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Causes of Diabetes
List of causes of Diabetes
Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Diabetes) that could possibly cause Diabetes includes:
- Metabolic syndrome - a syndrome with 4 key features (diabetes, hypertension, obesity/overweight, and high cholesterol).
- Insulin resistance
- Hemochromatosis - iron overload causes pancreas damage that can mimic Type 1 or Type 2 diabetes.
- Chronic pancreatitis - pancreas damage that can mimic diabetes.
- Polycystic ovary syndrome (PCOS) - ovary cysts inhibit natural female hormones causing insulin resistance
- Carcinoid syndrome - glucose intolerance, protean manifestations, serotonin inhibits insulin production
- Pancreas surgery
- Pancreas trauma (type of Pancreas conditions)
- Overactive pituitary gland
- Overactive adrenal glands
- Pancreatic insufficiency
- Acromegaly
- Cushing's disease
- Cystic fibrosis
- Adenocarcinomas
- Somatostatinoma
- Aldosteronoma-induced hypokalaemia
- Phaeochromocytoma
- Primary aldosteronism
- Wolfram's syndrome
- Leprechaunism
- Rabson-Mendenhall syndrome
- Insulin autoantibodies (IAAs) - can inhibit insulin and lead to insulin resistance.
- Type B insulin resistance - insulin receptor antibodies can inhibit insulin action.
- Stiff Man syndrome - about half have Glutamic Acid Decarboxylase (GAD) antibodies and get Type 1 diabetes.
More causes: see full list of causes for Diabetes-like symptoms
Causes of Diabetes: Online Medical Books
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Diabetes.
Hyperglycemia:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- Impaired fasting glucose
-
Medications
–Corticosteroids are a common cause
–Common medications include growth hormone, estrogen (including oral contraceptives), nicotinic acid, salicylates and NSAIDs, thiazide and loop diuretics, phenytoin, and epinephrine - Diabetes mellitus type I
–Diabetic ketoacidosis - Diabetes mellitus type II
-
Pancreatic disease
–Acute or chronic pancreatitis
–Pancreatectomy
–Pancreatic carcinoma
–Hemochromatosis
–Cystic fibrosis -
Increased counter-regulatory hormones associated with acute disease
–Myocardial infarction
–Stroke or other neurologic disease
–Renal insufficiency
–Hepatic insufficiency - Acromegaly
- Cushing's syndrome
- Pheochromocytoma
- Hyperthyroidism (thyroid storm)
- Glucagonoma
- Gestational diabetes
- Amyloidosis
Hyperglycemia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Type I diabetes mellitus
–Most common form of diabetes in children
–Prevalence: 1.9/1,000
–Autoimmune-mediated destruction of pancreatic islets (β-cells)
–Absolute insulin deficiency
–Often presents with ketosis and DKA
- Type II diabetes mellitus
–Increasing prevalence in children, especially among obese
–In children, onset usually in mid-puberty
–More frequent in blacks, Hispanics, Pacific Islanders, Asians, and Native Americans (Pima Indians)
–Strong association with family history of type II diabetes
–Insulin resistance and inadequate insulin secretion results in relative insulin deficiency
-
Maturity-onset diabetes of the young (MODY)
–Infrequent
–Autosomal dominant disease
–Onset usually between 9 and 25 years old
–Genetic defects in enzymes or nuclear transcription factors involved in islet cell development or the regulation of insulin secretion -
Drug- or chemical-induced diabetes
–Glucocorticoids, β-adrenergic agonists, phenytoin, asparaginase, cyclosporine, tacrolimus, vacor, pentamidine, diazoxide, nicotinic acid, thyroid hormone, thiazides - Other endocrinopathies: Cushing disease, acromegaly, pheochromocytoma
-
Exocrine pancreatic diseases
–Cystic fibrosis
–Hemochromatosis - Pancreatectomy
- Physiological stress (trauma, infection)
-
Infections
–CMV
–Congenital rubella - Genetic syndromes: Prader-Willi syndrome, Down syndrome, Turner syndrome, Klinefelter syndrome, Wolfram syndrome
Polydipsia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Diabetes mellitus (type I and type II)
–Hyperglycemia drives an osmotic diuresis that causes polyuria, which then leads to dehydration, increased thirst, and polydipsia -
Diabetes insipidus
–Abnormal water balance due to vasopressin (ADH) deficiency or resistance, causing excretion of large amounts of dilute urine -
Central or neurogenic diabetes insipidus
(vasopressin deficiency)
–Congenital
–Familial (autosomal dominant)
–Acquired: Neurosurgery, tumor (e.g., craniopharyngioma), head trauma, infiltrative/inflammatory, infectious-
Nephrogenic diabetes insipidus (decreased responsiveness of the kidneys to vasopressin)
–Familial (X-linked dominant and recessive forms)
–Acquired: Renal disease, obstructive uropathy, hypercalcemia/hypercalciuria
–Hypokalemia, drug-induced (e.g., lithium, diuretics, ethanol, cisplatin)
–Gestational DI: Increased clearance of ADH by placental vasopressinase, lower osmolar threshold for thirst and ADH release -
Primary polydipsia
–Compulsive water drinking
–Dipsogenic DI - Primary hyperaldosteronism
- Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (DIDMOAD) syndrome
- Bartter syndrome
- Hypertension (e.g., pheochomocytoma)
- Neuroblastoma
- Cystinosis
- Congestive heart failure
-
Nephrogenic diabetes insipidus (decreased responsiveness of the kidneys to vasopressin)
Polydipsia:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Diabetes insipidus
Diabetes insipidus characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Diabetes mellitus
Polydipsia is a classic finding with diabetes mellitus — a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur.
Hypercalcemia
As hypercalcemia progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, a decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
Hypokalemia
Hypokalemia is an electrolyte imbalance that can cause nephropathy, resulting in polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Psychogenic polydipsia
Psychogenic polydipsia is an uncommon disorder that causes polydipsia and polyuria. It may occur with any psychiatric disorder, but is more common with schizophrenia. Signs of psychiatric disturbances, such as anxiety or depression, are typical. Other findings include a headache, blurred vision, weight gain, edema, elevated blood pressure and, occasionally, stupor and coma. Signs of heart failure may develop with overhydration.
Renal disorders (chronic)
Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Sheehan’s syndrome
Polydipsia, polyuria, and nocturia occur with Sheehan’s syndrome, a disorder of postpartum pituitary necrosis. Other features include fatigue, failure to lactate, amenorrhea, decreased pubic and axillary hair growth, and a reduced libido.
Sickle cell anemia
As nephropathy develops, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers and bone deformities, such as kyphosis and scoliosis.
Other causes
Drugs
Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
Diabetic complications during pregnancy:
Causes
(Professional Guide to Diseases (Eighth Edition))
In diabetes mellitus, glucose is inadequately utilized either because insulin isn’t synthesized or because tissues are resistant to the hormonal action of endogenous insulin. During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes insulin’s effects; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, females who are prediabetic or diabetic are unable to produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant. As insulin requirements rise toward term, the patient who’s prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control, whereas the patient who’s insulin-dependent may need increased insulin dosage.
Hereditary fructose intolerance:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Transmitted as an autosomal recessive trait, hereditary fructose intolerance results from a deficiency in the enzyme fructose-1-phosphate aldolase. The enzyme operates at only 1% to 10% of its normal biological activity, thus preventing rapid uptake of fructose by the liver after ingestion of fruit or foods containing cane sugar.
In some European countries, hereditary fructose intolerance may have an incidence as high as 1 in 20,000 people.
Diabetes mellitus:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
DM affects an estimated 6% of the population of the United States, about half of whom are undiagnosed. Incidence is greater in females and rises with age. Type 2 accounts for 90% of cases.
In type 1 diabetes, pancreatic beta-cell destruction or a primary defect in beta-cell function results in failure to release insulin and ineffective glucose transport. Type 1 immune-mediated diabetes is caused by cell-mediated destruction of pancreatic beta cells. The rate of beta-cell destruction is usually higher in children than in adults. The idiopathic form of type 1 diabetes has no known cause. Patients with this form have no evidence of autoimmunity and don’t produce insulin.
In type 2 diabetes, beta cells release insulin, but receptors are insulin-resistant and glucose transport is variable and ineffective. Risk factors for type 2 diabetes include:
❑ obesity (even an increased percentage of body fat primarily in the abdominal region); risk decreases with weight and drug therapy
❑ lack of physical activity
❑ history of GDM
❑ hypertension
❑ Black, Hispanic, Pacific Islander, Asian American, Native American origin
❑ strong family history of diabetes
❑ older than age 45
❑ high-density lipoprotein cholesterol of less than 35 or triglyceride of greater than 250
❑ Seriously impaired glucose tolerance (IGT) test.
The “other specific types” of DM result from various conditions (such as a genetic defect of the beta cells or endocrinopathies) or from use of or exposure to certain drugs or chemicals. GDM is considered present whenever a patient has any degree of abnormal glucose during pregnancy. This form may result from weight gain and increased levels of estrogen and placental hormones, which antagonize insulin.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage in the fat deposits. Insulin deficiency compromises the body tissues’access to essential nutrients for fuel and storage.
Diabetes insipidus results centrally from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result nephrogenically from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial. (Note: Pituitary diabetes insipidus shouldn’t be confused with nephrogenic diabetes insipidus, a rare congenital disturbance of water metabolism that results from renal tubular resistance to vasopressin.)
Normally, the hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable. The absence of vasopressin in diabetes insipidus allows the filtered water to be excreted in the urine instead of being reabsorbed.
Nephrogenic diabetes insipidus involves a defect in the parts of the kidneys that reabsorb water back into the bloodstream. It occurs less commonly than central diabetes insipidus. Nephrogenic diabetes insipidus may occur as an inherited disorder in which male children receive the abnormal gene that causes the disease on the X chromosome from their mothers. Nephrogenic diabetes insipidus may also be caused by diseases of the kidney (such as polycystic kidney disease) and the effects of certain drugs (such as lithium and amphotericin B).
Diabetes insipidus is rare, affecting 1 in 25,000 people. Males and females are affected equally.
This disorder characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Polydipsia is a classic finding with this disorder—a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur.
As this disorder progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
This electrolyte imbalance can cause nephropathy, resulting in polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
This uncommon disorder causes polydipsia and polyuria. This condition may occur with any psychiatric disorder, but more common with schizophrenia. Signs of psychiatric disturbances, such as anxiety or depression, are typical. Other findings include headache, blurred vision, weight gain, edema, elevated blood pressure and, occasionally, stupor and coma. Signs of heart failure may develop with overhydration.
Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Polydipsia, polyuria, and nocturia occur within this syndrome of postpartum pituitary necrosis. Other features include fatigue, failure to lactate, amenorrhea, decreased pubic and axillary hair growth, and reduced libido.
As nephropathy develops, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers, and bone deformities, such as kyphosis and scoliosis.
This disorder infrequently causes polydipsia. Characteristic findings include tachycardia, palpitations, weight loss despite increased appetite, diarrhea, tremors, an enlarged thyroid, dyspnea, nervousness, diaphoresis, and heat intolerance. Exophthalmos may also occur.
Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
In diabetes mellitus, glucose is inadequately used either because insulin isn’t synthesized (as in type 1, insulin-dependent diabetes) or because tissues are resistant to the hormonal action of endogenous insulin (as in type 2, non–insulin-dependent diabetes).
During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes the effects of insulin; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, women who are prediabetic or diabetic can’t produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant.
As insulin requirements rise toward term, the patient who is prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control. The insulin-dependent patient may need increased insulin dosage.
The effects of diabetes mellitus result from insulin deficiency. Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the body tissues’access to essential nutrients for fuel and storage.
Type 1A results from autoimmune beta-cell destruction, resulting in insulin deficiency. Type 1B leaves these immunologic markers but results in insulin deficiency and kerosis.
Other risk factors include the following:
❑ Obesity contributes to the resistance to endogenous insulin.
❑ Physiologic or emotional stress can cause prolonged elevation of stress hormone levels (cortisol, epinephrine, glucagon, and growth hormone). This raises blood glucose levels, which, in turn, places increased demands on the pancreas.
❑ Pregnancy causes weight gain and increases levels of estrogen and placental hormones, which antagonize insulin.
❑ Some medications can antagonize the effects of insulin, including thiazide diuretics, adrenal corticosteroids, and hormonal contraceptives.
Pituitary diabetes insipidus results from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial.
The hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into the general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable.
In pituitary diabetes insipidus, the absence of vasopressin allows the filtered water to be excreted in the urine instead of being reabsorbed. In renal diabetes insipidus, the kidney doesn’t respond to vasopressin, which is usually present in high concentrations.
Diabetes insipidus characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Polydipsia is a classic finding with diabetes mellitus — a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur. (See Associated disorder: Diabetes mellitus, page 514.)
CULTURAL CUE:Diabetes is the fourth leading cause of death in Black, Native American, Hawaiian, and Filipino women. Also, Blacks are at greater risk for developing diabetes than Whites.
As hypercalcemia progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
An electrolyte imbalance — hypokalemia — can cause nephropathy, resulting in polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
As nephropathy develops in patients with sickle cell anemia, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers and such bone deformities as kyphosis and scoliosis.
Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
Diabetes insipidus.Diabetes insipidus characteristically produces polydipsia and may also cause excessive voiding of dilute urine and mild to moderate nocturia. Fatigue and signs of dehydration occur in severe cases.
Diabetes mellitus.Polydipsia is a classic finding with diabetes mellitus—a consequence of the hyperosmolar state. Other characteristic findings include polyuria, polyphagia, nocturia, weakness, fatigue, and weight loss. Signs of dehydration may occur.
Hypercalcemia.As hypercalcemia progresses, the patient develops polydipsia, polyuria, nocturia, constipation, paresthesia and, occasionally, hematuria and pyuria. Severe hypercalcemia can progress quickly to vomiting, decreased level of consciousness, and renal failure. Depression, mental lassitude, and increased sleep requirements are common.
Hypokalemia.Hypokalemia can cause polydipsia, polyuria, and nocturia. Related hypokalemic signs and symptoms include muscle weakness or paralysis, fatigue, decreased bowel sounds, hypoactive deep tendon reflexes, and arrhythmias.
Psychogenic polydipsia.Psychogenic polydipsia causes polydipsia and polyuria. It may occur with any psychiatric disorder, but is more common with schizophrenia. Signs of psychiatric disturbances, such as anxiety or depression, are typical. Other findings include headache, blurred vision, weight gain, edema, elevated blood pressure and, occasionally, stupor and coma. Signs of heart failure may develop with overhydration.
Renal disorders (chronic).Chronic renal disorders, such as glomerulonephritis and pyelonephritis, damage the kidneys, causing polydipsia and polyuria. Associated signs and symptoms include nocturia, weakness, elevated blood pressure, pallor and, in later stages, oliguria.
Sheehan's syndrome.Polydipsia, polyuria, and nocturia occur with Sheehan's syndrome, a disorder of postpartum pituitary necrosis. Other features include fatigue, failure to lactate, amenorrhea, decreased pubic and axillary hair growth, and a reduced libido.
Sickle cell anemia.With sickle cell anemia, as nephropathy develops, polydipsia and polyuria occur. They may be accompanied by abdominal pain and cramps, arthralgia and, occasionally, lower extremity skin ulcers and bone deformities, such as kyphosis and scoliosis.
Drugs.Diuretics and demeclocycline may produce polydipsia. Phenothiazines and anticholinergics can cause dry mouth, making the patient so thirsty that he drinks compulsively.
Other conditions that might have
Diabetes as a complication may,
potentially, be an underlying cause of Diabetes.
Our database lists the following as having
Diabetes as a complication of that condition:
Conditions listing Diabetes
as a symptom may also be potential underlying causes of Diabetes.
Our database lists the following as having
Diabetes as a symptom of that condition:
The following drugs, medications, substances or toxins are some of the possible
causes of Diabetes as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 76
medications causing Diabetes
When combined, certain drugs, medications, substances or toxins may react
causing Diabetes as a symptom.
The list below is incomplete and various other drugs or substances may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 78
drug interactions causing Diabetes
Causes: Diabetes:
Either reduced insulin production or poor insulin metabolism, depending on subtype.
People develop diabetes for two reasons: the pancreas does not make
enough insulin for the body's needs, or the cells in the muscles, liver,
and fat do not use insulin properly, or both. As a result, the amount of
glucose in the blood increases while the cells are starved of energy. Over
the years, high blood glucose damages nerves and blood vessels, leading to
complications such as blindness, heart and kidney disease, nerve problems,
gum infections, and amputation. (Source: excerpt from Am I at Risk for Type 2 Diabetes: NIDDK)
High blood sugar and high blood pressure damage the kidneys’ glomeruli.
When the kidneys are damaged, the protein leaks out of the kidneys into
the urine. Damaged kidneys do not do a good job of cleaning out waste and
extra fluids. So not enough waste and fluids go out of the body as urine.
Instead, they build up in your blood.
(Source: excerpt from Keep your kidneys healthy: NIDDK)
If you have diabetes, your body cannot properly convert
foods into the energy needed for daily activity. Our bodies change
the foods we eat into a form of sugar called glucose. Glucose
travels through the bloodstream to "fuel" or feed our cells.
Sometimes it is stored in the liver for future use. Insulin is a
hormone that is made in the pancreas and helps cells take in the
amount of glucose they need. People with diabetes do not make or
properly use insulin. As a result, glucose builds up in their blood
and causes many symptoms of diabetes such as feeling tired, losing
weight, feeling hungry or thirsty, urinating frequently or having
vision problems (Source: excerpt from Dealing With Diabetes - Age Page - Health Information: NIA)
The following medical news items are relevant to causes of Diabetes:
The following are statistics from various sources about the causes of Diabetes:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Diabetes may be found in:
Next articles: Tools & Services:
Medical Articles:
Diabetes insipidus:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Polydipsia:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Diabetes insipidus
Diabetes mellitus
Hypercalcemia
Hypokalemia
Psychogenic polydipsia
Renal disorders (chronic)
Sheehan’s syndrome
Sickle cell anemia
Thyrotoxicosis
Other causes
Drugs
Diabetic complications during pregnancy:
Causes
(Handbook of Diseases)
Protective mechanisms
Diabetes mellitus:
Causes
(Handbook of Diseases)
Diabetes insipidus:
Causes
(Handbook of Diseases)
Polydipsia:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Diabetes insipidus
Diabetes mellitus
Hypercalcemia
Hypokalemia
Renal disorders (chronic)
Sickle cell anemia
Other causes
Drugs
Polyuria and Polydipsia:
Principal Causes of Polyuria and Polydipsia
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Polydipsia:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Other causes
Diabetes as a complication of other conditions:
Diabetes as a symptom:
Medications or substances causing Diabetes:
Drug interactions causing Diabetes:
What causes Diabetes?
Article excerpts about the
causes of Diabetes:
Am I at Risk for Type 2 Diabetes: NIDDK (Excerpt)
Keep your kidneys healthy: NIDDK (Excerpt)
Dealing With Diabetes - Age Page - Health Information: NIA (Excerpt)
Medical news summaries relating to Diabetes:
Cause statistics for Diabetes:
Related information on causes of Diabetes:
» Next page: Risk Factors for Diabetes
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