Gonadal steroids and humoral immunity

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.

Other Assays Rarely Used- General availability of assays that can reliably measure suppressed TSH has made this the gold standard to which other tests must be compared, and has effectively eliminated the need for most previously used ancillary tests. There are only rare causes of confusion in the TSH assay. Severe illness, dopamine and steroids, and hypopituitarism, can cause low TSH, but suppression below µ/ml is uncommon and below µ/ml is exceptional, except in thyrotoxicosis. Thyrotoxicosis is associated with normal or high TSH in patients with TSH producing pituitary tumors and selective pituitary resistance to thyroid hormone.
If TSH, FT4, TRAb, and other tests noted above do not establish the diagnosis, it may be wise to do nothing further except to observe the course of events. In patients with significant thyroid hyperfunction, the symptoms and signs will become clearer, and the laboratory measurements will fall into line. Measurement of BMR, T3 suppression of RAIU, TRH testing, and clinical response to KI are of historical interest.

Thyroid hormones, gonadal and adrenocortical steroids, are glucoregulatory hormones. Thyroid hormones increase the provision of glucose to meet the enhanced energy demands which they impose. Glucose tolerance is decreased, associated with increased hepatic glucose production, although the glucose-raising effects of thyroid hormones are partially offset by an increased rate of glucose utilization especially in the postabsorptive state. The insulin secretory capacity of the pancreatic B cells is reduced by an excess of thyroid hormones, and the onset of diabetes may be hastened as pancreatic insulin reserves are depleted. Natural estrogens can improve glucose tolerance through a beta-cytotropic effect and enhanced insulin sensitivity. Progesterone may produce similar effects in the absence of estrogens, but progestins appear to antagonize the effects of estrogens. Testosterone exerts only marginal effects on glucose tolerance. Glucocorticoids decrease glucose tolerance by increased hepatic glucose production and impaired peripheral glucose utilization. Glucocorticoids reduce insulin sensitivity and responsiveness in peripheral tissues. However, the diabetogenic influence of glucocorticoid excess is partly compensated by a beta-cytotropic effect and a condition of diabetes develops when the functional reserve of the endocrine pancreas becomes limiting.

Cardiovascular risk factors include the alteration or diminishing of her glucose tolerance and hyperinsulinism (become resistant to insulin), a change in lipoproteins (carry cholesterol in blood) fraction which can cause cardiovascular disease and atherosclerosis (deposition of fatty substances onto inner walls of arteries causing blockage), increased triglyceride levels, hypertension (abnormally high blood pressure), changes in her myocardium (middle muscular layer of heart wall), and increased concentration levels of several different clotting factors.  Cardiomyopathy (a typically chronic disorder of heart muscle that may involve hypertrophy and obstructive damage to the heart), myocardial infarction (localized death of the myocardium tissue usually leading to heart failure), heart attack, stroke, and cerebro-vascular accidents have all been causes in deaths where AAS abuse was implicated.  Of course the liver, the body’s primary filtration system will come under attack as it has to accommodate the increased toxicity.  Among the liver problems promoted are holestatic jaundice (failure of bile flow that causes yellowish pigmentation of skin, tissues, and body fluids), peliosis hepatis (blood-filled cysts develop on liver), hepatocellular hyperplasia (unusual increase of an epithelial parenchymatous cell called hepatocytes in the liver), and cancer.  Secondary filters such as the kidneys and gallbladder also become more susceptible to disease.

Gonadal steroids and humoral immunity

gonadal steroids and humoral immunity

Cardiovascular risk factors include the alteration or diminishing of her glucose tolerance and hyperinsulinism (become resistant to insulin), a change in lipoproteins (carry cholesterol in blood) fraction which can cause cardiovascular disease and atherosclerosis (deposition of fatty substances onto inner walls of arteries causing blockage), increased triglyceride levels, hypertension (abnormally high blood pressure), changes in her myocardium (middle muscular layer of heart wall), and increased concentration levels of several different clotting factors.  Cardiomyopathy (a typically chronic disorder of heart muscle that may involve hypertrophy and obstructive damage to the heart), myocardial infarction (localized death of the myocardium tissue usually leading to heart failure), heart attack, stroke, and cerebro-vascular accidents have all been causes in deaths where AAS abuse was implicated.  Of course the liver, the body’s primary filtration system will come under attack as it has to accommodate the increased toxicity.  Among the liver problems promoted are holestatic jaundice (failure of bile flow that causes yellowish pigmentation of skin, tissues, and body fluids), peliosis hepatis (blood-filled cysts develop on liver), hepatocellular hyperplasia (unusual increase of an epithelial parenchymatous cell called hepatocytes in the liver), and cancer.  Secondary filters such as the kidneys and gallbladder also become more susceptible to disease.

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