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Biomedical subjects

I M Spitz

Publications and source records attributed to I M Spitz.

At least 109 records · Page 6Linked to original sources
PubMed1978

Gonadotrophin, thyrotrophin and prolactin reserve in beta thalassaemia.

Gonadotrophin (Gn), thyrotrophin (TSH) and prolactin (PRL) reserve was evaluated in patients (aged 12-26 years old) with beta thalassaemia. Abnormalities were detected in Gn reserve only. When compared with young adult controls, three of the four female patients and one of the two adult males had markedly impaired Gn responses to LH-releasing hormone (LHRH). Of the five prepubertal males, one had no Gn rise following LHRH, while responses in the other four patients were comparable to those in boys with delayed puberty. Only one adult male had an exaggerated LH response to LHRH. TSH and PRL dynamics were normal. No correlation could be found between the severity of the disturbance in the gonadal axis and the total number of blood transfusions. Our findings correlate best with the severity of the disease process itself.

Adolescent↗
PubMed1978

Induction of spermatogenesis in hypogonadotrophic hypogonadism.

A young male who presented with isolated bihormonal gonadotrophin deficiency is described, Basal levels of LH and FSH were low and there was no response to clomiphene citrate or LHRH. The remaining anterior pituitary function was intact. The administration of a combination of human menopausal gonadotrophin and human chorionic gonadotrophin caused testicular maturation with spermatogenesis and full androgenization. The patient was able to father a child.

Adult↗
PubMed1978

Pituitary insufficiency following head injury.

A 32-year-old man developed panhypopituitarism and diabetes insipidus shortly after sustaining a head injury. Hormonal investigation showed that basal prolactin levels were moderately elevated the first two years after the accident, but later returned to normal. There was no rise in prolactin after administration on chlorpromazine, and the response to thyrotropin-releasing hormone was attenuated. Basal luteinizing hormone and follicle-stimulating hormone levels were low and there was no change after administration of luteinizing-hormone-releasing hormone. There was also no growth hormone elevation following arginine infusion. On the other hand, there was a normal but delayed elevation of thyrotropin in response to thyrotropin-releasing hormone. Appropriate stimulation tests showed normal responsiveness of the thyroid, adrenals and testes. These findings are compatible with an injury to the pituitary stalk, damaging the neurohypophyseal tract and affecting the blood supply to the pituitary gland.

Adolescent↗
PubMed1978

Failure of bromocriptine to suppress prolactin in majeptil-induced hyperprolactinemia.

A case of hyperprolactinemic anovulation with amenorrhea and galactorrhea, due to Phenothizine derivative (Majeptil) is presented. Treatment with bromocriptine, 2.5 mg b.i.d., p.o., or L-Dopa, 500 mg, p.o., did not suppress serum prolactin and menstrual cycle was not resumed. Pituitary prolactin response to TRH and Pituitary LH and FSH response to LHRH were found to be normal. It seems that at the dose used, bromocriptine (a dopaminergic agonist) cannot counteract the phenothiazine induced hyperprolactinemia. Hence, it is not effective in induction of ovulation while the patient is under phenothiazine treatment.

Adult↗
PubMed1977

Diminished prolactin reserve: a case report.

A 17 year old male patient presented with short stature and delayed puberty. Investigations showed normal thyroid function and intact TSH response to TSH-releasing hormone (TRH). Although basal levels of LH were low, both LH and FSH rose following the administration of LH-releasing hormone (LHRH). ACTH secretion assessed indirectly by the cortisol response to insulin hypoglycemia was normal. Growth hormone levels increased following the onset of sleep, as well as after the administration of insulin, L-dopa and L-arginine. Basal levels of prolactin were low (2-5 ng/ml) compared with 5-12 ng/ml in controls. There was a markedly impaired prolactin response to TRH (maximum rise above basal values of 3 ng/ml compared to a rise of 12-29 ng/ml in controls). Prolactin levels did not rise after the administration of chlorpromazine or L-arginine. There was some suppression of prolactin levels after L-dopa. Similar patterns of prolactin are seen in panhypopituitarism, where they are usually associated with other hypophyseal hormonal deficiencies. The diminished prolactin reserve demonstrated in this subject in the presence of intact function of the remainder of the anterior pituitary is compatible with the diagnosis of diminished prolactin reserve.

Adolescent↗
PubMed1977

Dissociation of prolactin responsiveness to TRH and chlorpromazine in women with isolated gonadotropin deficiency.

The hormonal response to luteinizing hormone releasing hormone (LHRH) thyrotropin releasing hormone (TRH) and chlorpromazine has been evaluated in eleven female subjects with the syndrome of isolated bihormonal gonadotropin deficiency (IGD). Following LHRH, all subjects had elevations of both LH and FSH, but the gonadotropin responses were attenuated relative to those observed in normal female subjects studied in the early proliferative phase of the cycle. Similarly, peak TSH levels after TRH were significantly less in subjects with IGD relative to normal controls. Basal prolactin levels were low in the patient group. Prolactin levels following TRH increased at least two-fold in control subjects and in the group with IGD. Conversely, chlorpromazine failed to induce elevations of prolactin in eight of nine females with IGD.

Adult↗
PubMed1977

Hormonal response to exogenous luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in pregnancy and puerperium.

Luteinizing hormone-releasing hormone (LH-RH) and thyrotropin-releasing hormone (TRH) were injected into five women in the last month of pregnancy and three women in the postpartum period. In seven of the women, follicle-stimualating hormone (FSH) levels were at the limit of sensitivity of the assay and there was no response to LH-RH. One postpartum subject tested three weeks after delivery did show an FSH response to LH-RH. The thyrotropin response to TRH was within normal limits. When compared with control subjects, the pregnant and puerperal women had elevated basal levels of prolactin and an exaggerated response to TRH. Growth hormone levels were low and there was an inconsistent response to the administration of the releasing hormones. These results indicate that in pregnancy the thyrotroph and lactotroph are responsive to stimulation, whereas the gonadotroph is suppressed.

Adult↗
PubMed1977

Isolated hypogonadotropic hypogonadism: induction of ovulation with exogenous gonadotropins.

Six patients with all of the clinical and laboratory characteristics of isolated hypogonadotropic hypogonadism (bihormonal gonadotropin deficiency) were treated with human menopausal gonadotropins (hMG, Pergonal) and human chorionic gonadotropin (hCG). Of a total of 37 courses of treatment administered, there was evidence of ovulation in 32 (29%). The first four subjects had a total of six pregnancies in 13 treatment cycles. In the remaining two subjects, there were abnormalities in the seminal fluid of both husbands and, as a consequence, only one patient conceived. The average dose and duration of hMG therapy was 3310 IU (44 ampules), administered for 13 days. A wide range of hCG dosage was used to induce ovulation, but three subjects conceived following 5000 IU of hCG on 2 successive days. None of our subjects developed any evidence of the hyperstimulation syndrome, and there was only one instance of twin birth. Serial determinations of hLH performed during hMG therapy were lower than those noted during the normal follicular phase. In contrast, hFSH levels were in the normal follicular phase range. the high success rate in these subjects indicates that the prognosis for inducing ovulation in patients with hypogonadotropic hypogonadism is good.

Adult↗