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Excreted 17-ketosteroids

The urinary excretion of steroids is closely related to the gonadal and adrenocortical production of hormones. Because they can be determined quantitatively on the basis of color reactions, for example, with /w-dinitrobenzene, a relatively large amount of data is available with respect to the excretion of 17-ketosteroids. Exactly what is included in this group in specific instances must be ascertained by consulting the original publications. [Pg.124]

It is estimated that, of the total 17-ketosteroids excreted by men, about 60 per cent come from the adrenal cortices and 40 per cent from the testes. Anatomically the adrenal glands are said to vary in weight from about 7 to 20 gm. Some authors merely state that the... [Pg.124]

Although a number of studies have pointed to substantial variation in the 24-hr-urinary 17-ketosteroid excretion of men and women, the most definitive work dealing with inter-individual differences is that of Dobriner and co-workers23 which was referred to earlier (p. 99). In this study samples were collected from individuals over long periods of time and analyzed separately by exhaustive research methods involving the use of chromatography and infrared spectrometry in addition to the more usual techniques. [Pg.125]

Just as two human beings of the same weight, age, and sex may appear alike when examined in a cursory manner and yet be very different when examined in detail, so may two pituitary glands appear outwardly alike but be found very different when subjected to detailed study. We have just noted in the previous section a case involving the same principle. The total ketosteroid excretion for each of two individuals may be about the same, but the excretion of specific substances may be very different for the two. [Pg.126]

Gutierrez RM, Williams RJ. Excretion of ketosteroids and proneness to breast cancer. Proceedings of the National Academy of Sciences USA 1968 59 93843. [Pg.273]

A rhythmic variation has been observed in levels of plasma hydroxy-corticosteroids (A9, B13, D9) and in the excretion of 17-ketosteroids (P7). As shown in Table 5, urinary excretions of potassium, sodium, chloride, 17-hydroxycorticosteroids and water have been reported to be greatest between 10 am to noon and lowest between 4 am and 6 am (S21). In this study it was shown that within 5 weeks subjects could acclimate to similar patterns for a 21-hour, rather than a 24-hour, day. Heilman and his associates reported that about half of the day s cortisol production is achieved in the early morning hours during sleep and that production is minimal between noon and 10 pm (H7). In one study the plasma cortisol in normal men was 24.6 5.5 /xg/100 ml at 7 am 13.1 3.4 fig/100 ml at 9 am 11.8 fig/100 ml at noon 9.1 2.3 jag/100 ml at 7 PM and 6.3 /ig/100 ml at 10 pm (A9). [Pg.14]

P7. Pincus, G., Diurnal rhythm in excretion of urinary ketosteroids by young men. J. Clin. Endocrinol. 3, 195-199 (1943). [Pg.41]

Probenecid may inhibit the renal excretion of Phenolsulfonphthalein (PSP), 17-ketosteroids, and sulfobromophthalein (BSP). [Pg.948]

Most glucocorticosteroid are metabolized in the liver to hydroxy- and ketosteroid metabolites which are excreted by the kidneys as glucuronides, sulfates and unconjugated products. Enzyme-inducing agents will diminish the efficacy of glucocorticosteroids. [Pg.391]

The catabolism of plasma testosterone and other androgens occurs primarily in the liver (Fig. 63.3), where they are conjugated into water-soluble compounds that are excreted by the kidney as the urinary 17-ketosteroids. [Pg.727]

Because of its effects on the pituitary/adrenal system, ketoconazole has been used in the long-term control of hypercortisolism of either pituitary or adrenal origin (SED-12, 677). In seven patients with Cushing s disease and one with an adrenal adenoma, ketoconazole 600-800 mg/day for 3-13 months produced rapid persistent clinical improvement (585). Plasma dehydroepiandrosterone sulfate concentrations and urinary 17-ketosteroid and cortisol excretion fell soon after the start of treatment, and remained normal or nearly so throughout treatment. Urinary tetrahydro-ll-deoxycortisol excretion rose... [Pg.614]

In experiments on patients with breast cancer, it was found that up to a two-fold increase in serum /3-D-glucuronidase followed surgery, pregnancy, prolonged estrogen or cortisone therapy, etc.206 The /3-D-glucu-ronidase rise was usually accompanied by a fall in serum esterase, in both animal and human experiments. A rise in urinary ketosteroid excretion usually paralleled the changes, in man. [Pg.231]

From a study of the response to ACTH of the urinary excretion of 17-ketosteroids, Anderson et al. (Al) suggested that impaired adrenal function may be a factor in idiopathic hypercalcemia of infancy. [Pg.195]

Overall, other adrenal androgens also show a progressive decrease in urinary excretion in both men and women. Thus, the mean 17-ketosteroid urine levels of elderly people are about 50% of those in young adults. This is primarily secondary to decreased dehydroepiandrosterone (DHEA) and androsterone production. In men, about one-third of the daily 17-ketosteroids are of testicular origen, the remainder being mainly from the adrenals. Androstenedione is a prehormone for testosterone. [Pg.45]

Decreased serum cholesterol and decreased urinary excretion of 17-ketosteroids, reflecting the impairment of steroidogenesis. [Pg.355]

The composition of the excreted urinary 17-ketosleroids also reveals a close similarity between the hormones of different origin the testis accounts for 30% while the adrenal cortex contributes the remaining 70% of the total urinary 17-ketosteroids [383]. Androsterone, ep a-androsterone, and 5/8-androsterone (etiocholanolone) are the main urinary metabolities of testosterone, and dehydroepiandrosterone is the major urinary 17-ketosteroid derived from the adrenal cortex. [Pg.12]

I7(x-Methyl-17 -hydroxy-estra-4,9,l l-trien-3-one (Methyltrienolone, N-99). In the course of a steroid total synthesis [293] this compound (Methyltrienolone, N-99) was prepared it was reported [55] to possess 6000% of the androgenic (ventral prostate index), 7500% of the androgenic (seminal vesicles index), and 12,000% of the anabolic (levator ani index) activity of methyltestosterone. Later the anabolic activity was reported [74] to be 30,000% of that of methyltestosterone. As measured by multiple parameters methyltrienolone turned out to be the most hepatotoxic steroid, causing biochemical symptoms of intrahepatic cholestasis [75]. It was also reported [74] to reduce the excretion of 17-ketosteroids and 17-hydroxycorticosteroids and to cause enhancement of the blood coagulation factors V, VII, and X. It also increases the prothrombin content of the plasma [74]. [Pg.88]

Ether formation often leads to enhanced oral activity. 17/8-Hydroxy-5a-androstan-3-one 17-(rmethoxy)cyclopentyl ether (D-130), 17)3-hydroxy-5a-androstan-3-one 17-(l -ethoxy)cyclopentyI ether (D-132), 17j3-hydroxy-5a-androst-l-en-3-one 17-(r-ethoxy)cyclopentyl ether (A-163), and 17j3-hydroxy-5a-androst-l-en-3-one 17-cyclopent-r-enyl ether (A-164) are all reported to possess favorable anabolic-androgenic ratios with increased anabolic and androgenic properties. The enhancement of oral activity is interesting in view of the fact that the ether bond of these compounds is easily broken, as manifested by the strongly enhanced excretion of 17-ketosteroids in humans treated with the ether derivatives [144]. [Pg.89]

The only useful contribution of endocrine studies to diagnosis has been in the condition dystrophia myotonica, with its 80% incidence of eventual primary testicular atrophy in males. Many workers (Cl, Dl, G7, K15) have reported the urinary excretion of 17-ketosteroids in this condition to be subnormal in males, and even in females to be in the low normal range. Recent thorough investigations, however (B22, D18), have disclosed that, apart from an unexplained frequently low basal metabolic rate and the consequences of eventual testicular atrophy, there seems to be no reason to suppose that adrenal cortical, thyroidal, ovarian, and pituitary functions are other than normal in dystrophia myotonica. A majority of males examined had been fertile, and most women had brought one or more normal full-term pregnancies to spontaneous delivery. [Pg.146]

Tl. Tanaka, H., Manabe, H., Koshiyamo, K., Hamanaka, Y., Matsumoto, K., and Vozumi, T., Excretion patterns of 17-ketosteroids and 17-hydroxycorticosteroids in surgical stress. Acta Endocrinol. (Copenhagen) 65, 1-10 (1970). [Pg.284]

Bower BF, McComb R, Ruderman M. Effect of penicillin on urinary 17-ketogenic and 17-ketosteroid excretion. N Engl J Med 1967 277(10) 530-2. [Pg.2772]

Phenytoin decreases the urinary excretion of 17-ketosteroids and 17-hydroxycorticosteroids by stimulating the conversion of cortisol to 6-P-hydroxycortisol it also diminishes serum FSH and the sperm count in semen, and thereby reduces fertility, Phenytoin also lowers the serum thyroxine concentration, probably by competitive displacement of thyroxine from its protein-binding sites free thyroxine also tends to be low. Serum triiodothyronine is low, probably as a result of stimulated metabohsm in the liver, but the concentration of TSH is unaffected by the altered thyroxine metabolism. [Pg.459]

With blindness, the normal stimulation of the hypothalamic-pituitary axis is reduced. Consequently, certain features of hypopituitarism and hypoadrenalism may be observed. In some blind individuals, the normal diurnal variation of cortisol may persist in others it does not. Urinary excretion of 17-ketosteroids and 17-hydroxycorticosteroids is reduced. Plasma sodium and chloride are often low in blind individuals, probably as a result of reduced aldosterone secretion. Plasma glucose may be reduced in blind people, and insuhn tolerance is often less. The excretion of urate is reduced. Renal function may be slightly impaired, as evidenced by slight increases in serum creatinine and urea nitrogen. [Pg.465]

Fever provokes many hormonal responses. Hyperglycemia occurs early and stimulates the secretion of iasuHn, which improves glucose tolerance but insulin secretion does not necessarily reduce the blood glucose concentration because increased secretion of growth hormone and glucagon also occurs. Fever appears to reduce the secretion of thyroxine, as do acute illnesses even without fever. In response to increased corticotropin secretion, the plasma cortisol concentration is increased and its normal diurnal variation may be abolished. The urinary excretion of free cortisol, 17-hydroxycorticosteroids, and 17-ketosteroids is increased. As acute fever subsides, or if it lessens but still persists for a prolonged period, the hormone responses diminish. [Pg.465]

The main excretory metabohtes of androstenedione, testosterone, and DHEA are shown in Figure 53-5. Except for epitestosterone, these catabolites constitute a group of steroids known as 17-ketosteroids (17-KSs). These metabolites are excreted primarily in the urine (>90%), with approximately half as 17-KSs, and half as diols, triols, conjugates, and other polar compounds." ... [Pg.2099]


See other pages where Excreted 17-ketosteroids is mentioned: [Pg.125]    [Pg.146]    [Pg.328]    [Pg.400]    [Pg.688]    [Pg.725]    [Pg.730]    [Pg.565]    [Pg.218]    [Pg.12]    [Pg.25]    [Pg.26]    [Pg.28]    [Pg.1970]    [Pg.1206]    [Pg.452]    [Pg.461]    [Pg.465]    [Pg.466]    [Pg.785]    [Pg.66]    [Pg.78]    [Pg.128]   
See also in sourсe #XX -- [ Pg.3 ]




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