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Beta thalassemia genes are reported throughout the world, although more frequently in Mediterranean, African, and Southeast Asian populations. Symptoms of beta thalassemia occur when not enough oxygen gets to various parts of the body due to low levels of hemoglobin.

Beta-thalassemia also known as Cooley’s anemia. Beta-thalassemia happens when the body is unable to make an important blood protein called beta globin. Beta-thalassemia is caused by abnormalities in the beta-globin gene, located on chromosome 11. It is not a sex-linked genetic trait. Worldwide, beta thalassemia is affecting thousands of infants each year.

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. Male sexual development is affected in utero. Females appear normal at birth but have delayed puberty.

Apparent mineralocorticoid excess (AME ) are autosomal recessieve form of laag-reninhypertensie, cause of hypertensie and hypokalaemia which answers to glucocorticoid treatment. The syndrome of apparent mineralocorticoid excess is a rare form of severe juvenile hypertension that is usually transmitted as an autosomal recessive trait. Patients with apparent mineralocorticoid excess have low or absent activity of the enzyme 11 beta OH steroid dehydrogenase, and inappropriately high intrarenal levels of cortisol resulting in Na+ retention and hypertension. Although apparent mineralocorticoid excess is presumed to reflect inappropriate cortisol occupancy of mineralocorticoid receptors, several features also suggest inappropriate occupancy of glucocorticoid receptors.

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 Androgenetic alopecia is postulated to be a dominantly inherited disorder with variable penetrance and expression. Additionally, prostate cancer, disorders of insulin resistance, and high blood pressure have been related to androgenetic alopecia.

Androgenetic alopecia is an extremely common disorder affecting both men and women. This is essentially a cosmetic disorder. A variety of genetic and environmental factors likely play a role in causing androgenetic alopecia. Other than affecting the patient psychologically, the disorder is significant only in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. Androgenetic alopecia is a genetically determined condition. Androgen is necessary for progression of the disorder, as it is not found in males castrated prior to puberty. The progression of the disorder is stopped if postpubertal males are castrated.

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. Male sexual development is affected in utero. Females appear normal at birth but have delayed puberty.

Apparent mineralocorticoid excess (AME ) are autosomal recessieve form of laag-reninhypertensie, cause of hypertensie and hypokalaemia which answers to glucocorticoid treatment. The syndrome of apparent mineralocorticoid excess is a rare form of severe juvenile hypertension that is usually transmitted as an autosomal recessive trait. Patients with apparent mineralocorticoid excess have low or absent activity of the enzyme 11 beta OH steroid dehydrogenase, and inappropriately high intrarenal levels of cortisol resulting in Na+ retention and hypertension. Although apparent mineralocorticoid excess is presumed to reflect inappropriate cortisol occupancy of mineralocorticoid receptors, several features also suggest inappropriate occupancy of glucocorticoid receptors.

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Some forms of adrenal hyperplasia are more severe and cause adrenal crisis in the newborn due to salt wasting.

Adrenal hyperplasia refers to a radical of inherited adrenal gland disorders. People with this condition do no make enough of the hormones cortisol and aldosterone, and produce too much of androgen. Most of these conditions involve greater or lesser production of sex steroids and can alter development of primary or secondary sex characteristics in affected infants, children, and adults. Adrenal hyperplasia can affect both boys and girls. People with congenital adrenal hyperplasia lack of an enzyme needed by the adrenal gland to make the hormones cortisol and aldosterone. There are two major types of this disorder: classic adrenal hyperplasia, the more severe form of the disease affecting very young children; and nonclassic adrenal hyperplasia, a milder form that usually develops in late childhood or early adulthood.

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