Steroidogenesi corticosurrenalica

Vitamin A deficiency interfered with the pituitary-thyroid axis by: 1) increasing the synthesis and secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, 2) increasing the size of the thyroid gland, 3) reducing iodine uptake by the thyroid gland and 4) impairing the synthesis and iodination of thyroglobulin ( precursor to thyroid hormones ), thus leading to hypothyroidism. Hypothyroidism is associated with elevated thyrotropin releasing hormone (TRH), which is released to stimulate the pituitary gland to release TSH to stimulate the thyroid to increase thyroid hormone production. Vitamin A inhibits TSH secretion via the down regulation of TSH-β gene expression, protecting against elevated TRH levels. Elevated TRH leads to hypothyroidism and also increases prolactin.

Specificity and quantitation . Each sample was run in duplicate, and values not falling within 50% of their mean were rerun. Specificity of the PCR product was evaluated using the melting curve generated at the end of amplification and by running a 2% agarose gel to visualize the PCR product. Absolute quantitation of mRNA concentration in the original sample was achieved using a standard curve generated for each batch. Each standard curve included two nontemplate controls and eight serial dilutions covering the range of 10 3 to 10 7 molecules/µL. The standards for each gene were prepared as described previously ( Bhat and Epelboym 2004 ). The R 2 for the standard curve was between and ; the plate was rerun if it was < . The ratio of target gene mRNA molecules to 18S mRNA molecules was calculated for each.

Hershkovitz et al. (2008) reported 4 undervirilized males of an extended Bedouin family. One of these had been reported (Biason-Lauber et al., 1997) to carry mutations in the CYP17A1 gene (609300), encoding P450c17, causing isolated 17,20-lyase deficiency (202110). Gas chromatography-mass spectrometry (GC-MS) urinary steroid profiling and serum steroid measurements showed combined deficiencies of 17,20-lyase and 21-hydroxylase. Sequencing of exons 1 and 8 of CYP17A1 in 2 different laboratories showed no mutations. Sequencing of the POR gene showed that all 4 patients were homozygous for G539R (), which was shown by Huang et al. (2005) to retain 46% of normal 17-alpha-hydroxylase activity but only 8% of the 17,20-lyase activity of P450c17. Hershkovitz et al. (2008) conclude that POR deficiency can masquerade clinically as isolated 17,20-lyase deficiency.

The physiology of the reproductive system changes dramatically with the onset of major illness. The serum testosterone concentrations fall to pre-pubertal levels secondary to a decreased secretion of gonadotropins and a decreased Leydig cell response to luteinizing hormone. At the same time, the serum oestrogen concentration rises as the result of an increased rate of peripheral aromatization. The clinical consequences of these marked changes are not yet well understood. One line of evidence argues for the administration of anabolic steroids (derivatives of testosterone) to critically ill patients to improve their catabolic state. Another line of evidence in animal models suggests that testosterone may suppress the immune system and myocardial function in critical illness. No clinical trials of oestrogen administration to critically ill patients have been reported, although two animal studies suggest that oestrogen may have a positive effect on survival. This chapter reviews changes in the physiology of the reproductive system in major illness as well as current evidence regarding the clinical effects of androgens and oestrogens in critical illness and their potential therapeutic roles.

Steroidogenesi corticosurrenalica

steroidogenesi corticosurrenalica

The physiology of the reproductive system changes dramatically with the onset of major illness. The serum testosterone concentrations fall to pre-pubertal levels secondary to a decreased secretion of gonadotropins and a decreased Leydig cell response to luteinizing hormone. At the same time, the serum oestrogen concentration rises as the result of an increased rate of peripheral aromatization. The clinical consequences of these marked changes are not yet well understood. One line of evidence argues for the administration of anabolic steroids (derivatives of testosterone) to critically ill patients to improve their catabolic state. Another line of evidence in animal models suggests that testosterone may suppress the immune system and myocardial function in critical illness. No clinical trials of oestrogen administration to critically ill patients have been reported, although two animal studies suggest that oestrogen may have a positive effect on survival. This chapter reviews changes in the physiology of the reproductive system in major illness as well as current evidence regarding the clinical effects of androgens and oestrogens in critical illness and their potential therapeutic roles.

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