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PubMed1980

[3H-thymidine incorporation under endocrine influence and hormone receptor content of human mammary carcinoma (author's transl)].

The effect of medroxyprogesterone acetate, oestradiol-17 beta and testolactone on 3H-thymidine incorporation in human mammary carcinoma was studied in vitro. 54% of the tumours reacted to medroxyprogesterone, while testolactone and oestradiol-17 beta changed 3H-thymidine incorporation in 45.1 and 41.3%, respectively. Both inhibition and the in vivo undesirable stimulation of 3H-thymidine incorporation was observed. No relation could be established between oestrogen receptor content and reaction of the mammary carcinoma to oestradiol-17 beta. On the other hand, the gestagen receptor content and the reaction of the mammary carcinoma to medroxyprogesterone acetate correlated significantly (P < 0.001). This underlines the increasing significance of the gestagen receptor in the selective endocrine treatment of mammary carcinoma.

Breast Neoplasms↗
PubMed1986

Acute modulation of the hypothalamic-pituitary axis by intravenous testosterone in normal women.

Intravenous testosterone was infused for 6 hours in 23 ovulatory women, divided into five groups according to dose, to assess the effects of testosterone on gonadotropin secretion. Serum testosterone increased from 0.24 +/- 0.08 to steady-state levels of 1.63 +/- 0.18 ng/ml in the lowest-dose group (1) and to 42.1 +/- 3.3 ng/ml in the highest-dose group (4). In another group (5), patients were pretreated with testolactone, which prevented the estradiol rise associated with testosterone infusion. All groups except group 1 exhibited significant reductions in the delta maximum responses of luteinizing hormone to gonadotropin-releasing hormone during testosterone infusion compared with pretreatment levels (p less than 0.01). This was also evident for the testolactone group (5). There were no observed changes in serum follicle-stimulating hormone. Luteinizing hormone pulse frequency was decreased (p less than 0.05) with testosterone concentrations of 27.2 +/- 0.77 and 42.1 +/- 3.3 ng/ml (groups 3 and 4), but only in the highest group (4) was there a decrease in pulse amplitude (p less than 0.05). No luteinizing hormone pulse changes were observed with lower concentrations of testosterone. Plasma immunoreactive gonadotropin-releasing hormone levels remained undetectable or low in some of the groups sampled. These data suggest that short-term infusions of testosterone inhibit hypothalamic-pituitary function of normal women when high doses are used, and this effect may be independent of aromatization to estrogen.

Adult↗
PubMed1996

Testosterone decreases lipoprotein(a) in men.

We administered testosterone, with or without the aromatase inhibitor testolactone, to determine the effects of testosterone and its aromatization to estradiol on Lp(a) levels in normal men. Average Lp (a) values decreased by 37% during testosterone alone and by 28% when testosterone and testolactone were combined, suggesting that testosterone reduces Lp(a) in men primarily by an androgenic effect and not by its conversion to estradiol.

Adult↗
PubMed2002

McCune-Albright syndrome--the German experience.

The classical McCune-Albright syndrome (MAS) consists of peripheral precocious puberty (PPP), fibrous bone dysplasia and café-au-lait spots. We conducted a survey among pediatric endocrinologists in Germany, Austria and Switzerland, most of them participating in the German Working Group for Pediatric Endocrinology (APE). Thirty-three physicians reported 58 patients. A detailed questionnaire yielded extensive data from 41 patients. Patients (36 females, 5 males) were diagnosed between the 4th week of life and 8 years. Symptoms included precocious puberty (37 patients), café-au-lait spots (35), fibrous bone dysplasia (32), hyperthyroidism (5), liver disease (5), phosphate wasting (4), GH hypersecretion (3), anemia in infancy (2), hyperprolactinemia (1), and Cushing's disease (1). Therapy of PPP included testolactone (15), tamoxifen (7), cyproterone acetate (CPA) (5), anastrozole (1) and exemestane (1). Testolactone, tamoxifen and CPA showed varying degrees of clinical remission; none was unanimously effective, but side effects were very rare. New aromatase inhibitors were not well validated in MAS. Eleven children received bisphosphonate therapy (pamidronate i.v. q 3 months) for fibrous bone dysplasia. Pamidronate was well tolerated, and pain improved when present, but data on preventive effects are not yet available. In conclusion, this survey describes a large cohort of patients with MAS, many with severe clinical problems, including major physical handicaps. Our results show that there is no 'gold standard' for the therapy of PPP; tested treatment regimens are not ideal, and new aromatase inhibitors need to be evaluated in controlled studies. Pamidronate was well tolerated, but preventive effects on bone dysplasia have not yet been proven.

Child↗
PubMed1991

Gonadotropin-independent precocious puberty.

Gonadotropin-independent precocious puberty presents a challenge in diagnosis and management and in the elucidation of its pathophysiologic basis. Current therapeutic strategies reflect the fact that, irrespective of the underlying mechanism, the clinical and biochemical aspects of the disease process are consequences of gonadal autonomy. In MAS and in testotoxicosis, the most successful therapeutic maneuvers have focused on the local inhibition of steroidogenesis. Despite the positive reports on the use of MPA and cyproterone acetate, long-term experience with these preparations has been generally unsatisfactory, and there is a consensus that testolactone or ketoconazole represent optimal management. Although ketoconazole use, in our experience, has not been associated with any adverse effects either on liver function or on cortisol metabolism, the risk potential is always there. Nevertheless, its effects are dramatic in boys with testotoxicosis, and its mode of action allows for easy monitoring of its efficacy. Testolactone use in MAS, and in combination with spironolactone in testotoxicosis, appears to be relatively safe and reasonably effective. However, because serum testosterone levels are not lowered during treatment, assessment of efficacy depends largely on long-term evaluation of growth rate and of skeletal maturation. The etiology of these disorders remains unclear. The McCune-Albright syndrome is a multisystem disease and sporadic in nature. The organ involvement--ovary, thyroid, adrenal glands, bone, and kidney--is reminiscent of pseudohypoparathyroidism, ironically also bearing Albright's name (Albright's hereditary osteodystrophy, AHO). It is well established that in this syndrome, organ hypofunction associated with the AHO phenotype is caused by deficiency or dysfunction of the G-(or N) regulatory protein essential for production of intracellular cAMP and induction of specific protein kinases. The hypothesis that MAS is caused by abnormal regulation of the membrane receptor/kinase complex would seem logical. Despite its clinical similarity to MAS, the mechanism underlying testostoxicosis is clearly different. This disease is autosomal dominant and is expressed clinically only in boys. Its effects are confined to the production of gonadal autonomy. However, it is difficult to theorize how such autonomy could arise. The enzymatic reactions converting cholesterol to testosterone within the testis or adrenal gland are acquired typically through autosomal recessive inheritance, including the initial rate-limiting step of desmolase side-chain cleavage.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1997

The role of estrogen in bone growth and maturation during childhood and adolescence.

Twenty years ago it was believed that pubertal growth was stimulated by testicular androgen in boys and by adrenal androgen in girls. Estrogen, which was used to inhibit growth in excessively tall girls, was not thought to have growth-promoting effects. We hypothesized that estrogen has a biphasic effect on epiphyseal growth, with maximal stimulation at low levels. We showed that the administration of low doses of estrogen, corresponding to a serum estradiol level of about 4 pg/ml (15 pmol/l) caused more than a 60% increase over the prepubertal growth rate in both boys and girls. To test the hypothesis that estrogen is the principal mediator of the pubertal growth spurt in boys, we administered the aromatase inhibitor, testolactone, to boys with familial male-limited precocious puberty. Testolactone produced near normalization of both growth velocity and bone maturation, despite levels of serum testosterone that remained within the adult male range. The observation that low levels of estrogen stimulate growth and bone maturation suggested that estrogen might explain the more rapid epiphyseal maturation of prepubertal girls compared to boys. To determine whether prepubertal girls have higher estrogen levels than prepubertal boys, we developed an ultrasensitive recombinant cell bioassay for estrogen with a sensitivity of 0.02 pg/ml (0.07 pmol/l) estradiol equivalents. Prepubertal girls had approximately eight-fold higher levels of serum estradiol than did prepubertal boys (0.6 +/- 0.6 pg/ml (SD) (2.2 +/- 2.2 pmol/l) vs 0.08 +/- 0.2 pg/ml (0.29 +/- 0.73 pmol/l), P < 0.05). We concluded that the pubertal growth spurt of both sexes is driven primarily by estrogen, and that the more rapid epiphyseal maturation of prepubertal girls (vs boys) may be explained by their higher estradiol levels.

Adolescent↗
PubMed1975

Combined androgen and antimetabolite therapy of advanced female breast cancer. A report of the cooperative breast cancer group.

A clinical trial of androgen and antimetabolite therapy of advanced female breast cancer was conducted in 110 patients by the Cooperative Breast Cancer Group. An objective regression rate of 20% was achieved in women receiving oral testolactone, 6% in patients given intravenous fluorouracil alone, and 14% when the androgen and antimetabolite were administered together. This randomized trial according to the CBCG protocol did not produce the high regression rate noted previously in a nonrandomized, nonprotocol evaluation of these drugs.

Administration, Oral↗
PubMed1990

High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered.

We examined the influence of aromatization of testosterone on serum high-density lipoprotein cholesterol (HDL-C) and postheparin plasma hepatic triglyceride lipase activity (HTLA) in men. Eighteen healthy lean nonsmokers (ages, 20 to 33) were administered androgens in a weekly total dose of 280 mg for 12 weeks in one of three groups: testosterone enanthate (TE) (280 mg/wk intramuscularly [IM]); TE (280 mg/wk IM) + testolactone (TL) (250 mg orally [PO] four times daily); or methyltestosterone (MeT) (20 mg PO twice daily). Serum testosterone achieved steady state levels by 4 weeks with greater than 40 nmol/L (TE and TE + TL) and less than 15 nmol/L (MeT) while 17b-estradiol (E2) rose to greater than 250 pmol/L (TE) or remained below 70 pmol/L (TE + TL and MeT). LH fell to less than 5 U/L (TE and TE + TL) but remained unchanged with MeT. By 4 weeks, HDL-C had decreased significantly from 1.20 +/- 0.13 to 0.77 +/- 0.13 mmol/L (MeT), from 1.18 +/- 0.15 to 0.89 +/- 0.13 mmol/L (TE TL), and demonstrated no decrease in the TE group across the time course of the study. These changes were preceded by mean increases in HTLA of 102% (MeT) and 55% (TE + TL) over baseline, and no significant change with TE. The changes in HDL-C and HTLA returned to baseline within 2 weeks of steroid cessation. There were no changes in total cholesterol, triglycerides, or insulin in any group but, in the MeT group, apo AI levels decreased and low-density lipoprotein cholesterol (LDL-C) increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Diagnosis and management of precocious puberty.

The onset of pubertal development before the age of 8 years in girls or 9 years in boys constitutes precocious puberty. There are numerous causes of precocious puberty, which can be classified as central or peripheral precocious puberty. Central precocious puberty results from premature activation of the hypothalamic-pituitary-gonadal axis and thus presents with physical and hormonal findings similar to those found in normal puberty. Peripheral precocious puberty results from extrapituitary gonadotropin secretion or secretion of sex steroids independent of pituitary gonadotropins. All types of precocious puberty are characterized by rapid growth and advancement of skeletal age, leading to the paradox of the tall child becoming a short adult as a result of premature epiphyseal fusion. Long-acting GnRH agonists afford effective, selective, and reversible therapy of central precocious puberty without significant toxicity. GnRH agonists are not effective in managing the premature sexual maturation associated with peripheral precocious puberty, but a number of other agents have been used with some success. These agents include testolactone, ketoconazole, and medroxyprogesterone acetate. GnRH agonist treatment leads to an increase in predicted final height. To determine the true benefit of any of these agents in increasing ultimate height, there is a need for continuing studies in treated cohorts to follow growth patterns until adult stature is achieved.

Child↗
PubMed1999

Evaluation of the EDSTAC female pubertal assay in CD rats using 17beta-estradiol, steroid biosynthesis inhibitors, and a thyroid inhibitor.

The Endocrine Disrupter Screening and Testing Advisory Committee has recommended the female pubertal onset assay as a Tier I test to detect potential endocrine-disrupting chemicals (EDs). We evaluated this assay's ability to detect EDs acting through various mechanisms. In two similar experiments, weanling female rats were dosed for 20 days by gavage with vehicle (0.5% methocel) or the following test compounds (mg/kg/day): 17beta-estradiol (E2; 0.1, 2, or 4), ketoconazole (KETO; 24, 50, or 100), finasteride (FIN; 20), testolactone (TL; 220), fadrozole (FAD; 0.6, 1.2, or 6.0) or 6-propylthiouracil (PTU; 240). In vehicle-treated females, mean age at pubertal onset, as evidenced by vaginal opening (VO), varied interexperimentally from 32.3+/-1.6 days to 33.5+/-1.8 days. At 0.1 mg/kg E2, age at VO was reduced slightly to 31.0+/-1.6 days, but not significantly (alpha=0.05). Higher E2 doses (2.0 and 4.0) reduced age at VO to 28 days. KETO delayed VO, but this delay was significant only at 100 mg/kg (39.7+/-2.4 days). FIN and TL had no effect on age at pubertal onset; however, FAD significantly delayed VO. PTU delayed VO to 34.2+/-1.1 days and altered thyroid weight, histology, and hormone levels. With each compound, significant changes in age at VO were accompanied by decreased uterine or ovarian weights. Thus, although this assay did not detect TL or lower doses of E2 (0.1 mg/kg) or KETO (< or = 50 mg/kg), it was capable of detecting EDs operating through a variety of mechanisms.

5-alpha Reductase Inhibitors↗
PubMed2001

Evaluation of the male pubertal onset assay to detect testosterone and steroid biosynthesis inhibitors in CD rats.

The male pubertal onset assay has been recommended by the Endocrine Disrupter Screening and Testing Advisory Committee (EDSTAC) as an alternate Tier I screening assay to detect potential endocrine-active chemicals (EACs). Recently, this assay was evaluated by several laboratories using a variety of dosing schemes. This study used a 30-day dosing period to confirm and extend previous work on the assay's ability to detect steroid biosynthesis inhibitors. Weanling male rats were dosed by gavage from 21 to 50 days of age with vehicle (0.5% methocel) or chemicals from the following EAC classes: an androgen (testosterone propionate [TP], 0.1 or 0.4 mg/kg/day), a broad-spectrum steroid biosynthesis inhibitor (ketoconazole [KETO], 24 mg/kg/day), a 5alpha-reductase inhibitor (finasteride [FIN], 20 or 80 mg/kg/day), a moderately specific aromatase inhibitor (testolactone [TL], 220 mg/kg/day), or a highly specific aromatase inhibitor (fadrozole [FAD], 0.6 or 6.0 mg/kg/day). None of these treatments altered relative thyroid weights. However, TL, KETO, and FIN were positive for endocrine activity based on decreases in one or more reproductive or accessory sex gland organ weights. Of these three inhibitors, only TL significantly increased the age at PPS, indicating that PPS was less sensitive for detecting these EACs. Based on its profile of effects, TL may have been detected as an antiandrogen. TP and FAD were negative in this assay, even at doses that caused effects in other studies. With TP, oral administration limited assay sensitivity such that higher TP doses would be needed for detection. FAD decreased body weight gains, but did not significantly alter any other assay end points; thus, the capacity of this assay to detect aromatase inhibitors remains in question.

Animals↗
PubMed1984

Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens.

There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion.

Adult↗
PubMed1991

Reproductive endocrine considerations and hormonal therapy for men with epilepsy.

Androgen deficiency is unusually common among men with epilepsy. It may contribute to reproductive and sexual dysfunction and possibly exacerbate seizure frequency. The most important androgen is testosterone. it exists in the serum in a free form or bound to albumin or sex hormone-binding globulin (SHBG). Free testosterone levels have correlated significantly with measures of potency and sexual interest. The possibility that measures of non-SHBG-bound testosterone may provide a more sensitive assessment of biologically and perhaps clinically significant androgen levels is raised for consideration. Androgen deficiency may result from increased catabolism and binding induced by antiepileptic drugs (AEDs). It is a feature of the reproductive endocrine disorders that are often associated with epilepsy: hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, and functional hyperprolactinemia. It may be a consequence of medication-induced elevations in serum estradiol. Estradiol exerts a potent inhibitory influence on luteinizing hormone secretion and may contribute to premature aging of the reproductive system, both at the level of the testes and the hypothalamus. Testosterone therapy may moderately benefit reproductive and sexual function. Despite its antiseizure effects in animal experiments, however, it has not been reported to improve seizures clinically. One possible explanation is that AEDs that induce enzyme synthesis may enhance the conversion of testosterone to estradiol by aromatase. This possibility is supported by the improved seizure control achieved with the adjunctive use of the aromatase inhibitor testolactone or the antiestrogen clomiphene.

Anticonvulsants↗
PubMed1992

Familial adrenal feminization probably due to increased steroid aromatization.

5/10 members of a North African family (father, 2 male and 2 female siblings) had gynaecomastia, early growth and short final stature. The 8-year-old propositus had advanced bone age, facial acne, gynaecomastia, pubic hair and prepubertal testicular volume. Basal oestrone (E1) was elevated (670 pmol/l) and increased with adrenocorticotropic hormone (ACTH; 826 pmol/l). After human chorionic gonadotropin stimulation testosterone (T) responded normally whereas E1 and oestradiol (E2) remained unchanged. ACTH-dependent adrenal feminization was confirmed by a transient reduction of breast tissue following dexamethasone or cypropterone acetate treatment. Testolactone increased T/E2 (from 5.6 to 20.3) and A/E1 (from 3.4 to 31.4) ratios and temporarily reduced the breast tissue. In conclusion, this is a familial type of adrenal feminization with increased adrenal androgen aromatization. This is the first time that male-to-male and male-to-female transmission has been reported.

Adrenal Glands↗
PubMed1980

Influence of some antineoplastic agents on genetic exchange in Bacillus subtilis.

The influence of three categories of anti-cancer agents on competence development and on the binding of homologous DNA to cells have been studied in the Bacillus subtilis transformation system. Treatment of cells developing competence with testolactone resulted in a slight enhancement of transforamtion at high doses (50 and 100 micrograms/ml) of the drug, but this process was inhibited at 25 micrograms/ml. DNA binding was unaffected by this drug. DNA-interacting agents (daunomycin, prospidine, peptichemio and mithramycin) usually inhibited DNA-mediated transformation in a higher extent than DNA binding. Antimetabolites of DNA synthesis were also tested: dacarbazine did not greatly inhibit the binding and expression of donor DNA. 5-Fluorouracil appeared to slightly enhance transformation at low levels 1 microgram/ml), although it was inhibited at higher doses.

Antineoplastic Agents↗
PubMed1979

Evidence that testosterone can suppress pituitary gonadotropin secretion independently of peripheral aromatization.

Testosterone (T) was given to normal men with and without the concomitant administration of the aromatase inhibitor, delta 1-testolactone (Teslac), to examine the role of peripheral aromatization of T in gonadotropin regulation. When T was administered alone by continuous iv infusion (15 mg/day for 4 days), serum T increased 3-fold (P less than 0.01) and estradiol (E) increased by 50% (P less than 0.01). These changes were associated with a 50% decrease in serum LH and FSH concentrations (P less than 0.01). When T was infused into men taking Teslac (2000 mg/day), serum T levels doubled (P less than 0.01), but E levels did not change (13.4 +/- 1.5 vs. 13.5 +/- 1.0 pg/ml; P = NS). This pattern of plasma steroids, increased T and unchanged E, was also associated with significantly decreased serum LH and FSH concentrations (14.5 +/- 0.4 vs. 8.0 + 0.4 mIU/ml and 9.9 +/- 2.5 vs. 5.8 +/- 0.1 mIU/ml, respectively; P less than 0.01). These data support the hypothesis that T or one of its metabolites can modulate LH and FSH secretion independently of peripheral aromatization to E.

Adult↗
PubMed1991

Sex steroid control of gonadotropin secretion in the human male. I. Effects of testosterone administration in normal and gonadotropin-releasing hormone-deficient men.

The precise sites of action of the negative feed-back effects of gonadal steroids in men remain unclear. To determine whether testosterone (T) administration can suppress gonadotropin secretion directly at the level of the pituitary, the pituitary responses to physiological doses of GnRH were assessed in six men with complete GnRH deficiency, whose pituitary-gonadal function had been normalized with long term pulsatile GnRH delivery, before and during a 4-day continuous T infusion (15 mg/day). Their responses were compared with the effects of identical T infusions on spontaneous gonadotropin secretion and the response to a 100-micrograms GnRH bolus in six normal men. Both groups were monitored with 15 h of frequent blood sampling before and during the last day of the T infusion. In the GnRH-deficient men, the first three GnRH doses were identical and were chosen to produce LH pulses with amplitudes in the midphysiological range of our normal men (i.e. a physiological dose), while the last four doses spanned 1.5 log orders (7.5, 25, 75, and 250 ng/kg). The 250 ng/kg dose was always administered last because it is known to be pharmacological. In the GnRH-deficient men, mean LH (P less than 0.02) and FSH (P less than 0.01) levels as well as LH pulse amplitude (P less than 0.05) decreased significantly during T infusion, demonstrating a direct pituitary-suppressive effect of T and/or its metabolites. Mean LH levels were suppressed to a greater extent in the normal than in the GnRH-deficient men (58 +/- 15% vs. 28 +/- 7%; P less than 0.05). In addition, LH frequency decreased significantly (P less than 0.01) during T administration in the normal men. These latter two findings suggest that T administration also suppresses hypothalamic GnRH release. T was unable to suppress gonadotropin secretion in one GnRH-deficient and one normal man. In both groups, the suppressive effect of T administration was present only in response to physiological doses of GnRH. Because the pituitary- and hypothalamus-suppressive effects of T could be mediated by its aromatization to estrogens, five GnRH-deficient and five normal men underwent identical T infusions with concomitant administration of the aromatase inhibitor testolactone (TL; 500 mg, orally, every 6 h). As an additional control, four GnRH-deficient and four normal men received TL alone. TL administration completely prevented the effect of T administration to suppress gonadotropin secretion in both the normal and GnRH-deficient men, and mean LH levels increased significantly in both the GnRH-deficient (P less than 0.01) and the normal (P less than 0.001) men who received TL alone. The increase in mean LH levels was greater (P less than 0.01) in the normal men who received TL alone than in the normal men who received T plus TL, thus revealing a direct effect of androgens in normal men. Measurements of T and estradiol production rates in three men demonstrated that TL effectively blocked aromatization.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1991

Luteinizing hormone-releasing hormone (LHRH)-independent precocious puberty unresponsive to LHRH agonist therapy in two girls lacking features of the McCune-Albright syndrome.

Two girls with precocious puberty (chronological age, 1 and 4 yr; bone age, 3 and 6 yr, respectively) were initially given the diagnosis of idiopathic, central precocious puberty and treated with the LHRH agonist deslorelin (D-Trp6-Pro9-NEt-LHRH) for 5 yr. Unlike other girls with central precocious puberty, both had persistently elevated rates of growth and bone maturation, and both menstruated during therapy. One girl had episodic ovarian enlargement and markedly elevated serum estradiol levels due to recurrent unilateral ovarian cysts. Although the bone and skin manifestations of McCune-Albright syndrome were absent, we hypothesize that the underlying defect of McCune-Albright syndrome was expressed in the ovaries, but not in the skin or bones, of these two girls. One of these girls appeared to benefit from the aromatase inhibitor testolactone, which is effective in suppressing precocious puberty in girls with the McCune-Albright syndrome.

Child Development↗