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Biomedical subjects

L Gooren

Publications and source records attributed to L Gooren.

At least 19 recordsLinked to original sources
PubMed2003

Testosterone supplementation: why and for whom?

Androgen levels decline over a man's lifetime. In a proportion of men (increasing with age), levels fall below values that have been established by conventional laboratory criteria as indicative of hypogonadism. Testosterone has a wide range of non-reproductive actions: it preserves bone and muscle mass, it acts on non-sexual mental functioning and it stimulates red blood cell formation. Long-term androgen deficiency has a great impact on quality of life. The first intervention studies provide indications that androgen treatment of men with true androgen deficiency is helpful. Obviously, only men who are testosterone-deficient will benefit from androgen supplementation. The diagnosis of testosterone deficiency in old age is not unambiguous. Signs and symptoms of aging sometimes clinically overlap with those of testosterone deficiency. The groups that are at higher risk of testosterone deficiency are those men with disease (pulmonary disease, gastro-intestinal disease, rheumatoid disease, etc.). Usually, sex hormone binding globulin levels increase with aging, leading to lower levels of free, biologically available testosterone. For the time being, arbitrary criteria for testosterone deficiency in aging men have to be adopted. The best practical approach is to calculate the free testosterone level. The calculation can be found at www.issam.ch under 'Tools'.

Aged↗
PubMed2000

Dramatic suppression of plasma and urinary prostate specific antigen and human glandular kallikrein by antiandrogens in male-to-female transsexuals.

PURPOSE: Prostate specific antigen (PSA) and human glandular kallikrein (hK2) are mainly produced by the prostate and their genes are regulated by androgens through the androgen receptor. We determine whether PSA and hK2 change significantly in plasma and urine after antiandrogen treatment in male-to-female transsexuals. MATERIALS AND METHODS: Plasma and urine PSA and hK2 were measured with highly sensitive immunofluorometric procedures capable of detecting within 1 or 6 ng./l. PSA or hK2, respectively. Study groups consisted of 10 men treated with cyproterone acetate only (group 1), 15 transdermal estradiol plus cyproterone acetate (group 2) and 31 ethinyl estradiol plus cyproterone acetate (group 3). Plasma and urine samples were collected before initiation of treatment as well as after 4 months of hormonal therapy. For a subset of group 3 patients blood and urine samples were also obtained after 12 months of treatment. RESULTS: Cyproterone acetate, a steroidal antiandrogen, alone or with estradiol was able to suppress greater than 90% of plasma and urinary PSA and hK2 concentration after 4 or 12 months of therapy. CONCLUSIONS: Cyproterone acetate therapy causes dramatic suppression of plasma and urinary PSA and hK2 in men without prostate cancer. Since cyproterone acetate is used for prostate cancer treatment, suppression of PSA after hormonal therapy may not accurately reflect therapy success in reducing tumor burden.

Adolescent↗
PubMed1996

Effects of estrogens only on the prostates of aging men.

PURPOSE: The effects of estrogen only on prostate tissue were studied in 9 aging male transsexuals who had undergone orchiectomy. MATERIALS AND METHODS: Prostate volume was measured by ultrasound. Biopsies were stained for prostatic acid phosphatase (PAP), prostate specific antigen (PSA), Ki-67 and sex steroid receptors. RESULTS: Prostates were small, and biopsies showed PAP and PSA in most cases. No malignancy was found. Few androgen receptors were detectable but there were ample estrogen and progesterone receptors in stroma and epithelium. CONCLUSIONS: Prostates were small after long-term estrogens only. The sex steroid receptor content was considerably changed. PSA and PAP in the specimens suggested that their production does not depend on testicular androgens alone.

Acid Phosphatase↗
PubMed1996

The effect of one-year cross-sex hormonal treatment on bone metabolism and serum insulin-like growth factor-1 in transsexuals.

The effects of treatment with estrogens and antiandrogens in male to female (M-->F) transsexuals and androgens in female to male (F-->M) transsexuals on their respective bone metabolism, bone mineral density (BMD), serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) levels were investigated. BMD and variables of bone turnover in serum were measured at baseline and after 3 months (except for BMD) and 1 yr of treatment in 56 M-->F and 35 F-->M transsexuals. Serum IGF-I, IGFBP-3, and propeptide of type I procollagen (P1CP) were measured at baseline and after 1 yr of treatment in 10 M-->F and 10 F-->M transsexuals. In M-->F, BMD increased significantly. Bone turnover decreased, as shown by a significant decline in levels of osteocalcin, alkaline phosphatase, P1CP, and fasting urinary calcium/creatinine and hydroxyproline/creatinine ratios. Serum IGF-I levels decreased significantly without significant changes in IGFBP-3 levels. In F-->M, BMD did not change. Bone formation increased, as suggested by an increase in alkaline phosphatase and a borderline increase in P1CP values. IGF-I levels increased significantly, whereas no significant changes were seen in IGFBP-3 levels. We conclude that in males, estrogens (in combination with antiandrogens) decrease bone turnover, with a subsequent increase in BMD and a decrease in serum IGF-I. In females, testosterone administration increases bone formation, but this is not reflected in an increased BMD, whereas serum IGF-I increases.

Adolescent↗
PubMed1993

Homosexual and bisexual identity in sex-reassigned female-to-male transsexuals.

Descriptions of female-to-male transsexuals who are sexually attracted to men are rare. This is a report on nine of them. Their awareness of gender dysphoria preceded their awareness of their attraction to men. Their wish to undergo sex reassignment as a means of resolving their gender dysphoria superseded any concerns about their sexual orientation or sexual adaptation after surgery. Several had had sexual relationships with men before sex reassignment which were unsatisfactory because these men viewed our subjects as women. After sex reassignment, the subjects successfully established sexual relationships with gay men; in some of them even penovaginal intercourse was part of their sexual activities. While hormonally and surgically reassigned, none of our subjects had had phalloplasty. All nine subjects were interviewed and given psychological tests measuring sexual satisfaction and psychological adjustment. Their results were compared to those of a group of self-identified gay men. No major differences in sexual satisfaction and psychological adaptation were found. The phenomenon of female-to-male transsexuals who develop a sexual orientation toward men may be more common than previously thought. Regarding female gender dysphoric individuals, our findings challenge the issue of using sexual orientation in classification systems of gender dysphoria syndromes and as a risk factor in the decision regarding sex reassignment. Further, our study invites us to rethink the genital criterion in the assessment of sexual orientation.

Adult↗
PubMed1992

Male cross-gender behavior in Myanmar (Burma): a description of the acault.

Cross-gender behavior in Myanmar (formerly Burma) is reported. Western concepts of transsexualism, gynemimesis, transvestism, and homosexuality are not distinct categories by the Burmese. Males with cross-gender behavior are referred to as acaults. Although Myanmar is a profoundly Buddhist society, the people still have strong animistic beliefs with an elaborate system of 37 nats (spirit gods). One of these nats is a female named Manguedon who may take possession of males and impart femininity on them. The cross-gender status of the acaults is sanctioned by their spiritual marriage to Manguedon. The acaults, while not envied, are respected for their roles as shamans and seers.

Adult↗
PubMed1991

Development of male gender identity/role and a sexual orientation towards women in a 46,XY subject with an incomplete form of the androgen insensitivity syndrome.

Transsexualism and homosexuality have been theorized to originate in the male from insufficient androgenization of the brain. For verification of this hypothesis clinical science must rely on subjects with an abnormal prenatal/perinatal endocrine history. A case of a 33-year-old 46,XY subject with an incomplete form of androgen insensitivity syndrome (AIS) is presented. In adulthood the only genital sign of masculinization is a clitoris of 4 cm; the vagina is normal size. The diagnosis AIS was verified by androgen receptor studies. At birth there was confusion as to the sex of the newborn. Originally, the subject was assigned to the male sex, but this decision was reversed 5 days after birth and the subject was reared as a girl. At age 30 the subject applied for gender reassignment treatment to the male sex. Upon psychological evaluation the gender identity was unambiguously male and the sexual orientation was exclusively towards women. The estrogen feedback effect on LH, regarded by some as a marker of the sexual differentiation of the neuroendocrinium was negative before orchiectomy but positive after orchiectomy. Our observation demonstrates that in 46,XY subjects a male gender identity and a sexual orientation towards women can develop with a strikingly lower-than-normal level of biological action of androgens.

Androgen-Insensitivity Syndrome↗
PubMed1990

The endocrinology of transsexualism: a review and commentary.

Testicular hormones play a decisive role in the sexual differentiation of the genitalia. There is now also an impressive body of knowledge, gathered predominantly from laboratory animals, of the influence of gonadal steroid hormones on the prenatal/perinatal sexual differentiation of the brain. The well-documented mechanisms in animals have been extrapolated, sometimes dogmatically, to the development of sexual orientation and gender identity/role in humans. In principle, it is doubtful that an animal model of human gender identity can be found. Studies in humans have shown that levels of circulating sex steroids and estrogen feedback on luteinizing hormone do not differ between transsexuals and controls. The only reliable sources of information on hormonal influences on human gender identity formation are clinical syndromes in which the hormonal environment of the fetus has been atypical. Follow-up studies of such patients have provided evidence for possible effects of prenatal sex steroids on brain lateralization, sexual orientation and gender role stereotypes. However, a straightforward hormonal effect on gender identity (self-identification as male or female) has been difficult to ascertain up to the present time.

Disorders of Sex Development↗
PubMed1989

The effect of cross-gender hormonal treatment on bone metabolism in male-to-female transsexuals.

A deficiency of sex hormones leads in both sexes to increased bone loss, and hormonal substitution can prevent this. The effect of the change of hormonal environment on bone metabolism in transsexuals is unknown. Transilial bone biopsies were obtained from 23 male-to-female transsexuals (mean age +/- SD, 38.0 +/- 11.7 years) after estrogen (ethinylestradiol, 100 micrograms/day) and antiandrogen treatment (cyproterone acetate, 100 mg/day) for 8-41 months. Histomorphometric data were compared with those from 11 healthy men (39.6 +/- 9.4 years). There was no difference in bone volume, bone surface, or trabecular thickness between transsexuals and controls. Eroded surface and osteoclast number were not different between the groups. The osteoid volume, surface, and thickness were significantly lower in the transsexuals than in the controls. The mineral apposition rate and adjusted apposition rate were normal, but mineralizing surface and bone formation rate were suppressed in the transsexuals compared with data reported from the literature. The results indicate that antiandrogen and estrogen treatment in male-to-female transsexuals may suppress bone turnover and is not associated with bone loss.

Adult↗
PubMed1989

Androgens and estrogens in their negative feedback action in the hypothalamo-pituitary-testis axis: site of action and evidence of their interaction.

This paper reviews our research efforts with regard to the negative feedback effects of androgens and estrogens on the secretion of luteinizing hormone (LH) by the hypothalamo-pituitary unit. Three approaches were used: (1) administration of single sex steroids to eugonadal men, (2) administration of single sex steroids to agonadal men and (3) administration of antiandrogens and antiestrogens to eugonadal men. It was found that estrogen administration to agonadal men suppressed basal and LH-RH-stimulated LH levels and LH pulse amplitude while LH pulse frequency remained unaffected. Dihydrotestosterone did not suppress basal and LH-RH-stimulated LH levels in either eugonadal and agonadal men. Antiandrogens and antiestrogens evoked almost identical effects: an increase in LH pulse frequency and amplitude and in basal and LH-RH-stimulated LH levels. On comparison of results of studies with single sex steroid administration and of studies with the antihormones there were unexpected and even conflicting findings. These can be resolved by assuming an interaction of the receptor mechanisms of androgens and estrogens in their feedback action. Blocking of androgen receptors impairs the action of estradiol in this system and vice versa. A similar interaction between estradiol and progesterone exists in women. Androgens appear to regulate LH pulse frequency, the latter is determined at the level of the hypothalamus. Estrogens appear to regulate predominantly parameters of LH secretion as LH pulse amplitude and basal and LH-RH-stimulated LH levels. These effects must be viewed in terms of preponderance and not of mutual exclusion.

Androgens↗
PubMed1989

Improvement of spermatogenesis after treatment with the antiestrogen tamoxifen in a man with the incomplete androgen insensitivity syndrome.

A 32-yr-old man with a history of hypospadias, unilateral cryptorchidism, and pubertal gynecomastia (all surgically corrected) presented with complaints of infertility. Examination revealed scant virilization, recurrence of gynecomastia, small but normal sized testes, small prostate, and oligospermia. His plasma LH, testosterone, dihydrotestosterone, and estradiol levels were high, and his plasma FSH was below the reference range of adult men. An assay of pubic skin fibroblast androgen receptors confirmed the diagnosis of a form of incomplete androgen insensitivity syndrome. Administration of the estrogen receptor antagonist tamoxifen (10 mg, twice daily) induced an increase in plasma FSH greater than that which occurred in six men with idiopathic oligospermia. This man's wife conceived three times during a period of 5 yr, each time after he had received tamoxifen for 12-20 weeks and had considerable improvement of sperm parameters. Conversely, upon cessation of tamoxifen therapy, the semen abnormalities returned. These results indicate that estrogen action impaired this man's fertility, and the impairment could be reversed by administration of an estrogen receptor antagonist.

Adult↗
PubMed1988

Hypogonadotropic hypogonadal men respond less well to androgen substitution treatment than hypergonadotropic hypogonadal men.

This research asked whether androgen substitution therapy is as efficacious in hypogonadotropic hypogonadal men as in hypergonadotropic hypogonadal men. Erotosexual functions of two groups of six men of each diagnostic category were compared after 5-6 years of continuous androgen treatment. Treatment regimen was the same in both groups: Parenteral testosterone esters 250 mg/2 weeks. No difference was found in erectile and ejaculatory potency, but the number of sexual acts and scores of subjective quality of sexual acts, sexual excitement, and frequency of sexual thoughts and of nonsexual parameters as vigor, fatigue, anxiety were more negative in the hypogonadotropic men. The most obvious difference between the two groups is the value of LH/FSH and presumably of LHRH. Hypogonadotropic hypogonadal men may be better treated with gonadotropins (or with pulsatile LHRH, when the hypophysis is intact) than with androgens.

Adolescent↗
PubMed1988

Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinizing hormone (LH) pulse frequency, but not on basal LH levels and LH pulse amplitude in men.

We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 micrograms ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 +/- 1.3 (+/- SD) to 10.1 +/- 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7/7 h) and LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 +/- 1.5/7 h, while it was 5.9 +/- 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 +/- 7.0 vs. 34.3 +/- 8.6 and 4.1 +/- 1.8 vs. 7.4 +/- 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator.

Adult↗
PubMed1987

Sex steroids and pulsatile luteinizing hormone release in men. Studies in estrogen-treated agonadal subjects and eugonadal subjects treated with a novel nonsteroidal antiandrogen.

This study evaluated the effects of estrogens and androgens on LH pulse frequency and amplitude in male subjects. To assess the role of estrogens we compared the serum LH pulse frequency and amplitude between 3 groups: 8 agonadal subjects receiving no steroid treatment; 6 agonadal subjects continuously treated with 50 micrograms ethinylestradiol/day; and 17 eugonadal men. Mean serum LH levels and LH pulse amplitude were significantly lower in the agonadal subjects receiving estrogens (14.8 +/- 5.4 (SD) U/L and 4.1 +/- 1.5 U/L, respectively) than in the group of agonadal subjects not receiving sex steroid treatment (35.7 +/- 8.4 U/L and 7.3 +/- 2.0 U/L, respectively). The mean LH pulse frequency was 7.1 +/- 1.5/7 h in the group not receiving sex steroid treatment and 6.0 +/- 1.4/7 h in the group receiving estrogens (P NS). The LH pulse frequency in the eugonadal men (3.8 +/- 1.3/7 h) was significantly lower than the frequency in both groups of agonadal subjects. The LH pulse amplitude was of the same magnitude in the estrogen-treated agonadal subjects and in eugonadal men (4.1 +/- 1.5 U/L and 3.5 +/- 1.2 U/L, respectively). The role of androgens was studied in 15 eugonadal male subjects (who presented for female role reassignment) by determining the effects of a novel nonsteroidal androgen receptor blocker, Anandron, on basal and LH-releasing hormone (LHRH)-stimulated serum LH/FSH levels; LH pulse frequency and amplitude; sex steroid and sex hormone-binding globulin levels; and serum PRL levels during an 8-week period. Basal and LHRH-stimulated LH levels and testosterone rose progressively during the first 6 weeks and reached a plateau thereafter, while estradiol levels continued to increase somewhat. The LH pulse amplitude and frequency had increased after 6 weeks (3.1 +/- 0.6 vs. 4.5 +/- 1.2 U/L and 4.4 +/- 2.4 vs. 6.6 +/- 1.1 pulses/7 h, respectively). Basal FSH levels were not affected while LHRH-stimulated FSH levels progressively decreased from 2 to 6 weeks, after which they did not change. Along with the rise of estradiol levels an increase of sex hormone-binding globulin and PRL levels occurred.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

The neuroendocrine response of luteinizing hormone to estrogen administration in heterosexual, homosexual, and transsexual subjects.

The neuroendocrine response of LH to estrogen administration may be related to sexual dimorphism of the brain, and therefore, homosexual and especially transsexual individuals may differ from heterosexual individuals in their responses. This study failed to find such differences among groups of female heterosexuals, homosexuals, and transsexuals. Specifically, after single dose estrogen administration, all subjects had an initial decline in serum LH levels, followed by a brisk rise of equal magnitude. Among males, the type of response was less uniform. After an initial fall in serum LH levels, the individual responses varied. In 12 of 23 male homosexuals, 10 of 15 male heterosexuals, and all 6 genetic male transsexuals studied, serum LH levels remained below pretreatment levels. In the remaining 11 male homosexuals and 5 of the heterosexuals, serum LH levels increased to values exceeding those before treatment, resembling the response found in the 3 groups of women. Those homosexual and heterosexual men with a rise in serum LH levels to above pretreatment values also had the greatest fall in testosterone levels after estrogen administration, while these same men had the lowest testosterone response to hCG stimulation. I conclude from these results that 1) the similarity of LH responses to estrogen administration in all groups of women studied does not support a theory of brain androgenization as a factor in the establishment of gender identity of sexual orientation; and 2) individual differences in men in the type of LH response to estrogen administration can be satisfactorily explained by endocrine factors, such as Leydig cell function, and need not be related to gender identity, sexual orientation, or other possible causes.

Adult↗
PubMed1986

The neuroendocrine response of luteinizing hormone to estrogen administration in the human is not sex specific but dependent on the hormonal environment.

Mammals are known to have a sex-specific response of LH secretion to sequential estrogen administration. Females respond with an increase in LH secretion, while males have a decrease. This study of genetic male and genetic female transsexual subjects was done to determine if this sexual differentiation of the LH response to estrogen exposure applies to the human. All subjects were tested before hormone therapy while in the eugonadal state corresponding to their genetic sex and again during cross-gender hormone therapy subsequent to gonadectomy. Transsexuals of both genetic sexes had a LH response to estrogen administration appropriate to their genetic sex before gonadectomy and hormone therapy. The same individuals had the opposite response, appropriate to their reassigned sex, after gonadectomy and while receiving cross-gender hormone therapy. I conclude that the LH response to an estrogen stimulus is not sex specific in humans and is not irrevocably designated perinatally. Psychoneuroendocrine studies linking homosexuality and transsexualism to the type of LH response to estrogen administration should be viewed in the light of these results.

Adult↗