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Biomedical subjects

I M Spitz

Publications and source records attributed to I M Spitz.

At least 91 records · Page 5Linked to original sources
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

Diminished prolactin reserve in acromegaly.

Prolactin (PRL) secretion has been evaluated in twenty acromegalic patients. All had intact LH, FSH, and cortisol levels and normal thyroid function. Five patients had persistent hyperprolactinemia. The remainder had decreased basal PRL levels with impaired PRL responses to TRH and the dopaminergic antagonist metoclopramide (MET). Despite adequate hypoglycemia and an intact cortisol response, there was no PRL rise following insulin hypoglycemia. The imparied PRL response to TRH was evident in treated and untreated patients and was independent of GH levels. Basal hyperprolactinemia may be related to PRL secretion by the tumor cells or interference with the transport of PIF by the tumor. The decreased PRL reserve noted in the majority of the patients may be related to a decrease in lactotrope cell mass or, alternatively, to enhanced dopaminergic activity.

Acromegaly↗
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↗
PubMed1980

The hypothalamic-pituitary axis in diabetes mellitus.

The hormonal response to LHRH and TRH was evaluated in three groups of male diaetics. Five patients were receiving therapy with the hypoglycemic agent glibenclamide, five were on NPH insulin and five were on dietary therapy alone. When compared to controls, the latter two groups had intact gonadotropin responses to LHRH. Despite normal basal gonadotropin levels, however, the group receiving glibenclamide therapy showed significantly exaggerated LH and FSH responses to LHRH. Both basal PRL and TSH levels, as well as the responses to TRH were normal in all three groups. These results indicate that LH, FSH, TSH and PRL secretion is intact in uncomplicated diabetes mellitus. The exaggerated LH and FSH responses to LHRH in the glibenclamide treated subjects are probably related to primary gonadal involvement; alternatively, there may be augmented pituitary gonadotropin secretion in this group.

Adult↗
PubMed1980

Multiple abnormalities of anterior pituitary hormone secretion in association with pseudohypoparathyroidism.

A male with pseudohypoparathyroidism presented with several hormonal abnormalities. He was clinically euthyroid with no palpable goiter, His serum T4, total T3, T3 Sephadex retention, and 131I uptake were normal. However, elevated basal TSH levels and exaggerated TSH responses to TRH which normalized during the administration of thyroid extract suggested reduced thyroidal reserve. Despite these finding the 131I uptake increased after exogeneous TSH, and the T3 level rose after TRH. Basal testosterone levels and response to hCG were normal however, gonadotropins were elevated and there was an exaggerated response after LRH treatment. Both LH and FSH levels were suppressed by testosterone propionate. The patient demonstrated intermittent basal hyperprolactinemia and impaired PRL responsiveness after metolopramide, chlorpromazine, and insulin administration. There was, however, an intact response to TRH. Basal PRL, TSH, and LH levels decreased after the administration of L-dopa and bromocriptine. Although the precise mechanism underlying these finding is unknown, the elevated basal levels of TSH, LH, and FSH and the exaggerated responses to their respective releasing hormones suggest the presence of partial degree of end-organ resistance to these pituitary trophic hormones. Together with the resistance to PTH, this may imply a common defect, presumably at a postreceptor level. However, hyporesponsiveness of PRL to metoclopramide and chlorpromazine and normal responsiveness to TRH suggest that an abnormality of dopamine tone also exists in pseudohypoparathyroidism.

Adolescent↗
PubMed1980

Acid-induced gastric inhibitory polypeptide secretion in man.

This study has assessed the effect of oral or intraduodenal HCl, administered alone or in combination with glucose, on gastric inhibitory polypeptide (GIP) and insulin secretion. Eight young males were given the following three oral tests: 30 g glucose, 150 cc 0.1 N HCl and the glucose-acid combination. Another group of eight controls received intraduodenal infusions of 20 g glucose, 75 cc 0.1 N HCl and their combination. All tests were performed in a random fashion at weekly intervals. When given alone, HCl did not influence glucose or insulin levels. However, HCl did produce an increase in GIP. The GIP response to acid was less than that to glucose and was delayed. The peak insulin and GIP responses with the glucose and glucose/acid combinations were similar with both the oral and intraduodenal routes. There was, however, a potentiation of both the GIP and insulin responses when intraduodenal acid was given with glucose. This effect on GIP and insulin was not evident with the oral glucose/acid load. It is concluded that HCl by itself is capable of stimulating GIP secretion. Since there was only a potentiation of insulin and GIP secretion when large doses of HCl were given together with glucose via the intraduodenal route, the physiological relevance of acid-induced GIP secretion remains to be resolved.

Administration, Oral↗
PubMed1980

Dissociation of pituitary glycoprotein response to releasing hormones in chronic renal failure.

The LH, FSH and TSH response to LRH and TRH has been evaluated in patients with chronic renal failure. Basal gonadotrophins were elevated in 3 out of 6 males; one of 4 pre-menopausal females had increased basal LH. Exaggerated LH responses to LRH were noted in 4 out of 6 males and one of 4 females; FSH reponses were increased in 3 of these males. One male and one female had attenuated LH and FSH responses to LRH. Both testosterone and oestradiol levels were reduced. In 5 out of 6 subjects tested both pre- and post-dialysis there was a greater LH and FSH response to LRH following dialysis. This suggests the presence of a dialysable toxin which is inhibiting the gonadotrophin response to LRH. Gonadotrophin levels remained elevated during 4 h of dialysis suggesting prolongation of the metabolic clearance rate. Despite low T3 levels, TSH response to TRH (200 microgram) was only elicited in 2 of 6 cases. However, all 3 responded to 500 microgram and 2 out of 3 to 1000 microgram TRH, the third showing an attenuated response. TSH levels also remained persistently elevated in the responders. Dialysis however, failed to improve the relative TSH non-responsiveness to TRH. In conclusion the data has shown that there is a dissociation in glycoprotein hormone responses to releasing hormones in ureamia. Whereas the gonadotrophs retain their responsiveness to LRH, the thyrotrophs appear to be more effected by the uraemic process and demonstrate an impaired response to TRH.

Adult↗
PubMed1980

Hypothalamic-pituitary function in the Bardet-Biedl syndrome.

Four siblings with classic Bardet-Biedl syndrome were studied. The brother had hypogonadism of testiculr origin, with high gonadotropin levels and exaggerated responses to luteinizing-hormone-releasing hormone, whereas the three sisters showed a normal hypothalamic-pituitary-gonadal axis. The remaining pituitary hormone function was intact.

Adolescent↗
PubMed1979

Atropine suppression of basal and metoclopramide-induced human pancreatic polypeptide secretion in man.

The administration of metoclopramide (MET) increased human pancreatic polypeptide (hPP) levels in 17 of 18 male and female control subjects. In all the control subjects, the increase was from a mean (+/- SD) basal level of 96 +/- 60 pg/ml, to a peak of 221 +/- 170 pg/ml. The peak occurred at 30 min, and levels had decreased by 60 min in all subjects. Atropine pretreatment in five male control subjects significantly decreased basal hPP levels and completely abolished the response to MET. It thus likely that the hPP increase consequent to MET administration is related to the latter's cholinergic properties.

Adult↗
PubMed1979

Hyperprolactinaemia and hypogonadism in men: response to exogenous gonadotrophins.

Three male patients with pituitary tumours and marked hyperprolactinaemia were investigated. Their prolactin (PRL) levels ranged from 210 to 2500 ng/ml. The subjects had clinical and laboratory characteristics of hypogonadotrophic hypogonadism. All were treated with human chorionic gonadotrophin (HCG) and in one subject human menopausal gonadotrophin (HMG) was given in addition. In all three patients, despite the persistence of hyperprolactinaemia, serum testosterone had risen to normal levels within 4--17 days after starting HCG. Despite the normal testosterone level, impotence persisted in two patients and the third had persistently decreased libido. The hypogonadism in these patients may be related to an absolute reduction in gonadotroph number secondary to destruction by tumour mass. Alternatively, hyperprolactinaemia may inhibit the synthesis or release of the gonadotrophins or LHRH. Despite hyperprolactinaemia, pharmacological doses of HCG induced testosterone secretion in all these three subjects.

Adult↗
PubMed1979

Dissociation of prolactin response to thyrotropin-releasing hormone and metoclopramide in chronic renal failure.

PRL secretion was evaluated in 14 males with chronic renal failure on long term hemodialysis. Twelve had basal hyperprolactinemia. Ten subjects were challenged with TRH in doses ranging from 200--1000 micrograms. None of them responded to 200 or 500 micrograms TRH, although 2 of 4 subjects tested did respond to 1000 micrograms TRH. In contrast, all 4 subjects challenged with metoclopramide did have PRL responses which were indistinguishable from those of the controls. These results indicate that there is a dissociation in responsiveness to metoclopramide and TRH in chronic renal failure.

Adult↗
PubMed1979

Failure of metoclopramide to influence LH, FSH and TSH secretion or their responses to releasing hormones.

Intravenous metoclopramide (MET) (10 mg) induced a brisk PRL response with a mean +/- SEM peak of 85.3 +/- 7.7 ng/ml maximal at 30 min. L-Dopa, but not atropine pre-treatment, attenuated the prolactin (PRL) response to MET. This indicates that the antidopaminergic properties of MET mediate PRL secretion. MET did not influence basal levels of TSH, LH or FSH. Neither did it affect their response to the respective releasing of hormones. Our results indicate that dopaminergic blockade induced by iv MET, does not influence the secretion of the pituitary glycoprotein hormones.

Adolescent↗