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Biomedical subjects

Y Livshin

Publications and source records attributed to Y Livshin.

10 recordsLinked to original sources
PubMed1993

Pregnancy outcome in serologically indicated active Chlamydia trachomatis infection.

A serological test for chlamydial infection was administered to 281 Jerusalem women in order to determine the rate and influence of Chlamydia on pregnancy outcome. Serological indication of active infection was present in 7.8% of the tested women, while 15.3% were shown to be positive for Chlamydia. Among the ultraorthodox subpopulation of Mea Shearim, serological indication of active infection was present among 5.9% of the women, and 12.3% of this population tested positive. In comparison, women from the secular subpopulation had 12.7% serological indication of active infection and 22.95% tested positive (P < 0.01). There were no statistically significant differences between pregnancy duration, birthweight, incidence of premature uterine contractions, premature rupture of membranes, and postpartum febrile morbidity in the infected and noninfected groups. Women with a previous history of induced abortions showed a significantly higher evidence of past Chlamydia infection (9.3%) when compared with the women who did not have an infection (1.4%) (P < 0.006). Among the ultraorthodox women with positive or active infection, 41% had suffered at least one spontaneous abortion, as compared with 25% of the religious women who had no serological evidence of infection.

Abortion, Induced↗
PubMed1992

The effects of two fixed hormonal replacement therapy protocols on blood lipid profile.

Hormonal Replacement Therapy (HRT) is known to be accompanied by changes in blood lipid profile. The present prospective cohort study compared the blood lipid profile of healthy postmenopausal women treated with either (a) a preparation containing a fixed regimen of estradiol, estriol and norethisterone acetate (EENA, marketed under the trade name Trisequens); (b) a fixed protocol of conjugated equine estrogen and medroxyprogesterone acetate (CEEMPA, marketed under the trade name Premaril Plus); or with (c) a concurrent group which underwent no treatment. Blood lipid profiles (total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), and triglycerides (TG)) were performed at the beginning of the study and at 3-month intervals, for 9 months. The EENA-treated women showed a significant and profound decrease in TC and LDL-C when compared with their initial values, with the control group, and with the CEEMPA group. The CEEMPA group showed an increase in HDL-C values and a decrease in LDL-C values when compared with their initial values and with the control group, but no increase was shown when compared with an EENA group. There was a favorable decrease in the TC/HDL-C and LDL-C/HDL-C ratios in both treatment protocols. As the primary goal of prevention of coronary artery disease is total cholesterol reduction, the EENA protocol seems to be preferred.

Clinical Protocols↗
PubMed1984

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The dissociation of the exaggerated prolactin and thyrotropin responses in seminiferous tubule failure following the administration of a double-pulse of thyrotropin-releasing hormone.

PRL and TSH secretion has been evaluated in 11 patients with seminiferous tubule failure and 9 controls. When compared to the controls, the patients had increased basal FSH, TSH and PRL levels. However, LH, E2, T and thyroid hormone levels were similar to the controls. Both groups were given two pulses of TRH (200 micrograms) at 30 min intervals. Following the initial pulse of TRH, the patients demonstrated exaggerated TSH and PRL responses. The administration of a second pulse of TRH led to a further increment of TSH secretion in the patients. There was, however, no PRL response to the second TRH pulse in either patients or controls although mean PRL levels remained significantly greater in the patients.

Adult↗
PubMed1982

Clomiphene citrate does not modify the exaggerated thyrotrophin response to thyrotrophin-releasing hormone occurring in primary testicular failure.

Patients with primary testicular failure have increased basal TSH levels and an exaggerated TSH response to TRH in the presence of normal circulating levels of thyroid hormones. In order to evaluate it this TSH profile is an oestrogen-related phenomenon, sixteen patients with primary testicular failure were challenged with 200 micrograms TRH prior to and after the administration of clomiphene citrate. The latter was given in a dose of 100 mg/day for 4 weeks to ten patients; 200 mg/day for 4 weeks to three patients and 100 mg/day for 2 months to the final three patients. The patients demonstrated increased mean basal TSH levels with an exaggerated TSH response to TRH. Following the administration of clomiphene citrate, there were no changes in T4, T3 sephadex or total T3 levels and in basal or stimulated TSH levels. Clomiphene did produce an increase in oestradiol, testosterone, basal gonadotrophins and LH response to LHRH. Since the oestrogen antagonist, clomiphene citrate, had no effect on TSH secretion, it is unlikely that the exaggerated TSH response to TRH is mediated by oestrogens.

Adult↗
PubMed1982

Dissociation between sleep-related and TRH-induced prolactin secretion in seminiferous tubule failure.

Prolactin (PRL) secretion has been measured during sleep and following TRH administration in 8 patients aged 24-39 yr with seminiferous tubule failure and 36 controls. Basal LH levels were 25.7 +/- 14.7 mIU/ml in the patients compared to 11.5 +/- 4.2 mIU/ml in the controls (p less than 0.01) Corresponding FSH levels were 26.2 +/- 10.7 mIU/ml and 5.9 +/- 2.1 mIU/ml (p less than 0.001) Mean estradiol 17B and testosterone levels were similar in the 2 groups. The mean PRL secretion during sleep was 16.5 +/- 11.7 ng/ml in the patients and not different in 11 of the controls (12.4 +/- 3.2 ng/ml). One patient had a mean nocturnal PRL concentration of 44.1 ng/ml. In both groups, the mean sleep related PRL concentration was greater than that during waking hours. The average number of peaks in the 2 groups was similar. In the same patients, the peak PRL response to TRH (200 ug IV) was 81.9 +/- 18.8 ng/ml as compared to 32.1 +/- 10.7 ng/ml in the controls (p less than 0.001). It is concluded that PRL concentrations following pharmacological stimulation are increased in seminiferous tubule failure, whereas levels are normal in relation to the physiological stimulus of sleep.

Adult↗
PubMed1981

The TSH response to TRH is exaggerated in primary testicular failure and normal in the male castrate.

Basal TSH levels and the TSH response to TRH have been evaluated in 26 males aged 20-48 years with primary testicular failure, and 6 males aged 58-69 years who had been orchidectomised for prostatic carcinoma. The patients with testicular failure were sequentially challenged at 30 min intervals with iv LRH (100 microgram), TRH (200 microgram) and the dopaminergic antagonist, metoclopramide (10 mg). The castrates received a bolus of LRH and TRH given together. The responses in the 2 patient groups were compared to a group of 28 healthy male controls aged 20-40 years, who received the sequential protocol and 8 elderly controls aged 65-79 years, who were given the LRH, TRH bolus. Mean +/- SD basal TSH levels were 3.0 +/- 1.2 muU/ml in primary testicular failure and significantly greater than both control and castrate groups. The peak TSH response to TRH was 18.4 +/- 7.4 muU/ml in testicular failure and significantly greater than in the young controls, where it was 11.5 +/- 5.0 muU/ml. The peak levels in the castrates and in the elderly controls were similar to the young male controls. Total T4 and T3, as well as FTI, primary testicular failure had a reduction in their T3 resin uptake. The normal TSH profile in the castrates indicates that a testicular factor produces the exaggerated responses in primary testicular failure.

Adult↗
PubMed1980

Exaggerated prolactin response to thyrotropin-releasing hormone and metoclopramide in primary testicular failure.

Twenty-eight severely oligospermic and azoospermic men aged 20 to 42 years were challenged with luteinizing hormone (LH)-releasing hormone (LHRH), thyrotrophin-releasing hormone (TRH), and the dopaminergic antagonist, metoclopramide, given at 30-minute intervals. According to basal gonadotropin levels, the patients were subdivided into three groups: those with severe testicular failure (basal LH > 20 mIU/ml and FSH > 14 mIU/ml); those with moderate testicular failure with predominant seminiferous tubule involvement (LH < 20 mIU/ml and FSH > 14 mIU/ml) and those with mild testicular failure (LH < 20 mIU/ml and FSH < 14 mIU/ml. With one exception, mean basal prolactin (PRL) levels were normal in all patients. In all three groups, however, there was an exaggerated PRL response to TRH, the response in severe and moderate testicular failure being greater than that in mild testicular failure. The response to metoclopramide was increased only in the first two groups, not in the group with mild testicular failure. When individual patients and control subjects were considered together, the peak PRL response to TRH correlated with both basal and peak gonadotropin responses to LHRH. However, the PRL responses did not correlate with 17 beta-estradiol, estrone, testosterone, or the estradiol-testosterone ratio. It is concluded that oligospermic and azoospermic subjects with the most severe testicular failure and the highest gonadotropin levels have the greatest PRL increases after TRH and metoclopramide, indicating that the PRL response is related to the degree of testicular failure.

Adult↗