufficiency may result from a trauma, inflammation, sclereosis of the pancreatic vessels, infections, intoxication, psychological trauma, excessive consumption of carbohydrates, and overeating in general. The functional condition of the other endocrine glands—the pituitary, adrenals, thyroid, and so forth—and the central and autonomic nervous systems is another factor. Because of the insulin deficiency the liver and muscles become unable to convert sugar into glycogen, and all the tissues lose their capacity to oxidize sugar and use it as an energy source. Moreover, glyconeogenesis also takes place —that is, sugar is formed from proteins and fats. As a result, sugar accumulates in the blood—to as much as 0.2-0.4 g per 100 milliliters of blood or more (hyperglycemia). When the amount of sugar in the blood is more than 0.18 g (“kidney threshold”), some of the sugar in the renal tubules is not reabsorbed and is excreted in the urine (glycosuria).

In more severe cases, liver function weakens, glycogen ceases to be synthesized and accumulates, and the products of protein and fat decomposition are no longer rendered harmless. As a result, a substantial quantity of ketone bodies, especially acetoacetic and /3- hydroxybutyric acids appear in the blood and then in the urine. The accumulation of these acids disturbs the acid-base equilibrium, causing acidosis. Acidosis may result in a diabetic coma.

Diabetes mellitus patients suffer from an intensified appetite and thirst (hunger and thirst may not be very intense in mild cases), increased excretion of urine (up to 5–8 liters a day) with a high specific gravity, itching of the skin and external genitalia, inflammation of the oral mucosa, pain along the nerve trunks (polyneuritis), and muscular and sexual weakness. The menstrual cycle is disturbed in women; spontaneous abortions or stillbirths may occur in pregnant women. The blood cholesterol level rises in diabetics, promoting the early onset of atherosclerosis, which is often combined with hypertonia. Marked changes in the cardiovascular system, kidneys, and eyes are among the serious complications of diabetes mellitus.

Treatment is individualized, taking into account the specific metabolic disorder. In mild forms, a special diet is prescribed, taking into account individual energy expenditures, and exercise therapy (especially for obese persons); in some cases, sugar-reducing sulfanilamide preparations (which are particularly effective in elderly persons with a tendency toward obesity) are prescribed. In moderate and severe forms insulin therapy is undertaken; long-acting insulin preparations with a sugar-reducing action are used to prolong the action of insulin.


Genes, S. G. Sakharnyi diabet, 5th ed. Moscow, 1963. (Bibliography.)
Diabet, edited by R. Williams. Moscow, 1964. (Translated from English; bibliography.)


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The mean age of onset in the west is usually 1-3 years [10] and rare below 6 months.
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Statistical analysis showed that there was no significant correlation between nerve fiber density, the degree of distal muscle weakness of legs ([r.sup.2] = 0.04, P = 0.39), the age of onset ([r.sup.2] = 0.04, P = 0.36), and disease duration ([r.sup.2] = 0.06, P = 0.26).
The mean age of onset was 9.6 [+ or -] 4.3 years (2–16 years) and the mean age at diagnosis was 16.6 [+ or -] 6.1 years (8–31 years).
Early age of onset and faster progression of myopia in genetically predisposed might be due to the combined influence of genetic predisposition and environmental factors.
When the age of onset of the disease was observed, it was found to range between 10 and 63 years, whereas the mean age of onset was 34.11 [+ or -] 13.66 years (Table 1).
In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was linked with increased endothelial dysfunction as measured by brachial artery ultrasound.
Now the average ASD age of onset [bar.t] of a random cohort of patients in the MMM is defined by
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