Adrenal glands, atrophy

Giving exogenous corticosteroids suppresses ACTH secretion which results in adrenal gland atrophy. Therefore glucocorticosteroid doses should be tapered off to allow the patient to adjust and prevent symptoms of adrenal insufficiency. For the short acting glucocorticosteroids an alternate day regimen should be considered to lower the risks for adrenal suppression. 

Fluprednisolone has been shown to exist in seven different solid phases, of which six were crystalline and one was amorphous [107]. Of the crystalline phases, three were anhydrous, two were monohydrates, and one was a tert-butylamine solvate. The in vitro dissolution rates of the six crystalline phases of fluprednisolone were determined and compared with in vivo dissolution rates derived from pellet implants in rats [108]. The agreement between the in vitro and in vivo dissolution rates was found to be quite good, but the correlation with animal weight loss and adrenal gland atrophy was only fair. These results can be interpreted to indicate that, for fluprednisolone, differences in dissolution rates of the drug did not lead to measurable biological differences. 

Rats on a pantothenic acid-free diet show rapid depletion of adrenal corticosteroids, and reduced production of the steroids in isolated adrenal glands in response to stimulation with adrenocorticotrophic hormone (ACTH). This presumably reflects the role of acetyl CoA in the synthesis of steroids deficiency also results in atrophy of the seminiferous mbules of male rats and delayed sexual maturation in females. As deficiency progresses, there is enlargement, then congestion, and finally hemorrhage, of the adrenal cortex. In young animals, but not in adults, pantothenic acid deprivation eventually leads to necrosis of the adrenal cortex. 

Accutane is a potent rat and rabbit developmental toxin (teratogen). Testicular atrophy and evidence of lower spermatogenesis was noted in dogs given isotretinoin for 30 weeks at 20 or 60 mg kg day Fischer 344 rats dosed at 8 or 32 mg kg day for over 18 months had a dose-related raised incidence of pheochromocytoma, an adrenal gland tumor. The relevance in man is unknown since this animal develops spontaneous pheochromocytoma at a significant rate. 

Suppression of the pituitary-adrenal axis Inhibition of ACTH release Atrophy of adrenal glands reduced synthesis of natural corticosteroids Body unable to withstand stress if corticosteroid withdrawn - life threatening... 

Toxicology LD50 (oral, rat) > 2 g/kg low toxicity by ing. questionable carcinogen shown to cause urinary bladder polyps and atrophy of adrenal gland in animals tumorigen mutagen TSCA listed... 

Addison s disease is a rare, potentially fatal condition due to insufficient production of both aldosterone and cortisol caused by atrophy of the adrenal glands. It is characterised by low blood pressure, loss of sodium, weight loss and pigmentation of mucosal membranes. Adrenocortical insufficiency also results from pituitary failure with loss of adrenocorticotrophic hormone (ACTH) production. 

The adrenal insufficiency that develops in Addison s disease results from the extensive yet not total destruction of the cortex of both adrenal glands. Various pathological conditions that may be responsible for this destruction include bilateral tuberculosis (68%), destructive atrophy (19%), amyloid degeneration (2%), and neoplasm (1%). In the remaining 10% of cases, Addison s disease results from a number of miscellaneous degenerative processes (venous thrombosis, arterial emboli, syphilis, and pressure atrophy). The physician should beware of the sudden withdrawal... 

Castle knew that the acid- and pepsin-secreting part of the stomach in patients with pernicious anemia had atrophied. In the year Thomas Addison published his distinction between idiopathic anemia and the anemia of adrenal insufficiency, Charles Handheld Jones of St. Mary s Hospital wrote that no trace of the gastric tubules was to be seen in the stomach of a patient who had died of profound ane-mia. " Five years later, Samuel Fenwick of London Hospital cited Handheld Jones when he reported the results of an autopsy he performed on a patient who had died of what Fenwick clearly understood was the unremitting form of anemia described by Addison. Fenwick made certain that the patient did not have the characteristic pigmentation of adrenal insufficiency, and at autopsy he found the adrenal glands unaffected. In the same year, Arnold Cahn and Joseph von Mering, working in... 

Hypersecretion from the adrenal cortex leads to condition known as Cushing s syndrome which leads to feminism in males, which is the tendency to develop female sex characters and in females virilism develops, which is the tendency to develop male sex characters such as excess growth of hair on chest and pubic region, increase and darkening of facial hair, atrophy of mammary glands (breasts) and cessation of menstrual cycle (amenorrhoea). 

Rationale The administration of ACTH to normal subjects results in a rapid rise in the serum cortisol concentration. Patients with adrenal destruction (Addison s disease) show no change in serum cortisol concentration after ACTH administration. Patients with atrophy of the adrenal cortex, caused by exogenous glucocorticoid treatment or dysfunction of the pituitary gland or hypothalamus may show a shght rise in serum cortisol concentration, but not one of normal magnitude. 

Hypocalcaemia is associated with hypo- and pseudohypoparathyroidism while hypercalcaemia commonly relates to cirrhosis, adrenal insufficiency, osteoporosis, sarcoidosis, disease atrophy, and hyperparathyroidism. Calcium assays are rather important diagnostic aids especially since a routine screening on total serum calcium of 50 330 patients revealed 55 cases of unsuspected primary hyperparathyroidism [137] and the disease is on the increase in the U.S.A. and Sweden [138]. In primary hyperparathyroidism, the glands become autonomous and secretions of parathyroid hormone (PTH) are no longer controlled by the... 

The simple experiment of removing the pituitary and from the sella turcica to another site of the body also demonstrated the role of the hypothalamus in the control of anterior pituitary function. When the transplanted tissue is placed in a site remote from the sella turcica, for example, the anterior chamber of the eye, the kidney capsule or temporal lobe of the brain, partial or complete atrophy of the ovaries, testes, reproductive tracts, thyroid gland and adrenal cortices is observed together with a reduction in the rate of body growth. When, however, the transplanted tissue is placed in the vicinity of the hypothalamus and pituitary stalk, regeneration of the hypophysial portal vessels occurs and anterior pituitary function is restored as shown by the maintenance of reproductive, thyroid and adrenocortical activity [5]. 

Hypophysectomy, which produces an atrophy of the adrenal cortex, has been reported to inhibit [122, 298] and to enhance [425] the egg-white reaction or to have no effect on the egg-white [401] and dextran [396] reactions. More recently, Gabbiani and Bocskor [199] reported that hypophysectomy reduces the sensitivity of rats to iron-dextran and that normal sensitivity is restored by the transfusion of plasma from an animal with an intact pituitary. This suggests that a plasma substance is produced in the pituitary gland which has a permissive action on the anaphylactoid reaction. This report has yet to be confirmed. 

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