Prevalence and Incidence of MODY diabetes
MODY diabetes Prevalence: Book Excerpts
Prevalence/Incidence of MODY diabetes: Online Medical Books
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Diabetes insipidus:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
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.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
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.
ELDER TIP As the body ages, the cells become more resistant to insulin, thus reducing the older adult’s ability to metabolize glucose. In addition, the release of insulin from the pancreatic beta cells is reduced and delayed. These combined processes result in hyperglycemia. In the older patient, sudden concentrations of glucose cause increased and more prolonged hyperglycemia.
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
About prevalence and incidence statistics:
The term 'prevalence' of MODY diabetes usually refers to the estimated population
of people who are managing MODY diabetes at any given time.
The term 'incidence' of MODY diabetes refers to the annual diagnosis rate,
or the number of new cases of MODY diabetes diagnosed each year.
Hence, these two statistics types can differ:
a short-lived disease like flu can have high annual incidence but low prevalence,
but a life-long disease like diabetes has a low annual incidence but high prevalence.
For more information see about prevalence and incidence statistics.
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