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Biomedical subjects

H M Heshmati

Publications and source records attributed to H M Heshmati.

69 records · Page 4Linked to original sources

[Recent advances in hormonal detection of pituitary somatotropic adenomas (author's transl)].

The primary role of either the hypothalamus or pituitary in the origin of acromegaly has still to be determined, but some interesting progress has been made in the hormonal detection of pituitary somatotropic adenomas over recent years. The most valid explorations remain assays of basal GH and somatomedin levels, and the absence of blocking of GH by glucose. Abnormal and/or paradoxical responses to certain dynamic tests are seen with variable frequency: stimulation of GH by TRH (62.9 p. cent), or by LH-RH (35.9 p. cent), and bromocriptive blocking (70.8 p. cent). These findings could be of diagnostic value in the rare cases when the results of biological tests are inconclusive (basal GH levels normal, apparent persistence of the GH nycterohemeral cycle, or even blocking of GM by glucose). Other tests of stimulation or blocking proposed for the investigation of acromegaly are reviewed, but these are non-specific, non-reproducible, and give unreliable results.

Acromegaly↗

[Recent advances in post-therapeutic hormonal surveillance of prolactin adenomas (author's transl)].

Therapeutic results in 80 cases of pituitary prolactin adenomas, grouped according to Hardy's neurosurgical classification, are discussed as a function of the 5 types of treatment administered. These were: selective adenomectomy by the trans-sphenoidal approach under microscopic supervision; bromocriptine usually at doses of 5 to 7.5 mg per day; combined surgery and radiotherapy (50 to 60 grays 5 times per week for 5 to 6 weeks); surgery plus bromocriptine; surgery plus radiotherapy plus bromocriptine. Selective adenomectomy gives excellent results in stages 1 and 2, if performed by an experienced surgeon. Bromocriptine was remarkably effective in all cases, whatever the level of blood prolactin and the size of the adenoma. Prolactin levels never returned to normal after radiotherapy, which also markedly increased the frequency of post-therapeutic hormonal insufficiencies.

Adenoma↗

[Interference of meprobamate with adrenal hormone assays (author's transl)].

The authors draw attention to the fact that the decrease in 17-hydroxycorticosteroids and 17-ketosteroids observed in patients under meprobamate treatment is probably due to chemical interference with assay methods, since normal response to metyrapone indicates that the adrenal function is unimpaired. The asthenia usually reported by these patients is due to depression and should not be blamed on deficiency of the adrenal cortex.

Adrenal Cortex Hormones↗

[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)].

Twelve cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general) are reported. It is suggested that: 1 - Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a patent hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2 - Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3 - The hyperlipidemia can be familial or can result from growth hormone deficiency alone.

Adult↗

[Adrenocortical function in hyperprolactinemia. The study of glucocorticoids, mineralocorticoids and androgens in chronic and acute hyperprolactinemias (author's transl)].

Glucocorticoids, mineralocorticoids, and adrenal androgens were studied in 3 groups of patients: control subjects (group I), hyperprolactinemic subjects (group II) and miscellaneous patients including chromophobe adenomas and normalized hyperprolactinemic subjects treated with Bromocriptine (group III). All the patients were studied in the basal state and under various conditions: Metyrapone, ACTH, TRH for glucocorticoids, ACTH, TRH, saline perfusion for mineralocorticoids, ACTH and TRH for androgens. It is concluded that: the adrenal secretion of glucocorticoids, mineralocorticoids and androgens is not altered under basal conditions in chronic hyperprolactinemia nor during dynamic tests in chronic hyperprolactinemia (prolactin adenoma) nor in acute hyperprolactinemia (induced by TRH).

Acute Disease↗

[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)].

A serie of 12 cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general), is reported. It is suggested that: 1--Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a manifesting hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2--Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3--The hyperlipidemia can be familial or can result from growth hormone deficiency alone.

Adult↗

[Longitudinal study of 18 cases of prolactin adenoma. Therapeutic results (author's transl)].

Complete endocrinological studies were made before and after surgery in 18 cases of prolactin adenoma (2 giant adenomas and 16 macro-adenomas). Certain points are stressed: the frequency of the haemorrhagic nature of the adenoma in 4 cases, including 1 case of spontaneous necrosis; the great variability in dynamic responses to the TRH stimulation test or inhibition by I-Dopa; the persistence in 14 cases out of 16 of postoperative hyperproclactinaemia, requiring the prescription of 5 to 10 mg/day of bromocriptine, rarely more; the disappearance of total impotence in two male cases as a result of the latter drug, whilst testerone and dihydrotestosterone levels were normal before the beginning of medical treatment.

Adenoma↗

Prognostic value of suppressed thyrotropin level and positive thyrotropin-receptor antibody activity in Graves' disease with long-lasting clinical remission.

OBJECTIVE: To determine the prognostic value of suppressed thyrotropin (TSH) level and positive TSH-receptor antibodies (TSH-R Ab) in patients with Graves' disease who have long-lasting clinical remission. METHODS: We retrospectively studied patients with Graves' disease who underwent follow-up for a mean of 55 months after the withdrawal of antithyroid drug treatment. Study patients were 84 consecutive subjects in clinical remission, with normal serum free thyroxine (FT(4)) and free triiodothyronine (FT(3)) levels, regardless of serum TSH levels, a mean of 35 months (range, 6 to 135) after discontinuation of carbimazole therapy. Eighty-seven euthyroid subjects were used as control study participants. All subjects had serum determinations of FT(4) and FT(3) (radioimmunoassay), TSH (highly sensitive immunoradiometric method), TSH-R Ab (radioreceptor assay), and microsomal antibodies (M Ab, passive hemagglutination method). RESULTS: In the study patients, serum TSH was suppressed (</=0.10 mU/L) in 13 cases (15%), TSH-R Ab were positive (>/=15%) in 11 cases (13%), and M Ab were positive (>/=1:100) in 54 cases (64%). Simultaneous suppressed TSH and positive TSH-R Ab levels were present in six patients. During the follow-up, 11 patients had a relapse, demonstrated by above-normal values for serum FT(4) and FT(3) in association with clinical symptoms of hyperthyroidism. Five of them had a previously suppressed TSH level, three had a positive TSH-R Ab level, and six had a positive M Ab titer. Relapse was significantly more likely in patients with a previously suppressed TSH level (P<0.02) but not in patients with a previously positive TSH-R Ab level or positive M Ab titer. CONCLUSION: Patients with Graves' disease and long-lasting clinical remission after discontinuation of carbimazole therapy may have a suppressed TSH level, a positive TSH-R Ab level, or a positive M Ab titer (or some combination of these findings). Although positive TSH-R Ab and M Ab have no significant prognostic value, a suppressed TSH level is indicative of subclinical hyperthyroidism and higher risk of relapse.

Journal Article↗

[The study of the influence of prolactin on gonadal steroids metabolism by the human chorionic gonadotropin test. Plasma and urinary determinations in 27 subjects (control, hyperprolactinemic, normoprolactinemic but hypogonadic subjects) (author's transl)].

In order to determine whether hyperprolactinemia besides its action at the hypothalamic level, acts at the gonadal level, a serie of 28 stimulations by Human Chorionic Gonadotropin (HCG : 5 000 IU X 3) is reported. The following parameters were measured in plasma and in urine before and during 4 consecutive days following the injection of HCG : Progesterone (P), 17 OH Progestérone (17 OHP), Androstenedione (A), Testostérone (T), Dihydrotesterone (DHT), Estrone (E1), 17 beta estradiol (E2), Urinary Androstanediol (Adiol) Testosterone Glucuronide (G.T.) and phenolsteroids (PS). The test was performed in both sex, in 3 different groups including normal, hyperprolactinemic and normoprolactinemic but hypogonadic subjects (hypopituitarism). These data suggest that in hyperprolactinemic subjects: there is no steroid 5 alpha reductase abnormality in male patients, and there is no gonadal resistance to HCG stimulation in both sex, at least to the high doses of HCG used in this study.

Chorionic Gonadotropin↗

[Determination of 6 pituitary hormones in the cerebrospinal fluid. Control subjects, prolactin adenomas, empty sella syndrome and hypothalamic disorders (author's transl)].

Cerebrospinal fluid (CSF) and serum concentrations of TSH, ACTH, FSH, LH, GH and PRL were measured simultaneously in 34 subjects divided into 3 groups: I-12 normal subjects (6 males and 6 females); II-12 prolactin adenomas (3 males and 9 females); III-5 empty sella syndromes, 3 hypothalamic disorders, 1 chromophobe adenoma, 1 pituitary dwarfism. It is concluded that: 1) pituitary hormones are the normal constituents of CSF but the level can be undetectable and in any case lower than the serum level. 2) there is a positive correlation between serum and CSF concentration of PRL when serum PRL is higher than 20 ng/ml, indicating that the CSF level is influenced by serum level. 3) in prolactin adenomas, only prolactin is elevated in the CSF. 4) there is no correlation between the high level of CSF-PRL and a suprasellar extension of the adenoma.

Adenoma↗

[Determination of pituitary hormones in cerebrospinal fluid in normal subjects and in hypothalamo-pituitary diseases. Secreting or non-secreting pituitary adenoma, empty sella syndrome, hypothalamic syndromes].

Cerebrospinal fluid (CSF) and serum concentrations of TSH, ACTH, FSH, LH, GH and PRL were measured simultaneously in 34 subjects divided into 3 groups: I--12 normal subjects (6 males and 6 females); II--12 prolactin adenomas (3 males and 9 females); III--5 empty sella syndromes; 3 hypothalamic disorders; 1 chromophobe adenoma; 1 pituitary dwarfism. It is concluded that:--pituitary hormones are the normal constituents of CSF but the level can be undetectable and in any case lower than the serum level; --there is a positive correlation between serum and CSF concentration of PRL when serum PRL is higher than 20 ng/ml, indicating that the CSF level is influenced by serum level; --in prolactin adenomas only prolactin is elevated in the CSF; --there is no correlation between the high level of CSF-PRL and a suprasellar extension of the adenoma.

Adenoma↗