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J J Spijkstra

Publications and source records attributed to J J Spijkstra.

12 recordsLinked to original sources
PubMed2001

Intra-observer variability in APACHE II scoring.

Although the APACHE II score is the most widely used scoring system in intensive care units worldwide, its reliability and variability have not been extensively studied. Differences in case-mix may complicate comparison and interpretation of results. We hypothesised that a degree of variability might be inherent to use of the APACHE II scoring system, and decided to assess intra-observer variability in APACHE II scoring as a potential indicator of inherent score variability. APACHE II scores were assessed twice from the charts of 11 patients by 14 physicians, with a time interval of 4 (range 3.5-4.5) months between the two assessments. Intra-observer was found to be approximately 15%. These findings are in agreement with previous observations regarding inter-observer variability in APACHE II scoring, and strongly suggest that there is an inherent score variability of about 15%.

APACHE↗
PubMed1991

The effect of 6 weeks of testosterone treatment on pulsatile luteinizing hormone secretion in eugonadal female-to-male transsexuals.

Polycystic ovary disease generally is associated with elevated androgen levels and elevated luteinizing hormone (LH) levels, whereas follicle-stimulating hormone (FSH) levels are (sub)normal. To assess the role of androgens on gonadotropin secretion, we investigated the effect of 6 weeks of testosterone (T) undecanoate, 120 to 160 mg/d orally, on the parameters of the pulsatile secretion of LH in a group of six eugonadal female-to-male transsexuals with normal menstrual cycles. The treatment suppressed menstrual activity in all patients. Serum T and estrone were significantly elevated after treatment with oral T undecanoate. The parameters of the pulsatile secretion of LH were not affected by androgen administration. Levels of FSH, estradiol, and progesterone also did not change significantly.

Estrone↗
PubMed1989

Pulsatile luteinizing hormone release and ovarian steroid levels in female-to-male transsexuals compared to heterosexual women.

It has been suggested that there is a difference in the interaction between sex steroids and gonadotropin secretion between transsexual and heterosexual women. In this study we tested whether there is a difference in the pulsatile release characteristics of luteinizing hormone (LH) and in ovarian steroid concentrations between 16 female-to-male (f-to-m) transsexuals and eight eugonadal heterosexual women during the early follicular phase of the menstrual cycle. Blood samples for LH determination were collected every 10 min for 7 hr in the transsexual group, and every 10 min for 6 hr in the heterosexual group. There were no significant differences between the transsexual and heterosexual group in mean serum LH concentration (6.9 +/- 2.4 U/l vs. 7.5 +/- 2.6 U/l), mean LH nadir interval (77 +/- 37 min vs. 70 +/- 16 min), and mean LH pulse amplitude (2.9 +/- 1.1 U/l vs. 3.0 +/- 1.1 U/l). Serum estrone, 17-beta-estradiol, testosterone, progesterone and FSH concentrations also did not differ between the two groups. There also was not a higher prevalence of polycystic ovarian disease in our f-to-m transsexual group than in the general population.

Adult↗
PubMed1989

Effects of long-term testosterone administration on gonadotropin secretion in agonadal female to male transsexuals compared with hypogonadal and normal women.

We investigated the effects of long term testosterone (T) administration on pulsatile gonadotropin secretion in agonadal women and the effects of estradiol (E2) on gonadotropin secretion in eugonadal women in the follicular phase of the menstrual cycle. We studied 4 groups: A) 28 eugonadal women in the early follicular phase of the menstrual cycle, B) 11 hypogonadal women, C) 13 agonadal female to male (f-t-m) transsexuals treated for at least 3 months with 120-160 mg T undecanoate (TU)/day, orally, and D) 5 agonadal f-to-m transsexuals treated for at least 6 months with 250 mg of a mixture of testosterone esters, im (im T-esters), every 2 weeks. The eugonadal women in the early follicular phase had a mean serum E2 level of 193 +/- 94 (+/- SD) pmol/L, significantly higher (P less than 0.01) than that in the hypogonadal women (60 +/- 24 pmol/L), whereas there was no difference in the mean serum T levels (1.8 +/- 0.7 vs. 2.3 +/- 1.5 nmol/L). the higher serum E2 level in the eugonadal women was associated with a significantly lower mean serum LH level (6.9 +/- 2.6 vs. 44.6 +/- 17.6 U/L; P less than 0.01) and LH pulse amplitude (2.8 +/- 1.0 vs. 12.6 +/- 4.8 U/L; P less than 0.01), whereas the mean nadir LH interval did not differ between the two groups (75 +/- 29 vs. 81 +/- 49 min). The mean serum T level in the agonadal f-to-m transsexuals treated with oral TU was significantly higher (P less than 0.01) than that in the hypogonadal women (9.7 +/- 4.7 vs. 2.3 +/- 1.5 nmol/L). In spite of this elevated T level there was no difference in the mean serum LH level (38.4 +/- 14.7 vs. 44.6 +/- 17.6 U/L), LH pulse amplitude (14.3 +/- 5.7 vs. 12.6 +/- 4.8 U/L), or nadir LH interval (72 +/- 27 vs. 81 +/- 49 min) in these groups. Also, the mean serum E2 (64 +/- 16 vs. 60 +/- 24 pmol/L and FSH levels (62 +/- 17 vs. 64 +/- 28 U/L) did not differ between these groups. Treatment of the agonadal f-to-m transsexuals with im T-esters resulted in mean serum T and E2 levels of 34.4 +/- 27.0 nmol/L and 121 +/- 54 pmol/L, respectively, both significantly higher (P less than 0.01) than those in groups B and C.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

The effects of long term testosterone administration on pulsatile luteinizing hormone secretion and on ovarian histology in eugonadal female to male transsexual subjects.

Polycystic ovarian disease (PCOD) is associated with elevated serum LH and (sub)normal FSH levels, while serum androgen levels are often elevated. To clarify the role of androgens in this abnormal pattern of gonadotropin secretion, LH secretion was studied in 1) 9 eugonadal female to male transsexual subjects before and during long term (6 months) testosterone (T) administration (250 mg/2 weeks, im), and 2) in a woman with an androgen-secreting ovarian tumor both before and after surgical removal of the tumor. Finally, we studied the effects of high serum androgen levels on ovarian histology in 3) 26 transsexual subjects after long term (9-36 months) T administration (250 mg/2 weeks, im) to assess whether T-induced ovarian abnormalities are similar to those that occur in women with PCOD. Long term T treatment in the nine female to male transsexual subjects resulted in increases in the mean serum T level from 1.7 +/- 0.8 (+/- SD) to 40.8 +/- 31.9 nmol/L (P less than 0.01), the mean serum dihydrotestosterone level from 0.6 +/- 0.2 to 3.3 +/- 1.5 nmol/L (P less than 0.02), and the mean serum free T level from 9.5 +/- 5.2 to 149 +/- 46 pmol/L (P less than 0.02). Mean serum estrone and estradiol levels were similar before and during T treatment. The mean serum LH level decreased from 6.3 +/- 2.0 to 2.9 +/- 1.1 U/L (P less than 0.01), and the mean FSH levels decreased from 6.6 +/- 2.0 to 3.7 +/- 2.2 U/L (P less than 0.02). Pulsatile LH secretion before and during T treatment was studied in five subjects. Neither the mean nadir LH interval nor the LH pulse amplitude changed significantly in these five subjects. The serum T level in the woman with the androgen-secreting ovarian tumor was 9.6 nmol/L, and it declined to normal after removal of the tumor. Her mean serum LH and FSH levels, the mean nadir LH interval, and LH pulse amplitude were in the normal range before and after removal of the tumor. Studies of ovarian histopathology in 26 transsexual subjects after long term androgen treatment revealed multiple cystic follicles in 18 subjects (69.2%), diffuse ovarian stromal hyperplasia in 21 subjects (80.8%), collagenization of the tunica albuginea in 25 subjects (96.2%), and luteinization of stromal cells in 7 subjects (26.9%). Findings consistent with criteria for the pathological diagnosis of polycystic ovaries, that is 3 of the 4 findings listed above, were present in 18 of the 26 subjects (69.2%).(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗
PubMed1988

Short-term patterns of pulsatile luteinizing hormone secretion do not differ between male-to-female transsexuals and heterosexual men.

This study tested whether there is a difference in the pulsatile LH secretion between male-to-female transsexuals and eugonadal heterosexual men. The mean serum LH concentrations, the LH pulse frequency, and the LH pulse amplitude were compared between a group of eight male-to-female transsexuals and a group of 22 heterosexual men. Blood samples for LH determinations were collected every 10 min for seven hours. 17-beta-estradiol and testosterone were measured at the beginning of each test. There were no significant differences between the heterosexual and transsexual group in LH pulse frequency (3.9 +/- 1.3 vs. 3.9 +/- 1.7), LH pulse amplitude (3.7 +/- 1.3 U/l vs. 3.0 +/- 0.5 U/l), mean serum LH concentration (5.2 +/- 1.4 U/l vs. 5.4 +/- 1.1 U/l), 17-beta-estradiol (0.07 +/- 0.01 nmol/l vs. 0.08 +/- 0.02 nmol/l), or testosterone (22.9 +/- 3.7 nmol/l vs. 21.8 +/- 8.0 nmol/l). We conclude that the pulsatile release characteristics of LH do not allow a distinction between eugonadal heterosexual men and eugonadal male-to-female transsexuals.

Adult↗
PubMed1988

Effects of opiate receptor blockade on gonadotrophin secretion before and after administration of the oestrogen receptor blocker tamoxifen in eugonadal men.

Both gonadal steroids and endogenous opioid peptides (EOPs) exert an inhibitory effect on gonadotrophin secretion. It is thought that the negative feedback action of the gonadal steroids, testosterone (T) and oestradiol (E2), on the gonadotrophin secretion is mediated by EOPs. To assess the effects of EOPs and oestrogen and their interrelationship on pulsatile LH secretion we studied two groups of eugonadal men. The subjects of the first group were tested on three different occasions, firstly under basal conditions, secondly during infusion of the opiate receptor blocker naloxone (NAL) (bolus 5 mg + 2.1 mg/h for 7 h), and finally during NAL infusion after 6 weeks administration of the oestrogen receptor blocker tamoxifen (10 mg twice daily). The subjects of the second group were studied before and after 6 weeks administration of tamoxifen. NAL infusion produced a significant increase in mean serum LH levels (4.8 +/- SD 1.5 to 6.2 +/- 1.8 U/l) and LH pulse frequency (3.7 +/- 1.6 to 5.3 +/- 1.2 pulses/7 h). No change was seen in mean LH pulse amplitudes (3.5 +/- 1.5 vs 3.4 +/- 1.0 U/l). After tamoxifen administration alone there was a significant increase in mean LH level (from 5.7 +/- 1.3 to 10.1 +/- 2.4 U/l), LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.9 U/l) and LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7 pulses/7 h). A significant rise in mean serum LH levels was observed during NAL infusion after previous tamoxifen administration in comparison to the infusion of NAL alone (from 6.2 +/- 1.8 to 10.5 +/- 6.2 U/l). LH pulse frequency (5.3 +/- 1.2 vs 6.3 +/- 1.3 pulses/7h) and amplitude (3.4 +/- 1.0 vs 3.6 +/- 1.5 U/l) however, did not change. Mean serum LH level and LH pulse frequency after opiate receptor and oestrogen receptor blockade together did not differ from the results obtained after oestrogen receptor blockade alone. NAL however was expected not only to block opioid-mediated oestrogen action but also androgen action and therefore to have additional effect on LH secretion, whereas tamoxifen was supposed to block only oestrogen action. From these data we conclude that EOPs exert a negative feedback effect on LH secretion by slowing the GnRH pulse generator. Because there was no additional effect of opiate receptor blockade after oestrogen receptor blockade on pulsatile LH secretion we infer that androgens may be impeded in their negative feedback action in the presence of the antioestrogen tamoxifen.

Adult↗
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↗