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Biomedical subjects

H L Judd

Publications and source records attributed to H L Judd.

At least 163 records · Page 9Linked to original sources
PubMed1979

Hypercarotenemia in hypothalamic amenorrhea.

Six patients are described with hypothalamic amenorrhea and associated hypercarotenemia. The commencement of the hypothalamic amenorrhea followed weight reduction or stress in each case. The subjects were otherwise healthy and had none of the associated stigmata of anorexia nervosa. None of the subjects had ingested excessive quantities of vegetables or fruits rich in carotene. Although all six patients had elevated serum carotene levels, only three had clinically apparent yellow pigmentation of the skin. The exact mechanism responsible for hypercarotenemia in patients with hypothalamic amenorrhea is not apparent. Mobilization of lipid stores and catabolic changes occurring with weight-loss states appear to be related in some undefined way to the elevated carotene levels.

Adolescent↗
PubMed1978

Preoperative localization of virilizing tumors by selective venous sampling.

Two postmenopausal patients with virilization had preoperative localization of ovarian tumors by selective blood sampling from both ovarian and adrenal veins and assay of hormone levels. In the first patient, the peripheral concentrations of testosterone (T), androstenedione, and estrone were 936, 1,508 and 73 pg. per milliliter, respectively, levels which are above the ranges found in normal postmenopausal women. The catheterization study showed an increase in the left ovarian vein of all hormones except cortisol. It was predicted that a tumor was present in the left ovary. At operation a 7 by 4 mm. lipid cell tumour was found. In the peripheral blood of the second patient, the T level (4,518 pg. per milliliter) was markedly elevated and the estradiol concentration (73 pg. per milliliter) was increased. At retrograde catheterization the concentration of T in the right ovarian vein was markedly elevated at 120,400 pg. per milliliter. At operation a hilus cell tumor of the right ovary was found. These two cases represent the third and fourth consecutive androgen-secreting tumors from this institution that have been localized by selective ovarian and adrenal vein catheterization and sampling.

Adrenal Glands↗
PubMed1977

Correlation of the effects of dexamethasone administration on urinary 17-ketosteroid and serum androgen levels in patients with hirsutism.

Total 24 hour urinary 17-ketosteroid and serum testosterone (T), androstenedione (delta), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DS), and cortisol levels were measured before and during four days of dexamethasone administration in 28 hirsute patients and 10 women with normal ovulatory cycles. Both the base-line urinary 17-ketosteroids and serum androgen levels were significantly higher (p less than 0.05) in hirsute than in normal subjects. Cortisol levels were similar in the two groups. Dexamethasone administration resulted in a significant suppression (p less than 0.05) of all the urinary and serum androgen and cortisol levels in both groups. At the end of suppression the serum DHEA, DS and cortisol levels were similar, while the urinary 17-ketosteroids and serum T and delta levels were still significantly higher (p less than 0.05) in the hirsute than in normal women. There was poor correlation between total urinary 17-ketosteroid and serum androgen results. These finding suggest there is a dual abnormality of androgen production in hirsute patients. The adrenal glands appear to secrete increased quatities of DHEA and DA, while the ovaries appear to produce elevated amounts of T and delta.

17-Ketosteroids↗
PubMed1977

Sleep-wake patterns of LH and testosterone release in prepubertal boys.

Ten prepubertal boys who ranged in age from 6 11/12 to 14 2/12 years were studied for 2 consecutive nights. The subjects went to sleep at their usual times and sleep patterns were monitered polygraphically. Each night blood samples were drawn every 30 min from 1800 to 0600 h and plasma LH and testosterone (T) levels were measured on each sample. During evening wakefulness the mean LH (range 2.8-5.1 mIU/ml) and T (range 31-116 pg/ml) levels were in the normal prepubertal range for each subject. In the 5 youngest subjects (age 6 11/12 to 10 8/12 years) the mean hormone levels during sleep were significantly higher than the wakeful levels in 2 of 9 and 0 of 9 study nights for LH and T, respectively. In contrast, in the older prepubertal boys (age 13 2/12 to 14 2/12 years) the mean levels during sleep were significantly higher than wakeful values during 8 of 9 and 5 of 9 study nights for the same respective hormones. These data suggest that in young prepubertal subjects the sleep related rises of LH and T are either absent or not discernible in the peripheral blood. The prepubertal pattern of sleep-entrained LH and T release may be seen in prepubertal boys approaching the time of puberty and these hormonal rhythms are antecedent to the physical changes of puberty.

Adolescent↗
PubMed1977

Amniotic fluid androgens and estrogens in midgestation.

Amniotic fluid androgen and estrogen levels associated with 48 male and 72 female fetuses between 14 and 20 weeks of gestation were measured. Amniotic fluid testosterone levels were significantly higher (P less than 0.001) in the male (224 +/- 11 pg/ml) than the female fetuses (39 +/- 2 pg/ml) with no overlap of values. Amniotic fluid androstenedione concentrations were also significantly higher (P less than 0.001) with male (1024 +/- 53 pg/ml) than female fetuses (668 +/- 39 pg/ml), but there was overlap. There was no difference between anmiotic fluid dehydroepiandrosterone levels for the two sexes. Estrone concentrations were slightly but not significantly higher with the male (353 +/- 33 pg/ml) than with female fetuses (331 +/- 28 pg/ml), while estradiol concentrations were significantly higher (P =0.002) with the female (96 +/- 8 pg/ml) than male (64 +/- 4 pg/ml) fetuses. It is interpreted that the higher amniotic fluid testosterone and androstenedione levels for the male fetuses reflect fetal testicular secretion. The significantly higher estradiol concentrations for the female fetuses may reflect early ovarian secretion.

Amniotic Fluid↗
PubMed1976

Characterization of the inappropriate gonadotropin secretion in polycystic ovary syndrome.

To evaluate gonadotropin release in polycystic ovary syndrome (PCO), one or more of the following hypothalamic-pituitary function tests were performed on 24 patients with the syndrome. These tests included (a) the pulsatile pattern and day-to-day fluctuation of gonadotropin release; (b) effects of exogenous estrogen and antiestrogen (clomiphene) administration on gonadotropin release; and (c) pituitary responsiveness to maximal (150 mug) and submaximal (10 mug) luteinizing hormone-releasing factor (LRF) injections. In 10 of the 14 patients sampled frequently (15 min) for 6 h, luteinizing hormone (LH) levels were elevated above the concentration seen in normal cycling women (except the LH surge). These high LH concentrations appeared to be maintained by and temporally related to the presence of exaggerated pulsatile LH release, either in the form of enhanced amplitude or increased frequency. In all subjects, levels of follicle-stimulating hormone (FSH) were low or low normal, and a pulsatile pattern was not discernible. In four patients, daily sampling revealed marked day-to-day fluctuation of LH but not FSH. That the elevated LH levels were not related to a defect in the negative-feedback effect of estrogen was suggested by the appropriate fall of LH in four patients given an acute intravenous infusion of 17beta-estradiol. This infusion had no effect on FSH levels. In addition, clomiphene elicited rises of both LH and FSH that were comparable to the ones observed in normal women given the same treatment. The clomiphene study also suggested that the positive-feed-back mechanism of estrogen on LH release was intact when the preovulatory rises of 17beta-estradiol induced appropriate LH surges. The elevated LH levels appeared to be related to a heightened pituitary responsiveness to the LRF. This was found in the 11 and 2 patients given maximal (150 mug) and submaximal (10 mug) doses of LRF, respectively. The augmented pituitary sensitivity for LH release correlated with the basal levels of both estrone (P less than 0.025) and 17beta-estradiol (P less than 0.02). The net increase in FSH was significantly greater (P less than 0.001) in the PCO patients than the normal women with maximal doses of LRF. With the smaller dose study none of the injections had a discernible effect on FSH concentrations in either subject. The disparity between LH and FSH secretion could be explained by the preferential inhibitory action of estrogen on FSH release, coupled with a relative insensitivity of FSH release. These data indicate that in these PCO patients the abnormalities of the hypothalamic-pituitary regulation of gonadotropin secretion was not an inherent defect but represented a functional derangement consequent to inappropriate estrogen feedback, which led to a vicious cycle of chronic anovulation and inappropriate gonadotropin secretion.

Adult↗
PubMed1976

A testosterone-producing adrenal cortical adenoma in an elderly woman.

A 76-year-old woman with virilization had menopausal levels of circulating LH and FSH, and a markedly elevated concentration of plasma testosterone (9130 pg/ml) into the range for adult men. Plasma cortisol and androstenedione levels andurinary 17-ketosteroid secretion were normal. Ethinyl estradiol suppressed plasma testosterone, LH, and FSH levels into the normal range for premenopausal women, but the testosterone concentration was unaffected by the administration of dexamethasone or ACTH. Retrograde venous sampling and angiography localized a right adrenal adenoma preoperatively. Following adrenalectomy, there was a prompt fall in testosterone, but there was no change in the LH concentration. Thus, this patient had an adrenal adenoma which secreted only testosterone and appeared to be gonadotropin-responsive. Testosterone levels in the adult male range failed to suppress gonadotropins. The significance of these findings is discussed.

Adenoma↗
PubMed1976

Serum 17 beta-estradiol and estrone levels in postmenopausal women with and without endometrial cancer.

Serum 17 beta-estradiol (E2) and estrone (E1) levels were measured before and 6-8 weeks after ovariectomy in 16 postmenopausal women with endometrial cancer, and in 10 postmenopausal women with normal endometrium (preovariectomy only). For E2, no significant difference in the mean baseline (+/-SE) level was found between the tumor (13.5 +/- 1.1 pg/ml) and non-tumor patients (11.7 +/- 1.4 pg/ml). For the same patients, the mean baseline E1 levels of 33.8 +/- 2.4 pg/ml and 28.5 +/- 4.7 pg/ml were also not significantly different. The mean body weight of the tumor patients (141.1 +/- 7.3 lbs.) was similar to the mean weight of the non-tumor subjects (137.5 +/- 6.3 lbs.). This was of importance since both E2 and E1 levels correlated significantly with body weight and excess fat in these postmenopausal women. The circulating estrogen levels did not correlate significantly with the patients' height, age, or years of menopause. In the patients with endometrial cancer the mean E2 (14.1 +/- 1.7 pg/ml) and E1 (39.5 +/- 7.3 pg/ml) levels after ovariectomy were not significantly different from the preoperative concentrations. These data are consistent with the concept that in postmenopausal women most, if not all, circulating estrogen is produced by peripheral conversion of androgens and that this conversion is influenced by obesity. Circulating estrogen levels are not significantly different in postmenopausal patients with endometrial cancer compared with women of a similar age and weight who do not have the tumor.

Adenocarcinoma↗
PubMed1976

The effects of ovarian wedge resection on circulating gonadotropin and ovarian steroid levels in patients with polycystic ovary syndrome.

Serum gonadotropin, estrogen, and androgen levels were measured daily before and up to 35 days after surgery in 8 patients with polycystic ovary syndrome (PCO) undergoing ovarian wedge resection (WR). To serve as controls, similar assessments were made in 5 women having hysterectomies for non-ovarian disease during the early follicular phases of their cycles. Preoperatively, LH but not FHS, estrone (E1) but not estradiol 17 beta (E2), and both androstenedione (delta) and testosterone (T) levels were higher in the PCO patients than in the normal women. In the PCO patients, surgery had no discernible effect on FSH levels. In the 5 PCO patients who apparently ovulated after WR, LH levels did not fluctuate significantly until the midcycle LH peaks occurred 13-25 days after surgery. In the 3 patients who did not ovulate, there was a transient fall of LH, which reached a nadir on the sixteenth postoperative day and then returned to preoperative levels. In the total PCO group there was a significant fall of E1 (P less than 0.05) and a decrease of E2, which reached nadirs on the third postoperative day. Preovulatory rises of both E1 and E2 were seen only in patients who ovulated following WR. For the androgens, significant decreases (P less than 0.05) of both T and delta were seen during the first 3 days after WR. These were followed by steady increases of both androgens back to preoperative levels. Delta levels remained elevated while T concentrations fell again and were significantly lower (P less than 0.005) at the end of the sampling period than preoperatively. This pattern was seen whether the patients did or did not ovulate. Except for a small transitory fall of androgens, surgery had no discernible effect on the circulating levels of any of the hormones in the control subjects. These results show that in PCO patients, ovarian WR is followed by a profound, temporary reduction of ovarian delta secretion and a persistent reduction of T secretion. Smaller, but significant, decreases of estrogen production were also observed. The mechanism responsible for ovulation following WR appears to be local (intra-ovarian) rather than central since the alterations in ovarian hormone secretion had no discernible effect on circulating gonadotropin levels prior to the onset of midcycle surges.

Adult↗
PubMed1976

Amniotic fluid testosterone levels in midpregnancy.

Amniotic fluid testosterone levels were measured on specimens obtained between 12 and 25 weeks' gestation from 58 male-fetus and 77 female-fetus pregnancies. For the male fetuses the mean +/- SE amniotic fluid testosterone level of 223 +/- 10 pg/ml was significantly higher (P less than 0.001) than the concentration found for the female fetuses (40 +/- 2 pg/ml). The ranges were 104-424 and 18-82 pg/ml, respectively, for the same fetuses. In the male fetuses the highest mean level was found during the 17th gestational week, but the mean level observed during any 1 week was not significantly differenf from any other week for both sexes. These data are consistent with the concept that amniotic fluid testosterone levels may be a rapid and effective method for establishing fetal sex in utero during midgestation.

Amniotic Fluid↗
PubMed1975

Circulating gonadotropins, estrogens, and androgens in polycystic ovarian disease.

Serum gonadotropin, estrogen, and androgen levels were measured in samples obtained from 19 patients with polycystic ovarian disease (PCO) and from 10 normal women on day 2 to 4 of their menstrual cycles. In patients with PCO, the mean (plus or minus S.E.) concentration was significantly higher (P smaller than 0.001) than the concentrations found in the normal subjects for LH (35 plus or minus 4.6 vs. 12.7 plus or minus 2.6 m.I.U. per milliliter), but not for FSH (10.3 plus or minus 0.7 vs. 8.7 plus or minus 0.9 m.I.U. per milliliter). Estrone (E1) levels (92 plus or minus 4 vs. 52 plus or minus 5 pg. per milliliter) were also significantly higher (P smaller than 0.001), while estradiol (E2) concentrations (58 plus or minus 4 vs. 63 plus or minus 8 pg. per milliliter) were comparable. Testosterone (T) (468 plus or minus 41 vs. 325 plus or minus 34 pg. per milliliter, P smaller than 0.05), androstenedione (delta) (2,083 plus or minus 138 vs. 1,123 plus or minus 153 pg. per milliliter, P smaller than 0.001), and dehydroepiandrosterone sulfate (3.4 plus or minus 0.4 vs. 2.0 plus or minus 0.37 mug per milliliter, P smaller 0.02) were also significantly increased over the values in normal controls. The mean dehydroepiandrosterone (DHEA) was elevated in the patients with PCO (11.3 plus or minus 1.7 vs. 7.5 plus or minus 1.2 mug per milliliter), but was not significantly different. A positive correlation was found between LH levels and both E2 and E1 concentrations in the patients with PCO. These data show a distinct profile of gonadotropin, estrogen, and androgen levels in patients with PCO.

Adolescent↗
PubMed1975

Pubertal sleep-wake patterns of episodic LH, FSH and testosterone release in twin boys.

On 2 consecutive nights, plasma LH, FSH and testosterone (T) were measured every20 min for 12 h during evening wakefulness and polygraphic sleep in 5 pairs of male monozygotic twins in pubertal stages 1-4, and in a male dizygotic also studied in 3 twins. During sleep, significant enhancement of episodic LH release was seen on 16 of 18 nights on the stage 1-4 twins. During wakefulness, minimal episodic LH release was observed in the stage 1-3 twins, which then gradually increased in the more mature twins, until finally the significant sleep-wake difference in mean LH was lost in the stage 5 male. Testosterone also rose significantly in sleep on 19 of 20 study nights in the stage 1-5 twins. In the early pubertal twins this nocturnal rise in T was small, but in the midpubertal pairs it was profound, as peaks in T occurred which lay in the normal range for adult males. In these less mature twins the majority of the episodic secretion of T also was limited to sleep. In wakefulness, the T levels gradually increased across puberty until, in the stage 5 twin, wakeful peaks in T finally reached the adult male range. In the midpubertal twins, a close temporal relationship was seen between initiation of sleep-enhanced LH release and the subsequent initial rise in T (mean lag time 29.1 min). In the stage 5 twin, this episodic LH-T relationship persisted into wakefulness where the largest increments in T were seen just prior to sleep onset. Evidence of sleep-enhanced FSH release was more equivocal, and was limited mainly to pubertal stage 1 and 3 pairs. Similarities in hormonal patterns were seen within the monozygotic twin pairs and probably contributed to the parallel progress in puberty of the pair. Thus, sleep-wake rhythmicity in release of gonadotropins, particularly LH and thereby of testosterone, was seen to evolve transiently in twin boys across puberty. The existence of such rhythmicity suggests that a fundamental, sleep-entrained CNS mechanism plays an important, if not a dominant, role in sexual maturation in boys.

Adolescent↗