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Biomedical subjects

R J Chang

Publications and source records attributed to R J Chang.

At least 73 records · Page 4Linked to original sources
PubMed1985

Lack of tumor reduction in hyperprolactinemic women with extrasellar macroadenomas treated with bromocriptine.

Three patients with hyperprolactinemia and large extrasellar pituitary macroadenomas were treated with bromocriptine, 10 mg daily, for 8 weeks. In spite of correction of their amenorrhea, galactorrhea, and hyperprolactinemia, radiologic evaluation by CT scan failed to show evidence of tumor shrinkage. After surgical resection, histologic examination revealed that PRL-secreting cells comprised only a small portion of the tumor cell population in two patients and in the third patient were completely absent. These cases illustrate that large nonfunctional pituitary tumors may mimic signs and symptoms of a prolactinoma and stress the importance of adequate radiologic evaluation during medical management.

Adenoma↗
PubMed1985

Nelson's syndrome in pregnancy.

A patient with Nelson's syndrome whose pregnancy was complicated by symptomatic enlargement of an ACTH-producing pituitary tumor was described. Emergency ablative surgery was performed with successful outcomes for both mother and infant.

Adenoma↗
PubMed1985

Bromocriptine as primary therapy for prolactin-secreting macroadenomas: results of a prospective multicenter study.

To assess the effectiveness of bromocriptine in reducing the size of PRL-secreting macroadenomas with extrasellar extension, we conducted a prospective multicenter trial in patients without prior radiotherapy, applying a standard protocol of treatment and tumor size evaluation. Basal serum PRL levels [1441 +/- 417 (+/- SEM) ng/ml for women; 3451 +/- 1111 ng/ml for men] fell in all patients and to 11% or less of basal values in all patients but 1. Normal PRL levels were reached in 18 of the 27 patients. In 13 patients (46%), tumor size was reduced by greater than 50%, in 5 patients (18%) by about 50%, and in 9 patients (36%) by approximately 10-25%. The extent of tumor size reduction did not correlate with basal PRL, nadir PRL, percent fall in PRL, or whether PRL levels reached normal. However, a reduction in PRL levels always preceded any detectable change in tumor size. In 19 patients, reduction in tumor size was evident by 6 weeks, but in the other 8, such reduction was not noted until the 6 month evaluation. In the 4 patients in whom bromocriptine was discontinued at the end of 1 yr, tumor reexpansion occurred in 3. Visual fields improved in 9 of the 10 patients in whom they were abnormal. Because of the excellent results found in most of the patients in this series, we suggest that therapy with bromocriptine should be considered as initial management for patients with PRL-secreting macroadenomas.

Adenoma↗
PubMed1985

Associated non-ovarian problems of polycystic ovarian disease: insulin resistance.

It is evident from our current knowledge that women with PCO exhibit hyperinsulinaemia and are insulin resistant. Nevertheless, it remains to be determined whether the relationship of androgen to insulin is one of cause or effect in this syndrome. Elucidation of this mechanism may permit identification of the role of hyperinsulinism in the genesis or pathophysiology of this disorder.

Androgens↗
PubMed1984

Pregnancy after bromocriptine-induced reduction of an extrasellar prolactin-secreting pituitary macroadenoma.

In patients with a large prolactin-secreting pituitary adenoma, a marked reduction in tumor size may be achieved with bromocriptine therapy. However, before consideration of pregnancy, surgical removal of the lesion usually is advised. A 36-year-old woman with a large extrasellar pituitary macroadenoma was treated with bromocriptine, 10 mg/day, which resulted in dramatic reduction of the tumor mass. Subsequently, she became pregnant and drug therapy was maintained throughout gestation. This case illustrates the use of bromocriptine in the management of large prolactin-secreting pituitary tumors and the necessity for adequate radiologic follow-up.

Adenoma↗
PubMed1984

The incidence of late-onset congenital adrenal hyperplasia due to 21-hydroxylase deficiency among hirsute women.

Late-onset congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a cause of hirsutism in adult women. Its reported frequency of occurrence in hirsute women has varied from 0-30%, but the number of patients studied was small. To establish the incidence of CAH, 83 unselected hirsute women were studied prospectively with a standard ACTH stimulation test. On the basis of an exaggerated response of serum 17 alpha-hydroxyprogesterone to ACTH, 1 patient with CAH was found, for an incidence of 1.2%. The 95% confidence limits for the incidence of CAH among hirsute women were 0% and 3.4%. Five of seven hirsute women without CAH whose serum 17 alpha-hydroxyprogesterone levels rose above 3 ng/ml in response to ACTH had simultaneous serum progesterone values consistent with recent ovulation. Since routine screening of all hirsute women by means of ACTH stimulation does not appear to be cost effective, reported cases of CAH were reviewed in order to discern potentially helpful clinical clues. Severe hirsutism, virilization, early onset of symptoms, short stature, familial occurrence, and regular menses were identified as the clinical characteristics associated with late-onset CAH.

17-alpha-Hydroxyprogesterone↗
PubMed1984

Stimulation of LH fragments with reduced bioactivity following GnRH agonist administration in women.

In eumenorrheic women with endometriosis and in oligo-amenorrheic women with polycystic ovarian disease (PCO), chronic administration of a long-acting GnRH agonist (GnRH-a) reduced the circulating concentrations of estrogens and androgens to levels similar to those of castrated women. The concommittant elevation of LH in both groups suggested that the measured immunoreactive LH had reduced bioactivity. In seven women with endometriosis, bioactive LH (BA LH) measured as the in-vitro secretion of testosterone by dispersed Leydig cells, was significantly (p less than 0.001) reduced from 10.8 +/- 1.2 (SEM) to 4.4 +/- 0.2 mIU/ml at the end of 28 days of GnRH-a therapy. In five women with PCO, BA LH decreased from 44.2 +/- 15.5 to 5.7 +/- 0.6 mIU/ml (p = 0.06). These changes of BA LH appeared to be responsible for the suppression of ovarian androgen secretion during GnRH-a treatment and in turn may have contributed to the profound decreases of estrogen production by reducing the amount of precursor androgen available for aromatization. Free alpha subunit levels increased simultaneously with the decrease of BA LH at the end of therapy, suggesting a post-receptor effect of GnRH-a. Beta subunit levels became undetectable. Cross-reaction of alpha subunit in the RIA for LH was sufficient to only partially account for the LH levels measured. On sephadex G-100 chromatography the excess immunoreactive material was detected at and immediately following the alpha subunit tracer. Further studies will be necessary to elucidate the chemical nature of the immunoreactive LH secreted during GnRH-a therapy.

Endometriosis↗
PubMed1984

Further delineation of hypothalamic dysfunction responsible for menopausal hot flashes.

An association exists between pulsatile LH release and hot flashes (HFs). To further delineate the hypothalamic mechanism(s) responsible for HF, the basal levels and pulsatile release of LH, FSH, estradiol, and estrone and the rate of occurrence of HFs (measured objectively) were evaluated in patients with a defect of GnRH secretion [isolated gonadotropin deficiency (IGD)], patients with abnormalities of afferent input to GnRH neurons [hypothalamic amenorrhea (HA)], and postmenopausal women with severe HFs. Patients with IGD had received estrogens, which were discontinued before study. Patients with HA had experienced regular menses before disease onset, which followed emotional stress or weight loss. Studies were limited to HA patients with estrogen levels in the postmenopausal range. Pulsatile LH release was absent in patients with IGD and was absent or greatly reduced in women with HA. Objectively measured and subjectively experienced HFs occurred in IGD but not in HA patients. These results suggest that HFs are not an obligatory consequence of low endogenous estrogen levels and that the absence of episodic LH and GnRH release (IGD) does not influence the occurrence of HFs. It is possible that the dysfunction of afferent input to GnRH neurons in HA somehow prevents HFs in these women with low endogenous estrogen secretion.

Adult↗
PubMed1984

Origin of serum progestins in polycystic ovarian disease.

The glandular origin of excess circulating steroid hormones in women with polycystic ovarian disease has been difficult to establish with previously described perturbation techniques. Recently it was demonstrated that daily administration of a potent gonadotropin-releasing hormone agonist achieves complete and reversible suppression of ovarian steroid secretion. To examine the source of C-21 steroid hormones, circulating levels were measured before and after administration of the same agonist in polycystic ovarian disease subjects and normal control subjects. Serum levels of these hormones were also determined after administration of dexamethasone and adrenocorticotropic hormone (ACTH) as well as bilateral oophorectomy. Subjects with polycystic ovarian disease exhibited significant elevations of serum pregnenolone, 17OH -pregnenolone, and 17OH -progesterone by comparison with normal control subjects. The glandular origins of the excess levels of pregnenolone and 17OH -pregnenolone were more difficult to determine and appear to be different from that of 17OH -progesterone.

17-alpha-Hydroxypregnenolone↗
PubMed1983

Comparison of dopamine agonists in the treatment of hyperprolactinemic syndromes: a multicenter study.

Thirty-one patients with hyperprolactinemia were admitted for protocol study. Twenty-one of these patients had no findings of prolactinoma by computerized axial tomography (CAT) scanning; 10 had documented tumor by CAT scan. The patients were assigned to either Parlodel or Pergolide treatment on the basis of random numbers tables. They were treated for 6 months continuously and followed during this time with radiologic survey, hormonal evaluation, and blood chemistry determinations. Patients in both groups showed a decrease in prolactin levels, whether they were treated with Parlodel or Pergolide. The response was similar whether patients had hyperplasia or pituitary tumors. Patients with pituitary tumors tended to have a diminution in the size of their lesions regardless of the dopamine agonist used. The types of side effects experienced by various groups were similar regardless of the treatment. It is concluded that both Pergolide and Parlodel are useful in the treatment of hyperprolactinemic syndromes, although neither one appears to be superior to the other.

Adolescent↗
PubMed1983

Effect of coumadin-induced coagulopoietin plasma on vitamin K-dependent carboxylation of liver microsomes.

Coumadin-treated rabbits have a humoral substance(s) (coagulopoietin) which is capable of elevating vitamin K-dependent coagulation factors when injected into recipient rabbits (Karpatkin & Karpatkin, 1973). Biologic levels of coagulation factors II, V, VII and X; immunologic levels of factors II and X; and vitamin K-dependent liver microsomal carboxylase activity were measured in recipient rabbits receiving coumadin-induced coagulopoietin plasma. Factor II biologic activity increased 3.5-fold compared to the increase in immunologic activity. Factor X biologic activity increased 1.7-fold compared to the increase in immunologic activity. This indicates an increase in specific activity of factors II and X. Coumadin-induced coagulopoietin plasma had no effect on vitamin K-dependent liver microsomal carboxylase activity in vitro. However, livers obtained from recipient animals treated with coumadin-induced coagulopoietin plasma enhanced their carboxylase activity (compared to control animals) 2.4-fold employing endogenous microsomal precursor for carboxylation, and 6.2-fold employing synthetic substrate, phe-leu-glu-glu-val. Thus, coumadin-induced coagulopoietin plasma enhances the biologic activity of vitamin K-dependent coagulation factors II, VII, and X as well as the ex vivo vitamin K-dependent carboxylase activity of liver microsomes.

Animals↗
PubMed1983

HLA genotyping in family members and patients with familial polycystic ovarian disease.

To determine whether the familial occurrence of polycystic ovarian disease (PCO) is related to the major histocompatibility complex (HLA), four families in whom at least two siblings had clinical evidence of disease were examined. The diagnosis of PCO was confirmed by increased serum testosterone, androstenedione, and LH levels compared to those in normal women. Elevated concentrations of dehydroepiandrosterone sulfate indicated excess adrenal androgen secretion. The result of HLA genotyping in the families studied demonstrate that PCO does not exhibit linkage to the HLA system.

Androgens↗
PubMed1983

Steroid secretion in polycystic ovarian disease after ovarian suppression by a long-acting gonadotropin-releasing hormone agonist.

The principal glandular source of increased serum androgens in polycystic ovarian disease (PCO) is controversial), since complete separation of ovarian from adrenal function has not been achieved. The purpose of this study was to determine whether a long-acting GnRH agonist could be used to selectively inhibit ovarian steroid secretion in PCO and ovulatory women. Each of five typical PCO patients and six ovulatory subjects on day 2 of their menstrual cycles received D-Trp6-Pro9-NEt-LHRH (GnRH-a; 100 micrograms) for 28 consecutive days. Their results were compared to basal serum hormone values in eight oophorectomized women. In response to GnRH-a, PCO and normal subjects exhibited sharp and sustained rises of LH and gradual decreases in FSH. These levels were clearly less than basal levels seen in oophorectomized women. Episodic LH release was significantly attenuated in both groups at the end of GnRH-a treatment. After the administration of agonist, serum estradiol (E2), estrone (E1), androstenedione (A), and testosterone (T) were suppressed to castrate levels in both groups. The decrements of E2 and E1 in PCO were gradual and continuous compared to initial dramatic rises, which reached peaks at 14 days, and subsequent abrupt falls in the ovulatory controls. Serum A and T declined steadily in both groups. Basal serum dehydroepiandrosterone and dehydroepiandrosterone sulfate, but not cortisol, levels were elevated in PCO subjects. The 24-h secretion patterns and responses to ACTH of these hormones in PCO and ovulatory subjects were unaltered by GnRH-a administration. These data demonstrate that 1) in PCO subjects, GnRH-a induced complete suppression of ovarian steroid secretion, as circulating levels at the end of treatment were comparable to those seen in our oophorectomy subjects; 2) elevated A and T levels in PCO patients were derived primarily from the ovary; and 3) adrenal steroid secretion was unaltered by GnRH-a in both PCO and normal women.

Adrenal Cortex Hormones↗
PubMed1983

Insulin resistance in nonobese patients with polycystic ovarian disease.

To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Mean serum testosterone (T), androstenedione (A), dehydroepiandrosterone (D), D sulfate, and LH levels were significantly elevated in the PCO patients compared to those in control subjects. In PCO patients, the mean +/- SE basal insulin level (18.7 +/- 2.9 microU/ml) and the sum of the insulin levels in response to glucose (674 +/- 119 microU/ml) were significantly greater than those in the control group (11.0 +/- 0.8 microU/ml and 248 +/- 29 microU/ml, respectively). In all subjects, serum levels of T and A, but not D and D sulfate, were significantly correlated to basal insulin levels and insulin sums. Serum cortisol, GH, and PRL levels were similar in both groups. These results indicate that in PCO, a significant degree of insulin resistance exists, which clearly is not related to obesity. The positive correlation of serum T and A levels to circulating insulin levels in this study suggests that the insulin resistance in PCO may be, in part, a consequence of hyperandrogenism.

Androstenedione↗
PubMed1982

Circadian pattern of prolactin secretion in postmenopausal women receiving estrogen with or without progestin.

The circadian rhythm of prolactin secretion was assessed in postmenopausal women before and after daily administration of ethinyl estradiol for 4 weeks given in the morning (AM) or evening (PM) or in combination with a synthetic progestin, 17-medroxyprogesterone acetate. In response to AM ethinyl estradiol, mean circulating levels of serum prolactin during sleep and awake phases of the day rose 2.5-fold compared to untreated control values. The sleep/wake ratios for serum prolactin were comparable prior to and after AM administration of ethinyl estradiol. Altered time of administration, PM ethinyl estradiol or concomitant ethinyl estradiol and progestin treatment produced similar increases in mean prolactin levels, which were not different from the level observed during AM administration of ethinyl estradiol. These findings indicate that estrogen replacement therapy, in a dosage recommended for treatment of the menopause, stimulated a sustained rise in serum prolactin over 24 hours. This enhanced release of prolactin was not influenced by the time of administration of estrogen or concomitant administration of 17-medroxyprogesterone acetate.

Circadian Rhythm↗
PubMed1982

Acute phase (C-reactive) protein-like macromolecules from rainbow trout (Salmo gairdneri).

A protein which reacts with the Cx-polysaccharide of Streptococcus pneumoniae and is inhibited by phosphorylcholine was isolated from the serum of rainbow trout by affinity chromatography. The protein, which exists in monomeric and oligomeric forms in non-immune trout serum, is very similar with regard to specificity and size to the Cx-reactive protein from rabbits. A semi-quantitative analytical method for evaluating bacterial agglutination with an electronic particle counter and size distribution analyzer was developed to compare natural and acute serum levels of trout and rabbit Cx-reactive proteins. Results indicate that the poikilotherm has much higher concentrations in normal serum. The trout serum protein can also be rapidly induced to yet higher levels by both chemical and physical stress. The implications for such a protein in the teleost's natural defense system and overall homeostasis are discussed.

Agglutination Tests↗