Rise In Serum Follicle Stimulating Hormone Research Articles

Stimulation of a non-functioning pituitary macroadenoma after administration of goserelin acetate for locally advanced prostate cancer causing a sustained elevation in PSA and testosterone

Long-acting luteinizing hormone-releasing hormone (LHRH) agonists, such as goserelin, have been used for locally advanced and metastatic prostate cancer for many years and are the main forms of androgen deprivation therapy (ADT). Acting on pituitary LHRH receptors, they initially stimulate a transient rise in serum follicle-stimulating hormone (FSH) and LH. Long-term administration of an LHRH analogue will eventually lead to down regulation of LHRH receptors, thus suppressing FSH and LH secretion. This in turn suppresses testosterone production hence achieving and maintaining androgen deprivation. This case highlights the potential anomaly of a sustained elevated serum testosterone in the context of newly diagnosed locally advanced prostate cancer with a co-existing pituitary macroadenoma after administration of LHRH analogues. Alternative methods of androgen deprivation must be considered in such patients.

The effect of hysterectomy and endometrial ablation on follicle stimulating hormone (FSH) levels up to 1 year after surgery

Objectives: In this study the hypothesis was tested, that in premenopausal patients FSH-levels would rise after `simple hysterectomy'. As endometrial ablation is not supposed to compromise ovarian bloodflow, there would be no such change in ablated patients. Methods: Between January 1995 and April 1996, consecutive premenopausal patients with dysfunctional uterine bleeding who were scheduled for hysterectomy or endometrial ablation were asked to participate in the study. Bloodsamples were drawn before surgery, six weeks, six months and one year after surgery. FSH and oestradiol (E2) were assayed. In all patients data about length and weight were collected to calculate Body Mass Index (BMI). Every visit patients filled in a questionnaire, containing questions about typical climacteric complaints, combined in a five-point scale. Results: Except for a significant difference in preoperative FSH-level between both groups, there were no significant differences regarding age, Body Mass Index (BMI), oestradiol (E2) or the percentage of women with vasomotor complaints. Compared to the preoperative starting level, six weeks, six months and one year after surgery a significant rise in serum FSH in the hysterectomy group, as well as in the ablation group was found. However there was no significant difference in FSH increase between both groups. One third of the patients in both groups had typical climacteric complaints as flushing and nocturnal sweating. Conclusions: Assaying serum FSH-levels before and after uterine surgery and comparing hysterectomized patients and patients after endometrial ablation, we found a significant rise in FSH-level up to one year after surgery in both groups postoperatively, indicating impaired ovarian function. There was no difference in FSH-levels between both groups.Therefore major uterine surgery (hysterectomy, ablation) may prelude an earlier onset of menopause.

RU486 on an estrogen background blocks the rise in serum follicle-stimulating hormone induced by antiserum to inhibin or ovariectomy.

We used passive immunization with an antiserum to the alpha-subunit of inhibin (anti-I) or acute ovariectomy to investigate the relationship between serum inhibin levels and FSH secretion in the presence of the progesterone/glucocorticoid antagonist RU486. We demonstrated previously that 1) anti-I administered at 1700 h causes serum FSH to rise on the morning of estrus, even in the presence of a GnRH antagonist, when the two treatments are delivered on proestrus; and that 2) RU486 given on proestrus (1230 h), a time when serum estradiol levels are high, not only blocks the natural secondary FSH surge, but also suppresses the anti-I-induced rise in serum FSH on the morning of estrus. We have now extended our studies of the relationship between inhibin and RU486 to investigate treatment with RU486 and anti-I on a different day of the cycle, estrus, when serum estradiol levels are low. When both RU486 and anti-I were given on estrus (1230 and 1700 h, respectively), RU486 failed to block the anti-I-induced rise in serum FSH on the next morning of metestrus, in contrast to the blockade seen with RU486 treatment on the day of proestrus. However, pretreatment with estradiol benzoate (50 microgram) on the evening of proestrus, before the RU486 and anti-I treatment on estrus, caused RU486 to suppress the effects of anti-I on serum FSH, as it does when given on proestrus. We then repeated the study, using ovariectomy on proestrus or estrus (1700 h) to raise serum FSH, and assessed the effects of RU486 treatment at proestrus and estrus and estradiol benzoate treatment on proestrus. Our results indicate that treatment with RU486 can block the postovariectomy rise in serum FSH only in the presence of high circulating estradiol levels. We conclude that the inhibitory action of RU486 on FSH secretion after a fall in serum inhibin depends on a precedent estradiol background, probably due to induction of progesterone receptors by estradiol.

Adequacy of laparoscopic oophorectomy

Ovarian remnant syndrome occurs infrequently after oophorectomy, yet when present it can contribute greatly to pelvic discomfort. The syndrome may be difficult to diagnose, identify surgically, and treat without intraoperative or postoperative complications developing. Recently, laparoscopic oophorectomy has been performed with increasing frequency. We assessed the outcome after laparoscopic removal of both ovaries or the sole remaining ovary in 27 premenopausal women. No intraoperative or postoperative complications were identified, and no patients have experienced symptoms consistent with ovarian remnant syndrome. All women had a marked rise in serum follicle-stimulating hormone (FSH) levels (8±1 to 72±5 mlU/ml), and luteinizing hormone (LH) levels (8±1 to 37±3 mUl/ml) after oophorectomy, and all but one had FSH levels 40 mlU/ml or above. Thirteen women had gonadotropin levels measured after 4 weeks of hormone replacement therapy; all had reductions in FSH levels, but 10 had elevations of their LH levels. These findings indicate that ovarian remnant syndrome occurs infrequently after laparoscopic oophorectomy. In addition, the data suggest a different, nonovarian regulation of gonadotropin secretion.

Regulation of follicular development by diethylstilboestrol in ovaries of immature rats

Immature female rats received either one injection of 2 mg diethylstilboestrol (DES)/rat subcutaneously and were killed 12 h later or received two injections of DES at 0 and 24 h and were killed at 24, 36 and 48 h after the initial injection. The ovarian follicles were released by enzymic digestion with collagenase and separated into those of small, medium and large diameter (less than 200 microns, 200-400 microns and greater than 400 microns) by filtration through graded Teflon sieves and granulosa cells were extracted from these follicles. The ovaries of immature rats treated with pregnant mares' serum gonadotrophin (PMSG) were used for comparative purposes. Incorporation of [3H]thymidine into granulosa cell DNA was augmented by DES and by PMSG. Small follicles were more strongly stimulated by DES at 12 h than those of other sizes, but rates increased significantly in medium and large follicles at 48 h. Aromatase activity in the DES-treated group was low at all times and in all follicles. Rates of oestrogen and progesterone production in response to 36 h of exposure to follicle-stimulating hormone (FSH) in vitro were significantly lower than in the PMSG-treated group. FSH-stimulated steroid production in the DES group at 36-48 h was lower, particularly in the medium follicles. A significant rise in serum FSH, luteinizing hormone (LH) and progesterone concentrations was noted only at 36 h after DES treatment, while serum and follicular fluid oestrogen values remained unchanged. When these changes were compared with those in PMSG-treated rats, there were obvious differences. The pattern of thymidine incorporation and aromatase activity differed with time and follicle size. Serum FSH and LH values were not affected by PMSG treatment, but serum and follicular fluid oestradiol values increased with time. The PMSG-treated animals ovulated in response to human chorionic gonadotrophin, but the DES-treated rats did not ovulate in spite of the presence of some large antral follicles in the ovaries. These findings show that initial exposure of follicles to high concentrations of oestrogen results in follicles which fail to respond to subsequent gonadotrophin surges and are thereby restricted in their ability to differentiate fully.

Induction of ovulation with clomiphene citrate in women with polycystic ovary syndrome: the difference between responders and nonresponders

To identify why some women with polycystic ovary syndrome (PCO) fail to respond to clomiphene citrate (CC), the authors have monitored the endocrine and ovarian response to CC 100 mg/day given for 5 days. Of 40 cycles studied in 27 women, 73% were ovulatory. In 8 of 9 anovulatory women, there was no follicular development despite a significant rise in serum gonadotrophin concentrations within 3 to 5 days of starting CC. There were no significant differences between the ovulatory and anovulatory groups in the peak response of either luteinizing hormone (LH) or follicle-stimulating hormone (FSH). The authors conclude that, in women with polycystic ovaries, the most common reason for the failure to ovulate is an absent ovarian response to an appropriate rise in serum FSH.

Follicle-stimulating hormone beta subunit messenger ribonucleic acid concentrations during the rat estrous cycle.

Serum follicle-stimulating hormone (FSH), pituitary FSH content and FSH beta subunit mRNA concentrations were measured at 1 to 3h intervals throughout the 4 day estrous cycle in rats. Serum FSH was stable (range 200-320 ng/ml) apart from the biphasic proestrus surge (5 fold elevation) which was present from 1800h of proestrus through 0800 h on estrus. Basal FSH beta mRNA concentrations from late metestrus through the afternoon of proestrus were 0.10 +/- 0.04 f mol cDNA bound/100 micrograms pituitary DNA. The major increase in FSH beta mRNA began at 2000 h on proestrus, 2 h after the initial rise in serum FSH and peak mRNA concentrations (0.43 +/- 0.08 f mol cDNA bound) occurred at 0200 h on estrus. FSH beta subunit mRNA concentrations were again increased at 2300 h on estrus (peak 0.24 f mol cDNA bound) and remained elevated through 1700 h on metestrus. Pituitary FSH content was transiently increased during metestrus and diestrus, but was elevated at 1000 h through 1900 h on proestrus (peak 5-fold increase). FSH content fell rapidly at 2000h and remained low until 1400 h on estrus when values again rose. These data show that FSH beta mRNA is increased 4-5 fold during the proestrus FSH surge, and a smaller increase occurs on metestrus in the absence of elevated FSH secretion. The increased concentrations of FSH beta mRNA occurred at different times to the previously reported changes in alpha and LH beta mRNAs. Therefore, the data suggest that different mechanisms are involved in the regulation of LH and FSH beta subunit gene expression during the 4-day estrous cycle in rats.

Follicle-stimulating hormone beta subunit messenger ribonucleic acid concentrations during the rat estrous cycle.

Serum follicle-stimulating hormone (FSH), pituitary FSH content and FSH beta subunit mRNA concentrations were measured at 1 to 3h intervals throughout the 4 day estrous cycle in rats. Serum FSH was stable (range 200-320 ng/ml) apart from the biphasic proestrus surge (5 fold elevation) which was present from 1800 h of proestrus through 0800 h on estrus. Basal FSH beta mRNA concentrations from late metestrus through the afternoon of proestrus were 0.10 +/- 0.04 f mol cDNA bound/100 micrograms pituitary DNA. The major increase in FSH beta mRNA began at 2000 h on proestrus, 2 h after the initial rise in serum FSH and peak mRNA concentrations (0.43 +/- 0.08 f mol cDNA bound) occurred at 0200 h on estrus. FSH beta subunit mRNA concentrations were again increased at 2300 h on estrus (peak 0.24 f mol cDNA bound) and remained elevated through 1700 h on metestrus. Pituitary FSH content was transiently increased during metestrus and diestrus, but was elevated at 1000 h through 1900 h on proestrus (peak 5-fold increase). FSH content fell rapidly at 2000 h and remained low until 1400 h on estrus when values again rose. These data show that FSH beta mRNA is increased 4-5 fold during the proestrus FSH surge, and a smaller increase occurs on metestrus in the absence of elevated FSH secretion. The increased concentrations of FSH beta mRNA occurred at different times to the previously reported changes in alpha and LH beta mRNAs. Therefore, the data suggest that different mechanisms are involved in the regulation of LH and FSH beta subunit gene expression during the 4-day estrous cycle in rats.

Measurement of inhibin and an index of inhibin production by rat testes during postnatal development.

Our previous studies have shown that inhibin activity in rat testes can be measured using an in vitro inhibin bioassay. In animals that have undergone unilateral efferent duct ligation (EDL), the difference in inhibin content between the ligated and nonligated testis can be used as an index of the rate of inhibin production in vivo. In the present study we examined postnatal changes in inhibin content in the testes, and the production rates of inhibin and seminiferous tubule fluid in groups of neonatal, immature, and adult rats from 1 to 80 days old. We detected inhibin activity in testes of 1-day-old rats; the activity level rose linearly to Day 8, subsequently increasing markedly from Day 30 until it reached a plateau at Day 45. Increments in the content of inhibin and weight of the testis after unilateral EDL, interpreted to represent production of inhibin and seminiferous tubule fluid, commenced at Day 20 and increased rapidly between Days 30 and 50, decreasing thereafter to Day 80. The increase in content and production of inhibin was directly correlated to the rise in serum follicle-stimulating hormone (FSH) and testosterone, suggesting that these two hormones are important in controlling inhibin secretion. In addition, the changes in serum FSH from the high, postnatal levels to those typical of adults were inversely correlated to the content and production rate inhibin in the testes and concentrations of testosterone in the serum. These data support the hypothesis that inhibin is specifically involved in the feedback control of pituitary FSH secretion during postnatal development, although a role for testosterone or a synergistic interaction between the two hormones cannot be excluded.

Effect of gonadotropin-releasing hormone antagonists on serum follicle-stimulating hormone and luteinizing hormone under conditions of singular follicle-stimulating hormone secretion.

Previous work has indicated that in long-term ovariectomized rats a potent antagonist to gonadotropin-releasing hormone (GnRH) suppressed serum luteinizing hormone (LH) more successfully than follicle-stimulating hormone (FSH). The present studies examined whether the rise in serum FSH which occurs acutely after ovariectomy, or during the proestrous secondary surge, depends on GnRH. In Experiment A, rats were ovariectomized at 0800 h of metestrus and injected with (Ac-dehydro-Pro1, pCl-D-Phe2, D-Trp3,6, NaMeLeu7)-GnRH (Antag-I) at 1200 h of the same day, or 2 or 5 days later. Antag-I blocked the LH response completely, but only partially suppressed serum FSH levels. Experiment B tested a higher dose of a more potent antagonist [( Ac-3-Pro1, pF-D-Phe2, D-Trp3,6]-GnRH; Antag-II) injected at the time of ovariectomy. The analog suppressed serum LH by 79% and FSH by 30%. Experiment C examined the effect of Antag-II on the day of proestrus on the spontaneous secondary surge of FSH, as well as on a secondary FSH surge which can be induced by exogenous LH. Antag-II, given at 1200 h proestrus, blocked ovulation and the LH surge expected at 1830 h, as well as increases in serum FSH which occur at 1830 h and at 0400 h. Exogenous LH triggered a rise in FSH in rats suppressed by Antag-II. In Experiment D proestrous rats were injected with Antag-II at 1200 h and ovariectomized at 1530 h. By 0400 h the antag had suppressed FSH in controls, but in the ovariectomized rats, a vigorous FSH response occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Seminiferous tubule fluid and interstitial fluid production. I. Effects of age and hormonal regulation in immature rats.

Efferent duct ligation was used to assess seminiferous tubule fluid (TF) production and studies of the kinetics of TF production following this procedure were performed on 25-day-old rats. The rate of TF production was linear for 48 h, thereafter reached a plateau until 72 h and began decreasing at 96 h post-ligation. Using a 16-h ligation period, the onset of TF production was investigated in groups of immature rats from 15 days of age. TF secretion was not detected prior to 15 days but rose rapidly after Day 20 coincident with the prepubertal rise in serum FSH. The acute effect of hormone on TF production following unilateral efferent duct ligation (EDL) was evaluated in 25-day-old rats in which interstitial fluid production (IF) was also assessed in the unligated testis by the method of Sharpe (1977). Single subcutaneous injections of the following hormones were given to groups of rats at the time of EDL: a) NIH follicle-stimulating hormone (FSH) S13 (20 micrograms/rat); b) NIH luteinizing hormone (LH) S22 (200 micrograms/rat); c) testosterone propionate (2 mg/rat); d) human chorionic gonadotropin (hCG) (10 IU/rat); or e) NIH prolactin (Prl) 14 (200 micrograms/rat). A significant rise in TF production occurred following FSH treatment but no effect was noted in any of the other groups. In contrast, a marked stimulation of IF production occurred in rats treated with LH or hCG.

Intraventricular injection of follicle-stimulating hormone (FSH) during proestrus stimulates the rise in serum FSH on estrus in phenobarbital-treated hamsters through a central nervous system-dependent mechanism.

The serum gonadotropin profiles of 4-day cycling rodents exhibit LH and FSH surges during proestrus (P) and a second release of FSH during estrus (E). Peak serum levels of FSH during P occur between 1500–1800 h; the estrous FSH release starts late in the evening of P and reaches maximal serum levels during the morning of E. To delineate the mechanisms that regulate the estrous FSH rise and elucidate the role of FSH in its own secretion, hamsters were given Phenobarbital (ip) during P to block the endogenous gonadotropin surges and were subsequently injected systemically (iv) or intraventricularly (icv) with purified preparations of FSH or LH at 1500 h on P. Blood samples were obtained at regular intervals throughout P until 0900 h on E, at which time the animals were killed, and anterior pituitaries and hypothalami were collected. Serum and pituitary FSH and hypothalamic gonadotropin-releasing hormone were measured by RIA. Intact, saline-injected, and hypophysectomized (hypox) FSH-injected animals served ...

Hormonal profile of puberty in South Australian children I

ABSTRACT.Serum follicle stimulating hormone (FSH), luteinising hormone (LH) and testosterone (T) concentrations in 118 boys aged 8 to 17.9 years were related to chronological age (CA), bone age (BA), genital development (G1–5+), pubic hair development (PH1–5 +) and mean testicular volume (MTV).A progressive rise in serum FSH, LH and T was noted in relation to CA, BA and all pubertal parameters studied.FSH showed an approximate twofold increase, LH an eight to tenfold increase and T a fourfold increase from pre‐puberty through to full adult maturity.The FSH/LH ratio decreased with advancing CA, BA and pubertal development.

Inhibition of in vivo and in vitro FSH secretion by steroid-free hamster ovarian extracts.

We designed experiments to determine if a nonsteroidal substance capable of inhibiting the secretion of follicle-stimulating hormone (FSH) exists in the hamster ovary. Proestrous hamster ovaries were homogenized, centrifuged, and treated with dextrancoated charcoal for removal of steroids. Charcoal-treated ovarian extract (CTOE) was injected intraperitoneally at hourly intervals into phenobarbital-treated (phen-treated) proestrous hamsters immediately after ovariectomy at 1300. The CTOE inhibited the selective rise in serum FSH that occurred in phen-treated, ovariectomized (ovx) controls.KeywordsLuteinizing HormoneFollicular FluidPituitary CellLuteinizing Hormone LevelAnterior Pituitary CellThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Gonadotrophin response to luteinizing hormone releasing factor (LRF) in puerperal women.

Abstract. Synthetic luteinizing hormone releasing factor (LRF) was administered intravenously in a dose of 200 μg to twenty normal lactating puerperal women and serum follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) response to LRF was measured by double antibody radio‐immunoassay. Synthetic LRF failed to stimulate FSH secretion in all the eight volunteers in the 1st postpartum week. About half of the six subjects in the 3rd postpartum week responsed to LRF with a rise of serum FSH and LH. All the six lactating women in the 5th postpartum week were responsive to LRF and there was a concomitant rise in serum FSH and LH. These results suggest that gonadotrophic activity of the anterior pituitary is suppressed by an unknown mechanism during the first few weeks of puerperium and gonado‐trophin reserve function recovers completely around the 5th postpartum week. Thus, it might be assumed that puerperal anovulation or amenorrhoea is due to hypo‐thalamic‐pituitary dysfunction during the first few postpartum weeks and due to hypothalamic disorders after the 5th postpartum week.

The radio-immunoassay of follicle-stimulating hormone (FSH) during human pregnancy: serum concentration and response to luteinizing hormone releasing factor (LRF).

Abstract. Concentrations of follicle‐stimulating hormone (FSH) detectable by radio‐immunoassay and the FSH response to synthetic luteinizing hormone releasing factor (LRF) were measured in the sera of fourteen women during the first, the second and the third trimesters of pregnancy. Serum FSH was detectable, but relatively low in all the fourteen subjects throughout pregnancy. Moreover, exogenously administered synthetic LRF failed to stimulate serum FSH secretion from the anterior pituitary and there was no rise in serum FSH in all the fourteen pregnant women. Thus, it might be concluded that follicle‐stimulating activity of the hypophyseal gland is suppressed throughout human pregnancy by an unknown mechanism.

Pituitary-gonadal relations in male children and adolescents.

Extract: Data are provided on levels of circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in healthy male children and adolescents, and these levels are correlated with the stage of sexual maturation, bone maturation, whole body 40K content, and the 24-hr excretion of creatinine, estrogens, 17-hydroxy-corticosteroids, total 17-ketosteroids, and fractionated ll-deoxy-17-ketosteroids (see Tables I and II). Before age 6 there was no significant change with age in testis size or hormone concentrations. From age 6–10 years there was a gradual rise in testis size (Fig. 1), serum FSH (Fig. 4) and serum LH (Fig. 3), but no change in plasma testosterone (Fig. 2), which remained below 40 ng/100 ml. From age 11–17 years there was a doubling of mean testis length, continued rise in serum FSH, and a steeper rise in LH; these changes were accompanied by a 20-fold increase in plasma testosterone concentration, the appearance of male secondary sexual characteristics (Figure 5), more rapid bone maturation and whole body 40K accretion, and enhanced excretion of estrogens and ll-deoxy-17-ketosteroids. Mean levels of FSH in the adult range (> 10 μUg/100 ml) were achieved by age 8, and levels reached a plateau by age 15 (Fig. 6). Adult LH levels (> 2.5 μUg/100 ml) were reached by age 13 and a plateau was observed after 17 years. Plasma testosterone also ceased to rise after age 17. The data suggest that the testis may undergo progressive gonadotropin-mediated maturation in late childhood. Testosterone secretion by the Leydig cells at puberty may result from a further rise in LH levels. Speculation: Pituitary secretion of gonadotropins, particularly FSH, in male children is a gradual phenomenon, antedeating by several years the release of testosterone by the testis. This gradual rise may represent a progressive reduction in hypothalamic sensitivity to feedback by testicular steroids other than testosterone. In late childhood, rising FSH and LH levels may induce increased activity of the enzymes responsible for both synthesis and catabolism of tesoterone. At puberty, an LH-mediated reduction in reductase activity might then result in testosterone accumulation and secretion.

Hormonal changes in puberty. I. Correlation of serum luteinizing hormone and follicle stimulating hormone with stages of puberty, testicular size, and bone age in normal boys.

Extract: The concentration of luteinizing hormone (LH) and follicle stimulating hormone (FSH) in serum was determind using a double antibody radioimmunoassay method in each of 106 normal boys aged 5-16 years. The boys were grouped according to the stage of puberty (P1-P5) using the classification of TANNER. The serum LH and FSH, LH/FSH ratio, and testicular volume index (TVI) for boys prepuberty (P1) and at different stages of puberty (P2-P5) are shown in figure l and table. The mean value of LH in prepubertal boys was 4.2 ng/ml, which steadily rose to a concentration of 5.3 ng/ml at P4-5. The differences between the values for LH in early puberty (P2) and at a more advanced stage of puberty (P4-5) were statistically significant. The mean value for serum FSH in the prepubertal boy was 1.4 ng/ml. Serum FSH rose steadily through the early stages of puberty (P1-P3) with no further rise from P3 to P4-5. These changes were reflected in the LH/FSH ratio which fel between P1 and P2, but increased between P2 and P4. Tesricular size (TVI) showed a gradual increase from P1 through P4-5. A comparison of serum LH and FSH, LH/FSH ratio. and TVI with chronological age is indicated in table II. A slight increase in the mean levels of serum LH and FSH was observed from age 9 to age 12 with a continued rise to 15 years and older. Serum LH and FSH was obsereved from age 9 to age 12 with a continued rise to 15 years and older. Serum LH seemed to rise at an earlier age than serum FSH. The TVI showed a definite increase from chronologic age 8 through 11. A pronounced change in testicular size from age 11 through 15 was observed during the period of sharp rise in serum FSH. The correlation of bone age with concentrations of LH and FSH in serum, LH/FSH ratio, and TVI is shown in table III. A significant rise in LH was seen in boys with a bone age of 9-10 years, with a further increase at a bone age of 13-15 years and older. Serum FSH showed a steady increment from a bone age of 11 to 14 years. The most pronounced increase in TVI was seen at a bone age of 11 through 15 years. The relation of concerntrations of LH and FSH in serum and LH/FSH ratio to the TVI is presented in table IV. Mean LH and FSH showed a gradual rise from a TVI of <2 to 10.1-12. Serum LH rose and serum FSH fell, however, with the increase in TVI from 10.1-12 to 12.1-16. In four patients with chromatin-positive seminiferous tubular dysgenesis (Klinefelter's syndrome), the mean serum LH concentration was 11.3 ng/ml and the mean serum FSH concerntration was 21.6 ng/ml. The mean serum LH in 14 patients with multiple pituitary hormone deficiencies was 2.1 ng/ml and the mean serum FSH was 1.5 ng/ml. The small diffrences in the concentration of LH and FSH in prepubertal boys compared with that observed in children with hypopituitarism stress the need for further definition of the sensitivity of the assay for serum samples. The serum values reported are of relative not absolute significance. Speculation: The detection of serum FSH and LH prior to puberty, and the increase in serum FSH and LH coincident with advancing puberty suggests 1) that the hypothalamic-pituitary-testicular axis is functional befor puberty, and 2) that the onset of puberry may be associated with a change in sensitivity of the hypothalamus to feedback by testicular steriods.