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a general term referring to any of various disorders characterized by excessive urination (polyuria); when used alone, the term refers to diabetes mellitus. (See Atlas 4, Part D).
brittle diabetes diabetes that is difficult to control, characterized by unexplained oscillation between hypoglycemia and diabetic ketoacidosis. (This term was formerly much used, but it is not a classification used by the World Health Organization or the American Diabetes Association.)
bronze diabetes hemochromatosis.
central diabetes insipidus a metabolic disorder due to injury of the neurohypophyseal system, which results in a deficient quantity of antidiuretic hormone (ADH or vasopressin) being released or produced, resulting in failure of tubular reabsorption of water in the kidney. As a consequence, there is the passage of a large amount of urine having a low specific gravity, and great thirst; it is often attended by voracious appetite, loss of strength, and emaciation. Diabetes insipidus may be acquired through infection, neoplasm, trauma, or radiation injuries to the posterior lobe of the pituitary gland or it may be inherited or idiopathic.

Treatment of pituitary diabetes insipidus consists of administration of vasopressin. A synthetic analogue of vasopressin (DDAVP) can be administered as a nasal spray, providing antidiuretic activity for 8 to 20 hours, and is currently the drug of choice. Patient care includes instruction in self-administration of the drug, its expected action, symptoms that indicate a need to adjust the dosage, and the importance of follow-up visits. Patients with this condition should wear some form of medical identification at all times.
gestational diabetes diabetes mellitus with onset or first recognition during pregnancy, usually during the second or third trimester. In some cases mild, undetected glucose intolerance was present before pregnancy. It often disappears after the end of the pregnancy, but many women with this condition develop permanent diabetes mellitus in later life. Although the disordered carbohydrate metabolism is usually mild, prompt detection and treatment are necessary to avoid fetal and neonatal morbidity and mortality.
maturity-onset diabetes of youth (MODY) an autosomal dominant variety of type 2 diabetes mellitus characterized by onset in late adolescence or early adulthood.
diabetes mel´litus a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which may be secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins, and fats, diabetes is not limited to a disturbance of glucose homeostasis alone. Insulin resistance may also sometimes play a role in the etiology of diabetes. 

The American Diabetes Association sponsored an international panel in 1995 to review the literature and recommend updates of the classification of diabetes mellitus. The definitions and descriptions that follow are drawn from the Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. The report was first approved in 1997 and modified in 1999. Although other terms are found in older literature and remain in use, their use in current clinical practice is inappropriate. Epidemiologic and research studies are facilitated by use of a common language.

The Expert Committee notes that most cases of diabetes fall into two broad categories, which are called Type 1 and Type 2. There are also other specific types, such as gestational diabetes and impaired glucose homeostasis. See table for definitions of types of diabetes mellitus.
Incidence and Prevalence. It has been estimated that slightly over 6 per cent of the population is affected by some form of diabetes, or 17 million people in the USA and 1.2 to 1.4 million in Canada; many of these individuals are not diagnosed. Diabetes is ranked third as a cause of death, although the life span of patients with diabetes has increased due to improved methods of detection and better management. There is no cure for diabetes at the present time, but enormous strides have been made in the control of the disease. The patient must understand the importance of compliance with the entire treatment plan, including diet, exercise, and in some cases medication. The patient with diabetes is at increased risk for cardiovascular disease, renal failure, neuropathies, and diabetic retinopathy. Research studies such as the Diabetes Control and Complications Trial have indicated that tight control of blood glucose levels resulted in the delay or prevention of retinopathy, nephropathy, and neuropathy.
Diagnosis. The most common diagnostic tests for diabetes are chemical analyses of the blood such as the fasting plasma glucose. Capillary blood glucose monitoring can be used for screening large segments of the population. Portable equipment is available and only one drop of blood from the fingertip or earlobe is necessary. Capillary blood glucose levels have largely replaced analysis of the urine for glucose. Testing for urinary glucose can be problematic as the patient may have a high renal threshold, which would lead to a negative reading for urinary glucose when in fact the blood glucose level was high.
Clinical Manifestations. Diabetes mellitus can present a wide variety of symptoms, from none at all to profound ketosis and coma. If the disease manifests itself late in life, patients may not know they have it until it is discovered during a routine examination, or when the symptoms of chronic vascular disease, insidious renal failure, or impaired vision cause them to seek medical help.

The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.

Fatigue and muscle weakness occur because the glucose needed for energy simply is not metabolized properly. Weight loss in type 1 diabetes patients occurs partly because of the loss of body fluid and partly because in the absence of sufficient insulin the body begins to metabolize its own proteins and stored fat. The oxidation of fats is incomplete, however, and the fatty acids are converted into ketone bodies. When the kidney is no longer able to handle the excess ketones the patient develops ketosis. The overwhelming presence of the strong organic acids in the blood lowers the pH and leads to severe and potentially fatal ketoacidosis.

The metabolism of body protein when sufficient amounts of insulin are not available causes an elevated blood urea nitrogen. This first occurs because the nitrogen component of protein is discarded in the blood when the body metabolizes its own proteins to obtain the glucose it needs.

Persons with diabetes are prone to infection, delayed healing, and vascular disease. The ease with which poorly controlled diabetic persons develop an infection is thought to be due in part to decreased chemotaxis of leukocytes, abnormal phagocyte function, and diminished blood supply because of atherosclerotic changes in the blood vessels. An impaired blood supply means a deficit in the protective defensive cells transported in the blood. Excessive glucose allows organisms to grow out of control.

Another manifestation of diabetes mellitus is visual disturbance due to increased osmolarity of the blood and accumulation of fluid in the eyeball, which changes its shape. Once the diabetes is under control, visual problems should abate. Persistent vaginitis and urinary tract infection also may be symptoms of diabetes in females.
Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.

Visual impairment and blindness are common sequelae of uncontrolled diabetes. The three most frequently occurring problems involving the eye are diabetic retinopathy, cataracts, and glaucoma. photocoagulation of destructive lesions of the retina with laser beams can be used to delay further progress of pathologic changes and thereby preserve sight in the affected eye.

Another area of pathologic changes associated with diabetes mellitus is the nervous system (diabetic neuropathy), particularly in the peripheral nerves of the lower extremities. The patient typically experiences a “stocking-type” anesthesia beginning about 10 years after the onset of the disease. There may eventually be almost total anesthesia of the affected part with the potential for serious injury to the part without the patient being aware of it. In contrast, some patients experience debilitating pain and hyperesthesia, with loss of deep tendon reflexes.

Other problems related to the destruction of nerve tissue are the result of autonomic nervous system involvement. These include impotence, orthostatic hypotension, delayed gastric emptying, diarrhea or constipation, and asymptomatic retention of urine in the bladder.

Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
Management. There is no cure for diabetes; the goal of treatment is to maintain blood glucose and lipid levels within normal limits and to prevent complications. In general, good control is achieved when the following occur: fasting plasma glucose is within a specific range (set by health care providers and the individual), glycosylated hemoglobin tests show that blood sugar levels have stayed within normal limits from one testing period to the next, the patient's weight is normal, blood lipids remain within normal limits, and the patient has a sense of health and well-being.

The protocol for therapy is determined by the type of diabetes; patients with either type 1 or type 2 must pay attention to their diet and exercise regimens. Insulin therapy may be prescribed for patients with type 2 diabetes as well as any who are dependent on insulin. In most cases, the type 2 diabetes patient can be treated effectively by reducing caloric intake, maintaining target weight, and promoting physical exercise.

Diet. In general, the diabetic diet is geared toward providing adequate nutrition with sufficient calories to maintain normal body weight; the intake of food is adjusted so that blood sugar and serum cholesterol levels are kept within acceptable limits. Overweight diabetic patients should limit caloric intake until target weight is achieved. In persons with type 2 diabetes this usually results in marked improvement and may eliminate the need for drugs such as oral hypoglycemic agents.

The patient, physician, nurse, and dietician must carefully evaluate the patient's life style, nutritional needs, and ability to comply with the proposed dietary prescription. There are a variety of meal planning systems that can be used by the patient with diabetes; each has benefits and drawbacks that need to be evaluated in order to maximize compliance. Two of the most frequently used ones are the exchange system (see accompanying table) and the carbohydrate counting system.

In the exchange system, foods are divided into six food groups (starch, meat, vegetable, fruit, milk, and fat) and the patient is taught to select items from each food group as ordered. Items in each group may be exchanged for each other in specified portions. The patient should avoid concentrated sweets and should increase fiber in the diet. Special dietetic foods are not necessary. Patient teaching should emphasize that a diabetic diet is a healthy diet that all members of the family can follow.

The carbohydrate counting system focuses on matching the unit of insulin to the total number of grams of carbohydrate in food eaten. This system is the most accurate method for calculating insulin to food intake.

It is especially important that persons with diabetes who are taking insulin not skip meals; they must also be sure to eat the prescribed amounts at the prescribed times during the day. Since the insulin-dependent diabetic needs to match food consumption to the available insulin, it is advantageous to increase the number of daily feedings by adding snacks between meals and at bedtime.

Exercise. A program of regular exercise gives anyone a sense of good health and well-being; for persons with diabetes it gives added benefits by helping to control blood glucose levels, promoting circulation to peripheral tissues, and strengthening the heart beat. In addition, there is evidence that exercise increases the number of insulin receptor sites on the surface of cells and thus facilitates the metabolism of glucose. Many specialists in diabetes consider exercise so important in the management of diabetes that they prescribe rather than suggest exercise.

Persons with diabetes who take insulin must be careful about indulging in unplanned exercise. Strenuous physical activity can rapidly lower their blood sugar and precipitate a hypoglycemic reaction. For a person whose blood glucose level is over 250 mg/dl, the advice would be not to exercise at all. At this range, the levels of insulin are too low and the body would have difficulty transporting glucose into exercising muscles. The result of exercise would be a rise in blood glucose levels.

Insulin Therapy. Exogenous insulin is given to patients with diabetes mellitus as a supplement to the insufficient amount of endogenous insulin that they produce. In some cases, this must make up for an absolute lack of insulin from the pancreas. Exogenous insulin is available in various types. It must be given by injection, usually subcutaneously, and because it is a potent drug, the dosage must be measured meticulously. Commonly, regular insulin, which is a fast-acting insulin with a short span of action, is mixed with one of the longer-acting insulins and both types are administered in one injection.

Human insulin (Humulin) is produced by recombinant DNA technology. This highly purified biosynthetic insulin reduces the incidence of allergic reactions and the changes in subcutaneous tissues (lipodystrophy) at sites of injection.

Recently, battery-operated insulin pumps have been developed that can be programmed to mimic normal insulin secretion more closely. A person wearing an insulin pump still must monitor blood sugar several times a day and adjust the dosage, and not all diabetic patients are motivated or suited to such vigilance. It is hoped that in the future an implantable or external pump system may be perfected, containing a glucose sensor. In response to data from the sensor the pump will automatically deliver insulin according to changing levels of blood glucose.

Oral Agents. Oral antidiabetic drugs (see hypoglycemic agents) are sometimes prescribed for patients with type 2 diabetes who cannot control their blood glucose with diet and exercise. These are not oral forms of insulin; they are sulfonylureas, chemically related to the sulfonamide antibiotics. Patients receiving them should be taught that the drug they are taking does not eliminate the need for a diet and exercise program. Only the prescribed dosage should be taken; it should never be increased to make up for dietary indiscretions or discontinued unless authorized by the physician.
Patient Education. Successful management of diabetes requires that the patient actively participate in and be committed to the regimen of care. The problem of poor control can cause serious or even deadly short-term and long-term complications, with devastating effects on the patient's longevity and sense of well being. There are many teaching aids available to help persons with diabetes understand their disease and comply with prescribed therapy. In general, a patient education program should include the following components:

1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.

2. Home glucose monitoring using either a visually read test or a digital readout of the glucose concentration in a drop of blood. Patients can usually learn to use the necessary equipment and perform finger sticks. They keep a daily record of findings and are taught to adjust insulin dosage accordingly. More recent glucose monitoring devices can draw blood from other locations on the body, such as the forearm.

3. Pathophysiology of diabetes mellitus, including functions of the pancreas and the long-term effects of uncontrolled diabetes.

4. Insulin administration (if appropriate), including types of insulin and syringes, rotation of sites of injection, injection techniques, and pump therapy instructions.

5. Signs and symptoms ofhyperglycemiaandhypoglycemia, and measures to take when they occur. (See accompanying table.) It is important for patients to become familiar with specific signs that are unique to themselves. Each person responds differently and may exhibit symptoms different from those experienced by others. It should be noted that the signs and symptoms may vary even within one individual. Thus it is vital that the person understand all reactions that could occur. When there is doubt, a simple blood glucose reading will determine the actions that should be taken.

6. Oral antidiabetic agents, including information about drug-drug interactions, proper administration, and potential side effects.

7. Personal hygiene and activities of daily living, including general skin care, foot care, treatment of minor injuries to avoid infection, a formal exercise program as well as exercise at school or at work, recreational activity, and travel.

8. Identification tag and card and needed medical information.

9. Information on what to do on “sick days” when nausea, vomiting, or respiratory infection can interfere with the usual meals and exercise.

10. Importance of keeping appointments and staying in touch with a health care provider for consultation and assessment. Periodic evaluation of the binding of glucose to hemoglobin (glycosylated hemoglobin or hemoglobin A1C testing) can give information about the effectiveness of the prescribed regimen and whether any changes need to be made. The ADA position statement on tests of glycemia in diabetes recommends routine testing for all patients with diabetes. It should be a part of the initial assessment of the patient, with subsequent measurements every three months to determine if the patient's metabolic control has been reached and maintained.
See illustration.
Complications of diabetes mellitus. From Damjanov, 2000.
nephrogenic diabetes insipidus a rare form caused by failure of the renal tubules to reabsorb water; there is excessive production of antidiuretic hormone but the tubules fail to respond to it. Characteristics include polyuria, extreme thirst, growth retardation, and developmental delay. The condition does not respond to exogenous vasopressin. It may be inherited as an X-linked trait or be acquired as a result of drug therapy or systemic disease.
pituitary diabetes insipidus central diabetes insipidus.


abbreviation for maturity-onset diabetes of youth.

maturity onset diabetes of the young

Any of a number  of dominantly inherited, monogenic defects of insulin secretion occurring at any age (most commonly types 2 and 3). MODYs do not include any forms of type-2 diabetes, and comprise 1–2% of those initially diagnosed with diabetes. Given that MODYs are autosomal dominant, those with the faulty gene have a 95% chance of developing MODY during their lifetimes. Diagnosing MODY is important as some forms do not need insulin and may do well with oral hypoglycaemic agents, and because other family members can be identified and their treatment modified if appropriate.

MODY susceptibility genes:
• MODY type 1—HNF4A 
• MODY type 2—GCK     
• MODY type 3—HNF1A
• MODY type 4—PDX1
• MODY type 5—HNF1B
• MODY type 6—NEUROD1
• MODY type 7—KLF11
• MODY type 8—CEL
• MODY type 9—PAX4
• MODY type 10—INS
• MODY type 11—BLK


Maturity onset diabetes mellitus of young Endocrinology A mild form of type 2 DM, with onset before age 25. See Type 2 DM.


(di?a-bet'ez) [Gr. diabetes, (one) passing through]
A general term for diseases marked by excessive urination and elevated blood sugar, esp. diabetes mellitus (DM).

brittle diabetes

DM that is exceptionally difficult to control. The disease is marked by alternating episodes of hypoglycemia and hyperglycemia. Frequent adjustments of dietary intake and insulin dosage are required.


Diabetes may be brittle when insulin is not well absorbed; insulin requirements vary rapidly; insulin is improperly prepared or administered; the Somogyi phenomenon is present; the patient has coexisting anorexia or bulimia; the patient's daily exercise routine, diet, or medication schedule varies; or physiological or psychological stress is persistent.

Synonym: brittle diabetes mellitus

brittle diabetes mellitus

Brittle diabetes.

bronze diabetes


chemical diabetes

1. Asymptomatic DM, a stage in which no obvious clinical signs and symptoms of the disease are present but blood glucose measurements are abnormal.
2. Type 2 DM occurring in an obese child or adolescent. The syndrome is sometimes referred to as “mature onset diabetes of youth” (MODY).

cystic-fibrosis-related diabetes

Abbreviation: CFRD
DM arising in patients with cystic fibrosis (CF). It is the most common complication of CF other than those conditions that affect the lungs. It is caused by destruction of islet cells (the cells in the pancreas that make insulin) as well as a decrease in sensitivity of the liver and muscles to the actions of insulin. The disease usually first becomes clinically obvious in young adults.

Patient Care

Although CFRD can be diagnosed with fasting glucose blood tests or hemoglobin A1c levels, many experts recommend using an oral glucose tolerance test. Fifteen to thirty percent of patients with CF are affected by their 20th birthday, and perhaps as many as half have the disease by age 30. CFRD is associated with more severe lung disease than is experienced by patients with CF and normal glucose tolerance. Oral hypoglycemic agents, insulin, and exercise are the primary methods of treatment. Caloric restriction, a cornerstone of treatment for other forms of diabetes, is relatively contraindicated because of the need for aggressive nutritional supplementation in CF patients.

double diabetes

A colloquial term for hybrid diabetes, also called type 3 diabetes or type 1 and a half diabetes.

endocrine diabetes

DM caused by diseases of the ovaries, pituitary, thyroid, or adrenal glands.

fibrocalculous pancreatic diabetes

A rare form of DM caused by chronic tropical pancreatitis and destruction of insulin-producing islet cells.

gestational diabetes

Abbreviation: GDM
DM that begins during pregnancy owing to changes in glucose metabolism and insulin resistance.

GDM affects a large percentage of pregnant American women, ranging from about 1.5 to 14 %, depending on the ethnic group studied. Although gestational diabetes usually subsides after delivery, women with GDM have a 45% risk of recurrence with the next pregnancy and a significant risk of developing type 2 diabetes later in life.


Although many diabetic specialists recommend universal screening for GDM, it is agreed by all diabetologists that women at risk for GDM (women over age 25 who are overweight at the start of pregnancy; have a previous history of gestational diabetes; have had a previous infant weighing 9 lb or more at birth; have a history of a poor pregnancy outcome, glycosuria, or polycystic ovary syndrome; or who are from families or ethnic groups with a high incidence of type 2 DM) should undergo oral glucose tolerance testing as soon as possible to assess blood glucose levels while fasting and after meals. Testing should be repeated at 24 to 28 weeks' gestation if the first screening is negative.


A calorically restricted diet, regular exercise, and metformin or insulin are used to treat GDM.

Patient care

Blood glucose self-monitoring is essential to management, and patients should be taught to monitor glucose levels four times each day, obtaining a fasting level in the morning, followed by three postprandial levels (1 hr after the start of each meal). Blood glucose levels at 1 hr after beginning a meal are considered the best predictor for subsequent fetal macrosomia. Target blood glucose levels are 90 mg/dL or less (fasting) and 120 to 140 mg/dL postprandially. The patient and her partner should be instructed that food, stress, inactivity, and hormones elevate blood glucose levels and that exercise and insulin lower them. They will need to learn about both pharmacological (measuring and injecting insulin) and nonpharmacological (menu management and physical activity) interventions to maintain a normal glycemic state (euglycemia) throughout the pregnancy, while ensuring adequate caloric intake for fetal growth and preventing maternal ketosis. Women who have no medical or obstetrical contraindicting factors should be encouraged to participate in an approved exercise program, because physical activity increases insulin receptor sensitivity. Even performing 15 to 20 min of “armchair exercises” daily (while reading or watching television) can help the pregnant woman reduce hyperglycemia without increasing the risk of inducing uterine contractions. If euglycemia is not achieved by nutrition therapy and exercise within 10 days, insulin is started. Pregnant women require three to four times the amount of insulin needed by a nonpregnant woman. Human minimally antigenic insulin should be prescribed. Often one dose of long-acting insulin at bedtime is sufficient, with rapid-acting insulins, i.e., regular insulin, insulin aspart recombinant (Novolog), or insulin lispro recombinant (Humalog) used to aid optimal glycemic control. Insulin glargine (Lantus), once used for gestational diabetes, is no longer recommended for pregnant women. Because stress can significantly raise blood glucose levels, stress management is a vital part of therapy. The woman’s feelings about her pregnancy and diabetes as well as her support system should be carefully assessed. Coping strategies should be explored. The patient is taught about deep breathing and relaxation exercises and encouraged to engage in activities that she enjoys and finds relaxing. She and her partner should learn to recognize interaction tensions and ways to deal with these to limit stress in their environment.

Maternal complications associated with GDM include pregnancy-induced hypertension, eclampsia, and the need for cesarean section delivery.

hybrid diabetes

A form of DM that has characteristics of both types 1 and 2. The patient may have episodes of diabetic ketoacidosis but marked insulin resistance and an obese body type.

iatrogenic diabetes

DM due to administration of drugs such as corticosteroids or dextrose infusions.

idiopathic diabetes

Type 1b diabetes.

immune-mediated diabetes mellitus

Type 1 diabetes.

diabetes insipidus

Abbreviation: DI
Excessive urination caused either by inadequate amounts of circulating vasopressin (antidiuretic hormone) in the body (hypothalamic DI) or by failure of the kidney to respond to antidiuretic hormone (nephrogenic DI). Urinary output is often massive, e.g., 5 to 15 L/day, which may result in dehydration in patients who cannot drink enough liquid to replace urinary losses, e.g., those with impaired consciousness. The urine is dilute (specific gravity is often below 1.005), and typically the patient's serum sodium level and osmolality rise as free water is eliminated as urine. If water deficits are not matched or the urinary losses are not prevented, death will result from dehydration.


DI usually results from hypothalamic injury (such as brain trauma or neurosurgery) or from the effects of certain drugs (such as lithium or demeclocycline) on the renal resorption of water. Other representative causes include sickle cell anemia (in which renal infarcts damage the kidney's ability to retain water), hypothyroidism, adrenal insufficiency, inherited disorders of antidiuretic hormone production, and sarcoidosis.


The primary symptoms are urinary frequency, thirst, and dehydration.


When DI is a side effect of drug therapy, the offending drug is withheld. DI caused by failure of the posterior pituitary gland to secrete antidiuretic hormone is treated with synthetic vasopressin.

Patient care

Fluid balance is monitored. Fluid intake and output, urine specific gravity, and weight are assessed for evidence of dehydration and hypovolemic hypotension. Serum electrolyte and blood urea nitrogen levels are monitored.

The patient is instructed in nasal insufflation of vasopressin (desmopressin acetate, effective for 8 to 20 hr, depending on dosage), the oral tablet form being more useful for bedtime or administration of subcutaneous or intramuscular vasopressin (effective for 2 to 6 hr). The length of the therapy and the importance of taking medications as prescribed and not discontinuing them without consulting the prescriber are stressed. Hydrochlorothiazide can be prescribed for nephrogenic DI not caused by drug therapy; amiloride may be used in nephrogenic DI caused by lithium administration. Meticulous skin and oral care are provided; use of a soft toothbrush is recommended; and petroleum jelly is applied to the lips and an emollient lotion to the skin to reduce dryness and prevent skin breakdown. Adequate fluid intake should be maintained.

Both the patient and family are taught to identify signs of dehydration and to report signs of severe dehydration and impending hypovolemia. The patient is taught to measure intake and output, to monitor weight daily, and to use a hydrometer to measure urine specific gravity. Weight gain should be reported because this may signify that the medication dosage is too high. Recurrence of polyuria may indicate dosing that is too low. The patient should wear or carry a medical ID tag and have prescribed medications with him or her at all times. Both patient and family need to know that chronic DI will not shorten the lifespan, but lifelong medications may be required to control the signs, symptoms, and complications of the disease. Counseling may be helpful in dealing with this chronic illness.

insulin-dependent diabetes mellitus

Abbreviation: IDDM
Type 1 diabetes.

juvenile-onset diabetes

A dated term for type 1 diabetes.

latent diabetes

DM that manifests itself during times of stress such as pregnancy, infectious disease, weight gain, or trauma. Before the stress, no clinical or laboratory findings of diabetes are present. There is a very strong chance that affected people will eventually develop overt type 2 DM.

latent autoimmune diabetes in adults

Abbreviation: LADA
A form of type 1 diabetes usually diagnosed after 30 years of age, in which there are serum antibodies against insulin, pancreatic islet cells, or the protein products of those cells. Most patients affected by LADA eventually require insulin therapy, like patients with type 1 DM.

maternally inherited diabetes and deafness

See: maternally inherited diabetes and deafness

mature-onset diabetes of youth

Abbreviation: MODY
Type 2 DM that presents during childhood or adolescence, typically as an autosomal dominant trait in which there is diminished but not absent insulin production by the pancreas. Children with this form of DM are not prone to diabetic ketoacidosis.
Enlarge picture
WELL-CONTROLLED DIABETES MELLITUS: Daily blood sugar abstracted from the records of a patient whose DM is well controlled (hemoglobin A1c=6.4). The average capillary blood glucose level is 104 mg/dL, and the standard deviation is 19. Sixty-five percent of the readings are between 90 and 140 mg/dL; the lowest blood sugar is 67 mg/dL (on April 15) and the highest is about 190 (on March 21).

diabetes mellitus

Abbreviation: DM
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon

Type 1 DM usually presents as an acute illness with dehydration and often diabetic ketoacidosis. Type 2 DM is often asymptomatic in its early years. The American Diabetes Association (1-800-DIABETES) estimates that more than 5 million Americans have type 2 DM without knowing it.


Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.


Classic symptoms of DM are polyuria, polydipsia, and weight loss. In addition, patients with hyperglycemia often have blurred vision, increased food consumption (polyphagia), and generalized weakness. When a patient with type 1 DM loses metabolic control (such as during infections or periods of noncompliance with therapy), symptoms of diabetic ketoacidosis occur. These may include nausea, vomiting, dizziness on arising, intoxication, delirium, coma, or death. Chronic complications of hyperglycemia include retinopathy and blindness, peripheral and autonomic neuropathies, glomerulosclerosis of the kidneys (with proteinuria, nephrotic syndrome, or end-stage renal failure), coronary and peripheral vascular disease, and reduced resistance to infections. Patients with DM often also sustain infected ulcerations of the feet, which may result in osteomyelitis and the need for amputation.


Several tests are helpful in identifying DM. These include tests of fasting plasma glucose levels, casual (randomly assessed) glucose levels, or glycosylated hemoglobin levels. Diabetes is currently established if patients have classic diabetic symptoms and if on two occasions fasting glucose levels exceed 126 mg/dL (> 7 mmol/L), random glucose levels exceed 200 mg/dL (11.1 mmol/L), or a 2-hr oral glucose tolerance test is 200 mg/dL or more. A hemoglobin A1c test that is more than two standard deviations above normal (6.5% or greater) is also diagnostic of the disease.


DM types 1 and 2 are both treated with specialized diets, regular exercise, intensive foot and eye care, and medications.

Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels, i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides and a fall in HDL cholesterol. Participation in an intensive therapy program requires a motivated patient, but it can dramatically reduce eye, nerve, and renal complications compared to conventional therapy. See: insulin pump for illus.

Some patients with type 2 DM can control their disease with a calorically restricted diet (for instance 1600 to 1800 cal/day), regular aerobic exercise, and weight loss. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (such as glipizide), which increase pancreatic secretion of insulin; biguanides or thiazolidinediones (such as metformin or pioglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (such as acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. Both types of diabetics also may be prescribed pramlintide (Symlin), a synthetic analog of human amylin, a hormone manufactured in the pancreatic beta cells. It enhances postprandial glucose control by slowing gastric emptying, decreasing postprandial glucagon concentrations, and regulating appetite and food intake; thus pramlintide is helpful for patients who do not achieve optimal glucose control with insulin and/or oral antidiabetic agents. When combinations of these agents fail to normalize blood glucose levels, insulin injections are added. Tight glucose control can reduce the patient’s risk of many of the complications of the disease. See: illustration

Prevention of Complications

Patients with DM should avoid tobacco, actively manage their serum lipid levels, and keep hypertension under optimal control. Failure to do so may result in a risk of atherosclerosis much higher than that of the general public. Other elements in care include receiving regular vaccinations, e.g., to prevent influenza and pneumococcal pneumonia).


Diabetes is a chronic disease whose symptoms can be ameliorated and life prolonged by proper therapy. The isolation and eventual production of insulin in 1922 by Canadian physicians F. G. Banting and C. H. Best made it possible to allow people with the disease to lead normal lives.

Patient care

The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.

Home blood glucose self-monitoring is indispensable in helping patients to adjust daily insulin doses according to test results and to achieve optimal long-term control of diabetes. Insulin or other hypoglycemic agents are administered as prescribed, and their action and use explained to the patient. With help from a dietitian, a diet is planned based on the recommended amount of calories, protein, carbohydrates, and fats. The amount of carbohydrates consumed is a dietary key to managing glycemic control in diabetes. For most men, 60 to 75 carbohydrate g per meal are a reasonable intake; for most women, 45 to 60 g are appropriate. Saturated fats should be limited to less than 7% of total caloric intake, and trans-fatty acids (unsaturated fats with hydrogen added) minimized. A steady, consistent level of daily exercise is prescribed, and participation in a supervised exercise program is recommended.

Hypoglycemic reactions are promptly treated by giving carbohydrates (orange juice, hard candy, honey, or any sugary food); if necessary, subcutaneous or intramuscular glucagon or intravenous dextrose (if the patient is not conscious) is administered. Hyperglycemic crises are treated initially with prescribed intravenous fluids and insulin and later with potassium replacement based on laboratory values.

Regular ophthalmological examinations are recommended for early detection of diabetic retinopathy. The patient is educated about diabetes, its possible complications and their management, and the importance of adherence to the prescribed therapy. The patient is taught the importance of maintaining normal blood pressure levels (120/80 mm Hg or lower). Control of even mild-to-moderate hypertension results in fewer diabetic complications, esp. nephropathy, cerebrovascular disease, and cardiovascular disease. Limiting alcohol intake to approximately one drink daily and avoiding tobacco are also important for self-management. Emotional support and a realistic assessment of the patient's condition are offered; this assessment should stress that, with proper treatment, the patient can have a near-normal lifestyle and life expectancy. Long-term goals for a patient with diabetes should include achieving and maintaining optimal metabolic outcomes to prevent complications; modifying diet and lifestyle to prevent and treat obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy; improving physical activity; and allowing for the patient’s nutritional and psychosocial needs and preferences. Assistance is offered to help the patient develop positive coping strategies. It is estimated that 23 million Americans will be diabetic by the year 2030. The increasing prevalence of obesity coincides with the increasing incidence of diabetes; approx. 45% of those diagnosed receive optimal care according to established guidelines. According to the CDC, the NIH, and the ADA, about 40% of Americans between ages 40 and 74 have prediabetes, putting them at increased risk for type 2 diabetes and cardiovascular disease. Lifestyle changes with a focus on decreasing obesity can prevent or delay the onset of diabetes in 58% of this population. The patient and family should be referred to local and national support and information groups and may require psychological counseling.

Diabetic KetoacidosisHypoglycemia
OnsetGradualOften sudden
HistoryOften acute infection in a diabetic or insufficient insulin intakeRecent insulin injection, inadequate meal, or excessive exercise after insulin
Previous history of diabetes may be absent
MusculoskeletalMuscle wasting or weight lossWeakness
Muscle twitching
GastrointestinalAbdominal pains or cramps, sometimes acuteNausea and vomiting
Nausea and vomiting
Central nervous systemHeadacheConfusion, delirium, or seizures
Double or blurred vision
Orthostatic hypotension
SkinFlushed, dryDiaphoretic, pale
RespiratoryAir hungerVariable
Acetone odor of breathIncreased respiratory rate
Laboratory valuesElevated blood glucose (> 200 mg/dL)Subnormal blood glucose (0–50 mg/dL)
Glucose and ketones in blood and urineAbsence of glucose and ketones in urine unless bladder is full

non–insulin-dependent diabetes mellitus

Abbreviation: NIDDM
Type 2 diabetes. See: type 1 diabetes for table

pancreatic diabetes

Diabetes associated with destruction of the exocrine and endocrine functions of the pancreas, such as occurs in chronic or recurrent pancreatitis.

phlorhizin diabetes

Glycosuria caused by administration of phlorhizin.

renal diabetes

Renal glycosuria, marked by a low renal threshold for glucose. Glucose tolerance is normal and diabetic symptoms are lacking.

secondary diabetes mellitus

DM that results from damage to the pancreas (e.g., after frequent episodes of pancreatitis) or from drugs such as corticosteroids (which increase resistance to the effects of insulin).

steroid diabetes

Hyperglycemia caused by the use of exogenously administered corticosteroids, e.g., prednisone, methylprednisolone, or dexamethasone.

strict control of diabetes

Regulation of blood glucose to normal or nearly normal levels, both before and after meals. Tight control of blood sugar has been shown to improve the survival of patients in intensive-care units and to prevent long-term complications of DM, e.g., blindness, nerve damage, and kidney failure.

Patients with meticulously controlled DM typically have a hemoglobin A1c level of 6.5 to 7.0 or lower, fasting blood sugars that are less than 110 mg/dL, and after-meal blood sugar readings that are 140 mg/dL or less.

Synonym: tight control of diabetes

tight control of diabetes

Strict control of diabetes.

true diabetes

Diabetes mellitus.

type 1 diabetes

DM that usually has its onset before the age of 25 years, in which the essential abnormality is related to absolute insulin deficiency. It was formerly known as juvenile diabetes.
See: table
Type 1Type 2
Age at onsetUsually under 30Usually over 40
Symptom onsetAbruptGradual
Body weightNormalObese—80%
HLA associationPositiveNegative
Family historyCommonNearly universal
Insulin in bloodLittle to noneSome usually present
Islet cell antibodiesPresent at onsetAbsent
SymptomsPolyuria, polydipsia, polyphagia, weight loss, ketoacidosisPolyuria, polydipsia, peripheral neuropathy
ControlInsulin, diet, and exerciseDiet, exercise, and often oral hypoglycemic drugs or insulin
Vascular and neural changesEventually developWill usually develop
Stability of conditionFluctuates, may be difficult to controlMay be difficult to control in poorly motivated patients

type 1a diabetes mellitus

The most common form of type 1 DM. It is caused by autoimmune destruction of the beta cells of the pancreas and inadequate insulin production. In type 1a DM, antibodies against insulin, islet cells of the pancreas, or glutamic acid decarboxylase is often present in the blood. The patient is prone to develop diabetic ketoacidosis if he or she is not treated with insulin.

type 1b diabetes mellitus

A relatively less common form of type 1 DM (seen in only about 10% of type 1 diabetics) in which autoimmune antibodies against insulin, pancreatic beta cells, or their protein products are not found in the blood. Beta cells are nonetheless destroyed (by unknown means), and the patient develops hyperglycemia or ketoacidosis unless he or she receives insulin.
Synonym: idiopathic diabetes

type 2 diabetes

A type of DM that occurs predominantly in adults. The insulin produced is sufficient to prevent ketoacidosis but insufficient to meet the total needs of the body, and resistance to the effects of insulin on peripheral tissues is often present. This type of diabetes in nonobese patients can usually be controlled by diet and oral hypoglycemic agents (e.g., sulfonylurea drugs or metformin). Eventually, insulin therapy is often required. In some patients the condition can be controlled by careful diet and regular exercise. Synonym: non–insulin-dependent diabetes mellitus See: type 1 diabetes for table

unstable diabetes mellitus

Brittle diabetes.

mature-onset diabetes of youth

Abbreviation: MODY
Type 2 DM that presents during childhood or adolescence, typically as an autosomal dominant trait in which there is diminished but not absent insulin production by the pancreas. Children with this form of DM are not prone to diabetic ketoacidosis.
See also: diabetes

maturity-onset diabetes of the young

; MODY presentation of type 2 diabetes mellitus affecting overweight young adults or teenagers, similar to type 2 diabetes of older subjects, but usually without secondary complications (see alsodiabetes mellitusand type 2diabetes mellitus)
References in periodicals archive ?
Although much more research is needed, the strong evidence base for directed therapeutic strategies in the majority of patients with MODY, including discontinuation of glycemic therapies in MODY 2 and specific evaluation of response to sulfonylureas in MODY 1 and 3, provides a clear example of a beneficial application of molecularly driven personalized medicine in diabetes.
amp;quot;We do know a lot of money gets siphoned into Kenya where a lot of real estate is being picked up at double and triple the price it really is," said Mody.
Mody and Silliman have included articles from prominent scholars in the field of language disorders in the book.
More than anything else, what binds the Mody family together is this search - as also of his memory captured in a fading photo album, including his last image in his school uniform and holding the national flag.
The MODY group also tended to be older, heavier (BMI z score 1.
The flavours of absinthe are complex but the drink is smooth," said Mody.
We would like to see an urgent disclosure of the true costs of the PPF, which will allow an informed debate about whether greater fairness and transparency in setting the risk-based levy is needed, reducing the extent of cross-subsidy between companies,' Mr Mody said.
Drawing from existing literature (Lewis and Mody 1997, Mody and Patro 1996, Irwin and others 1997, Mody 2000), Llanto shows how the Philippine government may organize a management framework for contingent liabilities.
Istvan Mody and his colleagues at the University of California, Los Angeles examined brain slices from female mice.
As we grew (at an annual rate of 20%), our network of offices grew and our user needs became much more complex," says Vikram Mody, global head of information technology at MOW.
As the Army moves forward with its knowledge management and information technology modernization efforts, SIGNAL continues to play an integral role in the Army's transformation," said SIGNAL President & CEO Roger Mody.