Download Cushing’s Syndrome by Dorothy T. Krieger M. D. (auth.) PDF

By Dorothy T. Krieger M. D. (auth.)

The unraveling of our wisdom of the services of the adrenal gland constitutes one intriguing improvement of contemporary medication and biochemistry. We owe those advances to the felicitous cooperative efforts of the medical investigator and the biochemist. 3 centuries elapsed among the 1st recorded anatomical descrip­ tion of the adrenals and the demonstration via Dr. Addison within the mid-nineteenth century of the deadly result of the destruction of those glands by way of affliction. It turned obvious from this commentary that the adrenals secreted a "factor" or "factors" necessary to existence. It took nearly ninety years to isolate this elusive very important issue - cortisone - from pork adrenal cortices, independently via either Reichstein and his co-workers in Basle and Kendall and his workforce within the usa and one other 10-15 years prior to it turned extra often to be had for experimental and scientific use. it truly is probably tricky to think that as lately as 35-40 years in the past, ahead of cortisone and cortisol have been clinically to be had, the surgical elimination of a benign adrenal cortical tumor in sufferers with Cushing's syndrome was once linked to a prohibitive postoperative mortality cost. inside of 12-36 h after operation, such a lot of such sufferers constructed an intractable nation of outrage, which was once now not manifested by way of major electrolyte abnormalities or hypoglycemia and used to be unresponsive to the standard remedy for surprise plus the beneficiant use of salt-retaining hormone.

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2); 4 transport to smooth endoplasmic reticulum (SER); 5a hydroxylation and 5b oxidation and isomerization in SER; 6 hydroxylation in SER; 7 mitochondrial hydroxylation; 8 mitochondrial hydroxylation and oxidation 38 Actions of Adrenocortical Hormones proteins induced by glucocorticoids. In those instances where glucocorticoids induce catabolic effects and eventual cell death (such as in rat thymocytes, which are lysed by glucocorticoids), it is postulated that these events are also initiated by induction of a protein or some other transcriptional event, the nature of which is unknown.

It is now known that adrenal hyperresponsiveness to ACTH administration can be attributed to sensitization of this gland by exposure to greater-than-normal amounts of corticotropin. When exogenous ACTH is given, therefore, such a primed gland secretes more corticosteroids. It was also not realized at that time that the presence of normal plasma ACTH concentrations was inappropriate for the elevated plasma cortisol concentrations present in such patients, in whom, if normal feedback mechanisms were operative, plasma ACTH levels should be markedly suppressed.

Endocrinol, Melbourne, p 157 (Abstract) Schwyzer R (1977) ACTH: A short introductory review. In: Krieger OT, Ganong WF (eds) ACTH and related peptides, Structure, regulation and action. NY Acad Sci 297:3-26 Scow RO, Sticker FA, Pick TY, Clary TR (1965) Effect of ACTH on FFA release and diglyceride content in rat adipose tissue. Ann NY Acad Sci 131:288-301 Segal BM, Christy NP (1968) Potentiation of the biologic activity of ACTH by human plasma. A preliminary study. J Clin Endocrinol 28:1456-1472 Simpson ER, Carr BR (1979) Metabolism of serum lipoproteins by the human fetal adrenal.

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