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The effects of garlic supplementation on protein metabolism were investigated by measuring testis testosterone and plasma corticosterone in rats fed diets with different protein levels. In Experiment 1, rats were fed experimental diets with different protein levels (40, 25 or 10 g/100 g casein) with or without 0.8 g/100 g garlic powder. After 28 d of feeding, testosterone contents in the testis were significantly higher and plasma corticosterone concentrations were significantly lower in rats fed 40 and 25% casein diets with garlic powder than in those fed the same diets without garlic powder. Urinary excretion of 17-ketosteroid (an index of testosterone), nitrogen balance and hepatic arginase activity were significantly higher in rats fed the 40% casein diet with garlic powder than in the 40% casein controls. In Experiment 2, the effect of diallyldisulfide (a major volatile sulfur-containing compound in garlic) on the secretion of luteinizing hormone (LH) from the pituitary gland, which regulates testosterone production in the testis, was investigated in anesthetized rats. Plasma LH concentration increased dose dependently after administration of diallyldisulfide (P < 0.01, r = 0.558). These results suggest that dietary supplementation with 0.8 g/100 g garlic alters hormones associated with protein anabolism by increasing testicular testosterone and decreasing plasma corticosterone in rats fed a high protein diet.

A 28-year old female patient with virilization due to left adrenocortical adenoma was studied. The patient had clinical features of hyperandrogenism such as hirsutism and a low pitched voice, but not of hypercorticoidism. Plasma testosterone and dehydroepiandrosterone-sulfate (DHEA-S) were high. Although the basal plasma cortisol concentration and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were within the normal range, the absence of diurnal variation in plasma cortisol and loss of suppressibility by dexamethasone suggested constitutive secretion of cortisol by the tumor. Inappropriate cortisol secretion was also supported by blunted ACTH response to provocative stimuli. After successful removal of the left adrenal tumor, such endocrinological abnormalities were all normalized. Immunohistochemical analysis revealed that tumor cells were positively stained for C21 hydroxylase cytochrome P-450 (P-450C21) and P-450(11) beta which convert 17-hydroxy (OH) progesterone to cortisol as well as P-450SCC, 3 beta-hydroxysteroid dehydrogenase and P-450(17) alpha which are involved in testosterone biosynthesis. These findings suggest that adrenocortical adenoma secretes predominantly testosterone and constitutively cortisol in a young woman patient with virilization.

Serum testosterone concentrations and excretion of 17-Ketosteroid in urine were determined in 32 caterpillar vehicle drivers exposed to low frequency vibration of the whole body and to noise. Testosterone concentrations were assessed by the RIA method in fasting after 3 hrs of work. 17-Ketosteroid excretion was measured in the 8-hr collection of night urine and in urine collected during the day's work. No significant differences were found in exposed workers, either in mean testosterone concentration in fasting and after 3 hrs of work or in 17-Ketosteroid excretion, before and during the work, when compared with the control group.

After the wedge resection of the ovaries the authors obtained the normal menses in 100%, the reduction of total testosterone in blood of 41.8% and of 17-KS in urine of 20%, an increase of fertility of 62.5% and in hirsutism a correction only of 12%, the stopping of 12% and no correction of 76%. The authors conclude that the cause of the healing or of the correction is placed in the resection of 3/4 of the changed ovaries with cysts follicles with distinct thecal layer what is accompanied by the reduction of testosterone on average of 41.8%. On contrary a weak correction in hirsutism has the explanation that the existent hirsutism is supported even by the normal level of testosterone in organism.

The paper is concerned with the results of investigation of 15 patients with virile ovarian tumors (VOT). The following methods were employed for instrumental diagnosis: USI, computerized tomography and laparoscopy. Hormonal investigation included the determination of basal levels of serum testosterone (T), excretion with urine of 17-ketosteroids and their time course against a background of suppression tests with dexamethasone and stimulation tests with CG. The results of hormonal investigations were compared with those of similar investigations of 14 patients with stromal ovarian thecomatosis and 8 patients with androgen producing adrenal tumors. Ovarian tumors were detected in 40% by instrumental and clinical methods. Hormonal studies revealed a high level of T in patients with virile ovarian and adrenal tumors exceeding 3-3.8-fold a similar indicator in patients with stromal thecomatosis. All patients with a "tumor" level of T underwent laparotomy after excluding an adrenal lesion. Ovarian tumors of 1.0-2.5 cm in diameter were detected.

Previous studies carried out by the Authors had shown an increased urinary excretion of epitestosterone, a poorly active androgen mostly believed to be of adrenal origin, after HCG administration to presenescent and aging subjects. Purpose of this study was to ascertain whether or not this held in the young too. Testosterone excretion sharply decreased after the age of 60 (P less than 0,001); 17 KS on the other hand, decreased progressively in such a way that the aging group showed significantly lower (p less than 0,05) excretion rates than the only young-adult group. ET excretion decreased steadily but not significantly with age. ET showed a very good correlation to T (p less than 0,01) both under basal and poststimulatory conditions in each of the three age groups. ET percent increase showed a good correlation (p less than 0,01) to T percent increase only in young-adult and presenescent people, not in the elderly. Poor was the correlation between ET percent increase and 17 KS percent increase. Thus ET excretion pattern showed to be somewhat different from that of T and very different from that of 17 KS. As a conclusion (a) epitestosterone excretion rate seems to decrease steadily but not significantly with age; (b) epitestosterone probably is not mainly secreted by the adrenal gland. A major source may be the testis, but liver, prostate and blood red cells metabolism are not definitely ruled out.

A 27-yr female patient was admitted to the hospital because of secondary amenorrhea and a severe and complex virilization syndrome. The urinary 17-Ks, 17 OHCS and testosterone glucuronide values were greatly increased. The plasma testosterone through very high, was within the normal limits in males (3.52 ng/ml). Urography, echography and CT scan revealed a large right adrenal tumor. Removal of the tumor brought about a considerable clinical improvement: reoccurrence of the menstrual cycle, a progressive decrease in the virilization syndrome and normalization of the urinary 17-Ks, 17-OHCS and of the plasma testosterone.

Oral testosterone undecanoate (TU) in arachis oil has been evaluated with a view to its possible use as a means of androgen replacement therapy. A single 100 mg dose was found to elevate plasma androgen levels and urinary 17-ketosteroid excretion in 6 normal men. Ninety mg/day and 60 mg/day doses taken by a hypogonadal man resulted in sustained levels of androgen which appeared physiological when measured by radioimmunoassay without chromatography. However, upon separation of the steroids by chromatography it was found that much of the androgen present was in fact dihydrotestosterone not testosterone. Both TU and dihydrotestosterone undecanoate were detected in plasma by gas chromatography and it is suggested that the ester is absorbed as such from the intestine and the unesterified steroid subsequently released by hydrolysis. The convenience of oral administration, the resulting prolonged elevated plasma androgen levels and the probable lack of deleterious effects on the liver may render oral TU of value where androgen replacement therapy is indicated.

The study presents the data gathered along the years on the antisteroid action of the pineal gland. Thus, it was demonstrated that administration of pineal polypeptides to the rabbit lowers the urinary 17-KS both of testicular and adrenal origin. Conversely, pinealectomy caused an increase in the level of these steroid hormones. The same pineal material induced a marked decrease both in the serum and testicular testosterone and in the plasma and adrenal corticosterone in the rat. At the same time administration of pineal polypeptides lowered the cholesterol in the serum, bile, liver, testis and adrenal. Melatonin had no effect on these biochemical indices, which demonstrates that the effects obtained with pineal polypeptides are not mediated by melatonin.

Alterations of sexual hormones in plasma of ageing males occur between the 50th and 60th year of life with individual variations: 1. Decreased values of testosterone in plasma and a poor response to gonadotrophins demonstrate a diminished synthesizing capacity of the testes in old men. 2. The decreased testosterone plasma values are followed by an increase in LH. The response of the anterior pituitary gland to LH-RH stimulation in old men is normal. 3. Under basal conditions estrone as well as estradiol plasma concentrations increase significantly with age because of increased conversion from androgens. 4. Parallel to estrogen plasma values an increased concentration of the sexual hormone binding globulin (SHBG) is found, resulting in a steep decrease of the free (= active) testosterone fraction. 5. Decreased testosterone, which is more strongly bound to SHBG and increased estrone and estradiol plasma values result in an androgen/estrogen imbalance in old men.

A patient with virilization was studied. The basal urinary excretion of 17-ketosteroids was at the upper limit of normal, but the plasma testosterone concentration was greatly elevated. Testosterone secretion could be stimulated by hCG, suppressed by dexamethasone, and was not affected by ACTH. At operation, an arrhenoblastoma of the left ovary was found. Isolated tumor cells in culture secreted testosterone. The addition of a LRH agonist (10 ng/ml) suppressed the secretion of testosterone by 50% (P less than 0.01). The inhibiting effect of a LRH agonist on steroidogenesis suggests that LRH receptors were present on this tumor and that treatment with LRH agonists might be beneficial in patients with metastatic steroid hormone-secreting ovarian and testicular tumors.

Plasma follicle stimulating hormone, luteininzing hormone, testosterone, urinary 5-hydroxyindole acetic acid and 17-ketosteroids were measured in patients seen at an infertility clinic. Plasma folicle stimulating hormone and luteinizing hormone levels, and urinary 5-hydroxyindole acetic acid levels were increased in patients with sperm concentrations less than 10 times 10(6) per ml. Plasma testosterone levels were lower in patients with sperm concentrations less than 10 times 10(6) per ml. The results suggest that in patients with sperm counts less than 10 times 10(6) per ml. there is not only impaired spermatogenesis but also decreased Leydig cell function. Urinary 17-ketosteroid levels were not related to sperm cell concentration.

Plasma testosterone levels were suppressed in 6 of 8 mature male patients with Cushing's disease, all of whom complained of loss of libido and decreased sexual potency. Gonadotrophin levels, both under basal conditions and in response to LH-RH, were generally normal. The testicular response to stimulation with hCG was brisk in the 2 patients examined. Oestradiol levels were slightly elevated in 2 patients and prolactin levels were normal in all patients. Thus, male patients with Cushing's disease demonstrated normal gonadotrophin levels in the presence of suppressed testosterone, or, viewed from a slightly different prospect, low testosterone levels despite normal gonadotrophins. Neither oestradiol nor prolactin excess appeared to account for the observations. Possible explanations for these findings include (a) a combination of impaired hypothalamic and testicular function, and (b) a resetting downwards of the level of testosterone that is seen as appropriate by the disordered bypothalamic-pituitary unit. Following correction of cortisol excess in Cushing's disease, testosterone levels rose into the normal range.

The administration of human chorionic gonadotrophin (HCG) to dexamethasone-suppressed men caused parallel changes in the concentration of plasma testosterone and in the urinary output of androsterone+aetiocholanolone, total 17-oxosteroids and oestrogens. Discrepant results occurred in only four of the thirty-seven men tested. With these exceptions, the response to HCG could by followed as well by measuring androsterone+aetiocholanolone, 17-oxosteroid or oestrogen excretion rates as by following plasma testosterone levels. The most sensitive index of response was the rate of appearance of oestrogens in urine, and the next that of androsterone+aetiocholanolone.

The research here reported concerns 9 hirsute women, four of them with PCO and five with idiopathic hirsutism, who underwent treatment with spironolactone. 4 non hirsute hypertensive cases served as control. For one year hair growth, testosterone, 17 Ks, estradiol and gonadotropins behaviours were studied in all of the patients. Results clearly show that the peripherical response (the hair) to the therapy is only just sufficient, and corresponds to a good reduction of the androgenic hormones in blood. However, there is also an LH gonadotropin secretion reduction which is statistically scarcely significant. If the therapeutic response of hair were good, fetal risk could be prevented with safe and contemporaneous contraception. However, since the response is scarcely sufficient, we do not think this therapy is more advisable than other ones.

Concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in serum and 17-ketosteroids (17-KS) in urine of 10 paraplegic and 10 quadriplegic subjects were measured from onset of injury and followed once a week for 4 months. Compared with age-matched normal controls, paraplegic subjects showed significantly lower serum levels of LH and FSH for 2 weeks and of testosterone for 6 weeks after spinal cord trauma, following which periods of time these hormones attained normal levels. By contrast, in quadriplegic subjects, serum testosterone concentrations remained significantly lower than those of the controls during the entire 4-month testing period. Furthermore, in another group of 10 chronic (1 to 6 years after onset of injury) paraplegic and 10 chronic quadriplegic subjects, serum testosterone and FSH concentrations were comparable to those of the normal controls. Serum LH concentrations were at control levels in chronic paraplegic but significantly depressed in chronic quadriplegic subjects. The concentrations of urinary 17-KS exhibited sharp fluctuations over the 4-month period and were below control levels in paraplegic but within control limits in quadriplegic subjects. The results indicate that the function of the hypothalamic-pituitary-gonadal axis is disturbed for at least 4 months in quadriplegic subjects.

To evaluate the usefulness of blood testosterone (T) in monitoring the effects of therapy in congenital virilizing adrenal hyperplasia due to 21- or 11- hydroxylation defect (CVAH), T levels were measured on 45 occasions in 13 patients with CVAH; 32 urinary 17-ketosteroid levels and 31 preganetriol values were available for comparison. Bone age levels, growth data, and medication are listed to help assess the clinical state of the patient at the time of each T determination. Blood T values were above normal for age and sex in untreated patients with CVAH and declined with glucocorticoid suppression. A blood T value of 20 ng/100 ml appeared to distinguish between well-controlled cases and those with inadequate steroid suppression. Serial measurement of blood T in girls and in prepubertal boys with CVAH provides assistance in evaluating chemical control of the disease, particularly when accurate 24-h urine collections cannot be obtained for 17-ketosteroid and pregnanetriol assessments.

In 11 children aged between 2 and 17 years with (nonsalt-losing) congenital adrenal hyperplasia (21-hydroxylase deficiency) blood was drawn at 90-minute intervals during a 24-hour period and levels of 17-hydroxyprogesterone, testosterone, and cortisol were measured. Levels of 17-ketosteroids and pregnanetriol were measured too in 24-hour urine samples. These measurements were taken under different regimens of treatment and after interruption of treatment. Cortisol level rose and fell rapidly after administered corticosteroid, and reached unphysiologically high levels. Testosterone levels showed pronounced variations but stayed in the normal range for most of the time even in untreated patients; thus testosterone provides a poor control parameter. Levels of 17-hydroxyprogesterone showed extreme fluctuations and very high peak levels in untreated patients; standard treatment with two or three daily doses of corticosteroids did not prevent a pronounced rise in its level after midnight. After the first morning dose of hydrocortisone a very steep fall was observed. The 24-hour pregnanetriol excretion correlated well with the corresponding total integrated 17-hydroxyprogesterone area. It is concluded that single 17-hydroxyprogesterone values are unlikely to give adequate information about the quality of treatment.

The authors present the results of study of the basic blood testosterone level and of the 17-ketosteroid urinary excretion under conditions of a test with dexamethasone and choriongonin. The results obtained were compared with the results of analogous examination of a group of patients with the virile form of the Stein-Loewenthal's syndrome. Blood testosterone level served as a significant criterion in the diagnosis of virilizing tumours of the testes. Besides, a study was made of the remote results of sparing surgical tactics in the treatment of virilizing tumours of the testes lasting up to 13 years in 37 patients. Favourable results pointed to the benign course of these tumours and justified conservative therapy.

The excretion of the C19O2-fraction of 17-oxosteroids in urine (C) and the concentration of testosterone in serum (T) have been compared in 15 women with hirsutism during tests with suppression of the adrenals and the ovary and with stimulation of the ovary. The behaviour of both parameters seemed to be only qualitatively similar in all three phases of the tests. In one of the test phases a statistically significant correlation between the percentage of decrease or increase of C and T has been observed (First phase: r = 0.242; second phase; r = 0.457; third phase r = 0.392). The mean relative changes of C in the adrenal suppression phase was more distinct (P less than 0.002) than that of T. Both parameters seem to be of different diagnostic meaning.

Three children with Fanconi's anemia belonging to a family where 6 children had the disease were investigated. One child had growth hormone deficiency, a second child showed subnormal response of testosterone to gonadotropin stimulation and the third child had a missing insulin release following arginine. This report shows that growth hormone deficiency is not necessarily liniked with Fanconi's anemia when it occurs in a family. Multiple endocrine insufficiencies do no appear to be part of the disease.

Both pregnenolone and 17-OH-pregnenolone were found to be higher in the plasma of patients with poorly controlled congential adrenal hyperplasia than in normal subjects. The plasma levels of these precursor steroids were significantly correlated with urinary 17-ketosteroid and pregnanetriol excretion and with plasma testosterone. The mechanism where by plasma pregnenolone and 17-OH-pregnenolone levels are elevated in patients with 21-hydroxylase deficiency is unknown, but the phenomenon of product inhibition is suggested as a possible explanation. As 17-OH-pregnenolone in plasma is almost entirely of adrenal origin, its measurement promises to be useful in the management of patients with congenital adrenal hyperplasia. Acute stimulation with ACTH caused negligible changes in the plasma levels of pregnenolone and 17-OH-pregnenolone and failed to distinguish between overly, appropriately, and under-treated patients. However, following repeated stimulation with repository ACTH, the steroid levels rose. These findings indicate limited adrenal responsiveness to ACTH following chronic glucocorticoid treatment of congenital adrenal hyperplasia, even in under-treated patients, and suggest that normal precursor steroid levels in plasma and normal 17-ketosteroid and pregnanetriol excretion can only be achieved by the suppression of total steroidogenesis to less than that occurring in normal subjects.

The mean basal plasma testosterone level in 28 patients with chromatin positive Klinefelter's syndrome was significantly lower than in 58 healthy male controls. In 12 of the patients the hormone levels were in the normal range. In both the eugonadal males and the Klinefelter patients the plasma testosterone levels spontaneously decreased throughout the day, the relative decrease in both groups being of the same order of magnitude. Short term ACTH infusion and the administration of dexamethasone did not significantly influence the plasma testosterone concentration in the Klinefelter patients. These findings do not support the view that the adrenal cortex plays a major role in contributing to the circulating plasma testosterone levels in this syndrome.

The aim of the study was clinical evaluation of a new marker of pituitary tumours--the alpha subunit of glycoprotein hormones. The studies were performed in 152 patients with manifestations of intersellar tumours; an elevated serum alpha subunit concentration was found in 49 of these cases. The determinations of alpha subunit were performed by double antibody radioimmunoassay. Iodination of alpha subunit was made by chloramine T technique with subsequent purification of Ultrogel AcA54 column. The remaining pituitary hormones were also determined by radioimmunoassay. The incidence of pituitary tumours of alphoma type was 30 percent. Tumours occurred frequently in association with an increased serum growth hormone and manifestations of acromegaly, less frequently with hyperprolactinemia and signs of prolactinoma. Following neurosurgery of 60Co pituitary irradiation hypopituitarism was of high occurrence.

Interactions between gonadal hormones and adrenocortical function have been studied in the male rat. After injection (im) of testosterone, the accessory reproductive organs are more stimulated in the castrated rats than in the castrated adrenalectomized rats. Gonadectomy increases lipids, cholesterol and corticosterone in adrenal glands and plasma corticosterone levels. Testosterone reverses these effects.

Two brothers with Reifenstein syndrome underwent LH-RH and HCG tests at various ages ranging from 13 to 17 years. We found that at age 13 the plasma LH and FSH response to one LH-RH injection was normal. After the age of 14, the basal plasma concentration of LH and FSH and their response to LH-RH became elevated. Concomitantly the plasma testosterone levels rose to abnormal levels. These findings are compatible with progressive development of primary gonadal dysfunction and with peripheral insensitivity to testosterone.

After reviewing the principal studies on the interferences of lead on the endocrine system, this paper reports the results of a survey carried out on 30 subjects in which the effects of lead on serum FSH, LH and testosterone and on urinary steroid hormones excretion were examined. Statistically significant differences were not demonstrated between lead exposed subjects and control group for serum LH and testosterone (total and free) and for urinary steroids. A significant increase of FSH has been detected in lead exposed workers even if this increase remains between the "normal limits" of the laboratory which performed the determinations. The results are discussed in the light of the more recent knowledge about the endocrine effects of xenobiotics in general and heavy metals in particular and some interpretations to justify the detected FSH increase are proposed.

Considering the larynx as a hormone dependent secondary sex characteristic has previously led to successful antiandrogentherapy of pachydermia of the vocal cords, which may constitute a precancerous state. As a first step to further evaluate the endocrine state of patients with precancerous lesions or cancer of the larynx, the urinary excretion of 17-hydroxysteroids, 17-ketosteroids, testosterone and estrogens has been determined in male patients with pachydermia laryngis (n = 15) or cancer of the larynx (n = 20) as compared to controls with different other otorhino-laryngological affections (n = 20). No difference between groups was found in 17-hydroxysteroids and no significant difference in 17-ketosteroid excretion. The pachydermia group as a whole showed significantly increased levels of testosterone (p = 0.01) and estrogen (p = 0.04) of 64.6 +/- 39.9 microgram/24 hr testosterone versus 34.7 +/- 19.3 microgram/24 hr in controls and 31.7 +/- 16 microgram/24 hr in laryngeal cancer and 277 +/- 14.8 microgram/24 hr total estrogens versus 19.1 +/- 12 microgram/24 hr and 17.8 +/- 8.1 microgram/24 hr respectively. These data further support the idea of hormonal factors playing an important role in the pathogenesis of pachydermia and thus possibly cancer of the larynx. So far, however, they do not permit definite conclusions on the pathogenetic mechanisms involved.

To determine whether a single morning plasma level of 17-hydroxyprogesterone (17OH-P), androstenedione, testosterone and progesterone reflected the degree of control of 21-hydroxylase congenital virilizing adrenal hyperplasia (CVAH) as indicated by 24-hour urinary 17-ketosteroid and pregnanetriol excretion, 142 simultaneous 24-hour urine and morning blood collections were made from 65 patients with CVAH. Patients were grouped into five categories on the basis of age, skeletal age, and sex. Paired blood and urinary data were analyzed. The results suggest that androstenedione is the most reliable indicator for all patient categories. Testosterone is an excellent indicator for children of both sexes and for adolescent and adult females. Levels of 17OH-P are difficult to interpret, as they can be several fold higher than the normal values when adrenal suppression appears adequate on the basis of urinary data. In general, progesterone is a poor indicator.