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Biomedical subjects

S Reichlin

Publications and source records attributed to S Reichlin.

At least 145 records · Page 8Linked to original sources
PubMed1981

Normal immunoregulation of in vitro antibody secretion in autoimmune thyroid disease.

Defective suppressor cell function may be a causative factor in autoimmune disease in animals and man. In autoimmune thyroid disease, decreased suppressor cell activity could, under appropriate conditions, account for excess production of thyroid autoantibodies. We evaluated suppressor cell function in patients with Graves' disease and Hashimoto's thyroiditis and in normal controls. The method used is based on the principle that immunoglobulin synthesis by pokeweed mitogen (PWM)-stimulated lymphocytes is inhibited by Concanavalin A (Con A) stimulation of suppressor T cells. We studied suppressor cell control of polyclonal immunoglobulin G (IgG) and the thyroid-specific autoantibody, antimicrosomal antibody. PWM-stimulated IgG secretion (mean +/- SD) by lymphocytes from patients with Graves' disease (2797 +/- 718 ng/ml) and Hashimoto's thyroiditis (2201 +/- 423 ng/ml) did not differ from normal subjects (2431 +/- 485 ng/ml). The addition of Con A to PWM-stimulated lymphocytes suppressed IgG production in all three groups: Graves', 475 +/- 137 ng/ml; Hashimoto's, 507 +/- 74 ng/ml; and normal subjects, 460 +/- 156 ng/ml. The degree of suppression by the disease groups did not differ from the normal controls. Antimicrosomal antibody was detected in the concentrated, PWM-stimulated culture media of two of four Hashimoto's lymphocytes, three of five Graves' lymphocytes, and none of nine normal controls. Con A induced marked suppression of this organ-specific antibody in all cases. We conclude that Con A-stimulated lymphocytes from patients with Hashimoto's thyroiditis and Graves' disease can suppress antimicrosomal antibody and polyclonal IgG synthesis. These findings do not support the postulate of a generalized defect of suppressor cell function in these thyroid disorders.

Adult↗
PubMed1981

Precocious puberty and hypothalamic hamartoma.

A 3-year-old boy with true precocious puberty and hamartoma of the hypothalamus is described. Preliminary diagnosis was established by the presence of unusually advanced puberty and skeletal age without other evidence of central nervous system dysfunction, elevated blood gonadotropin and testosterone concentrations, and positive computed tomography scans. Pneumoencephalography further delineated the tumor. Hypothalamic-pituitary-gonadal and adrenal functions were studied. Release of gonadotropins after the injection of synthetic luteinizing hormone-releasing hormone and the suppression of luteinizing hormone and of testosterone by oral fluoxymesterone were comparable to maximal responses of normal men. The diagnosis was confirmed by histologic and electron microscopic study of an excised portion of the tumor. Immunofluorescence studies indicated the presence of luteinizing hormone-releasing hormone in the hamartoma and radioimmunoassays detected thyroid-stimulating hormone-releasing hormone and somatostatin. The hamartoma resembles an autonomously functioning accessory hypothalamus. The ectopic neuroendocrine pathways, however, are responsive to hormonal stimulation and feedback. The clinical, endocrinologic, and pathologic features of published cases of precocious puberty and hypothalamic hamartoma are reviewed. Advanced or rapidly progressive true precocious puberty in the very young with elevated concentrations of blood gonadotropins and gonadal steroids and positive pneumoencephalography appear to be characteristic.

Child, Preschool↗
PubMed1980

Somatostatin: occurrence in urinary bladder epithelium and renal tubules of the toad, Bufo marinus.

Immunohistochemical techniques were used to detect immunoreactive somatostatin-like material in toad urinary bladder epithelium and in kidney distal tubules and collecting ducts. This material has immunological and chromatographic properties identical to those of synthetic cyclic somatostatin. The occurrence of somatostatin-like material in antidiuretic hormone-sensitive portions of the renal urinary system suggests a local regulatory or paracrine role for somatostatin.

Animals↗
PubMed1980

The hypothalamic 'tuberoinfundibular' system of the rat as demonstrated by horseradish peroxidase (HRP) microiontophoresis.

Microiontophoresis of horseradish peroxidase (20%) into the median eminence of the rat has allowed visualization of perikarya and axon projections of the tuberoinfundibular system after retrograde transport. Cells projecting to the median eminence were found in the periventricular regions of the hypothalamus and were particularly pronounced in dorsal portions of the rostral arcuate nucleus, the medial division of the paraventricular nucleus, and within the anterior periventricular nucleus. Labeling of perikarya within the ventromedial nucleus was rarely found. No labeling by HRP was found within cells of the dorsomedial, anterior, suprachiasmatic, preoptic, lateral hypothalamic nuclei or within the septal and amygdaloid nuclei. Axons from identifiably cells were located within the periventricular neuropil and contained within the baso-lateral portions of the hypothalamic-hypophysial tract.

Animals↗
PubMed1980

Somatostatin: an endogenous peptide in the toad urinary bladder inhibits vasopressin-stimulated water flow.

Somatostatin (somatotropin release-inhibiting factor; SRIF) is a tetradecapeptide present in brain, pancreas, gastrointestinal tract, and thyroid that inhibits the secretion or action of several hormones in these tissues. We observed that the toad urinary bladder contains concentrations of endogenous somatostatin (8.0 pg/micrograms of protein) comparable to those found in the mammalian pancreas and gastrointestinal tract. To determine if somatostatin directly alter the action of vasopressinn we studied the effects of this polypeptide on vasopressin-stimulated transport processes in the toad urinary bladder in vitro. Somatostatin produced a dose-dependent, reversible inhibition of vasopressin-stimulated osmotic water flow; it inhibited theophylline-stimulated osmotic water flow but not the water flow stimulated by 8-p-chlorophenylthioadenosine 3',5'-cyclic monophosphate. These data are consistent with an inhibition of both basal and hormone-stimulated adenylate cyclase. Vasopressin-stimulated short circuit current was not inhibited by somatostatin. These studies provide direct evidence for an effect of somatostatin on hormone-modulated epithelial transport in tissues other than the gastrointestinal tract. We propose that endogenous somatostatin may function as a local regulator of the cellular action of vasopressin on osmotic water flow.

Animals↗
PubMed1980

Galactorrhea, oligo/amenorrhea, and hyperprolactinemia in patients with craniopharyngiomas.

We report three patients with craniopharyngiomas who had galactorrhea, oligo/amenorrhea, and abnormal sellar tomograms, clinically suggesting the presence of a prolactinoma. One patient had an intrasellar craniopharyngioma (Rathke's cleft cyst) diagosed during surgical exploration of the pituitary fossa for removal of a suspected prolactinoma, and two had suprasellar caraniopharyngiomas whose presence was suspected on the basis of computed tomography. This finding emphasizes the importance of computed tomography in the evaluation of patients with the clinical presentation of a prolactinoma. In two patients, PRL levels were elevated before surgery and remained elevated after removal of the craniopharyngioma. In the third case, an initially normal serum PRL level became elevated after removal of the tumor.

Adult↗
PubMed1980

Effects of L-dopa and bromocriptine on calcitonin secretion in medullary thyroid carcinoma.

The secretion of calcitonin (CT) by thyroid C cells has been reported to be reduced by dopamine in vitro and by L-dopa in patients with medullary thyroid carcinoma (MTC). These results have suggested that dopa uptake ad decarboxylation to dopamine may play an inhibitory role in the control of CT secretion. We studied the effects of either L-dopa or bromocriptine, a dopamine agonist, on CT secretion in 11 patients with MTC. Seven patients had multiple endocrine adenomatosis type II (MEA II), 1 had MEA III, and 3 had sporadic MTC. Metastatic disease was confirmed in 8, was probable in 2, and was absent in 1. L-Dopa (500 mg orally) was given to 10 patients in 12 trials. Serum obtained serially for CT measurement RIA over a 4-h period showed a fall in 4 instances in 3 patients; there was no decrease in 7 patients. Absorption of L-dopa was confirmed by the finding of the expected rise in serum GH concentration in all nonresponders except 1. Bromocriptine administered in increasing doses (7.5-50 mg/day) for periods from 4-18 weeks in 5 patients with metastatic disease failed to lower the serum CT concentration in any patient. In 2 of 4 cases, pentagastrin-induced CT release was augmented during bromocriptine administration. These results show L-dopa suppression of CT secretion only in a minority of patients with MTC; the lack of response to bromocriptine suggessts that dopamine receptor stimulation by dopaminergic ergots does not inhibit CT secretion in this same group of patients.

Adolescent↗
PubMed1979

Selective transsphenoidal adenomectomy in women with galactorrhea-amenorrhea.

Thirty women with prolactin (PRL)-secreting adenomas underwent selective adenomectomy via a transsphenoidal route. All had abnormal sella polytomes or visual fields, amenorrhea with low basal serum gonadotropin levels despite decreased serum estradiol concentrations, and elevated basal serum PRL levels with blunted PRL response to neuroendocrine stimulation tests )thyrotropin-releasing hormone, levodopa, chlorpromazine, and hypoglycemia). Of 17 patients with microadenomas, 14 (82.4%) were cured and three (17.6%) improved. None were unchanged or worse. Three (60%) of five patients with larger, but still intrasellar tumors, had normalization of PRL levels, return of menses, and resolution of galactorrhea. The patients with tumors extending out of the sella did not fare as well. Overall, 21 (70%) were cured, six (20%) improved, two (6.7%) were unchanged, and the condition of one (3.3%) became worse. All preoperative neurologic deficits resolved. Postoperative complications were minimal with no neurologic morbidity. When tumors are small, surgical results are excellent with minimal risk.

Adenoma↗