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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty patients with the Prader-Willi syndrome have been examined. The typical features begin in gestational life with poor fetal vigor and difficulties with birth and post-partum feeding. The classical features of hypotonia, small hands and feet, cryptorchidism can be identified at this time. The delayed milestones, mental retardation and obesity become more prominent later. The average height of the patients in this series who were admitted to the Clinical Study Center was 149 cm and their weight was 114 kg. The weight and height curves show that Prader-Willi individuals are consistently shorter and heavier than normal children. Tests of endocrine function showed normal glucose tolerance. Insulin secretion was increased in relation to obesity. The rise in growth hormone (hGH) after injecting insulin to induce hypoglycemia and after the infusion of arginine was comparable to other obese individuals but was low in comparison to normal weight subjects. There was no rise in growth hormone with L-dopa administration, but there was a rise in hGH with the administration of 2-deoxy-D-glucose. The hypoglycemia produced by insulin was greater in the Prader-Willi patient than in obese controls. The rise in TRH (thyrotropin-releasing hormone) following the injection of TSH (thyrotropin stimulating hormone) was greater in the Prader-Willi patients than in the obese controls. Hypogonadism was routine in this series, and the response to LRH (luteinizing releasing hormone) was absent in all tested subjects. Treatment with clomiphene for 30 to 90 days significantly increased the response to LRH in three adult individuals who had not been treated with gonadal steroids previously and who were hypogonadal. Rectal temperature declined in three of the five Prader-Willi patients during exposure to an ambient temperature of 4 degrees C, but none of the three obese controls showed a decline. Food intake averaged 5167 kcal/d when six patients were given trays containing more food than they could eat. Food intake was not reduced when tryptophan was added to the diet. Salivary secretion was reduced in the Prader-Willi patients. A number of pulmonary function tests were significantly reduced in the study patients compared to obese or normal weight controls. The anatomic findings in four autopsied patients with the Prader-Willi syndrome showed no significant differences from those of obese subjects without this syndrome. The chromosomal pattern showed a deletion or translocation at chromosome 15 in 3 of 12 patients in whom this test was performed. These findings in 40 patients with the Prader-Willi syndrome have been compared with the information contained in 159 reports published in the medical literature.
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PMID:The Prader-Willi syndrome: a study of 40 patients and a review of the literature. 633 43

In two girls (14 and 16 years) and one boy (19 years) with PLW-syndrome and pronounced obesity (240, 210 and 77% overweight) endocrine function tests were carried out. Growth hormone secretion was decreased but normalized after reduction of weight. Thyroxin levels as well as basal and TRH stimulated TSH concentrations were normal. HCG application in the boy induced no rise of the normal basal testosterone levels. Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. In the LHRH test an insufficient rise of gonadotropins was found. However, after two weeks of pernasal application of an LHRH analogue (D-Leu6-des-Gly10-EA) the gonadotropin stimulation was distinctly improved and onset of puberty was induced in the male patient. These results are indicative of a hypothalamic disturbance in patients with PLW-syndrome.
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PMID:[Endocrine studies on the Prader-Labhart-Willi syndrome: puberty induction in a 19-year-old boy after long-term treatment with an LHRH analog]. 641 33

We studied plasma concentrations of TSH (basal and after TRH), thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3; rT3), free T4 and free T3 in thirty obese subjects, twenty patients with anorexia nervosa, fifteen malnourished subjects and twenty normal weight subjects. Total serum T4 values were similar for the four groups of subjects while serum free T4 values were slightly increased in anorexia nervosa and normal in the other groups. Serum total and free T3 levels were both significantly decreased in anorexia nervosa and malnutrition, and within normal limits in obesity. The mean serum rT3 level was increased in anorexia nervosa and malnutrition while was reduced in obesity. A delay in peak response of TSH to TRH stimulation (30' rather than 20') was noted in anorexia and malnourished patients. The results suggest that these alterations of serum iodothyronines are due to a different peripheral conversion of T4 to T3 according to nutritional status.
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PMID:Thyroid function in altered nutritional state. 641 28

TSH response to TRH stimulation was studied in 40 non-obese control females and in 40 obese female subjects 40-148 per cent in excess of their ideal weight prior to receiving dietary advice. One patient was found to be hypothyroid and was excluded from further study. There was no significant difference between the basal serum TSH concentration in the subjects and controls. Obese subjects however had significantly greater serum TSH concentrations at 20 and 60 min following TRH stimulation. The implciations of these findings are at present unexplained.
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PMID:TSH response to TRH in substantial obesity. 677 84

The TSH response to exogenous TRH may be diminished or absent not only on overt hyperthyroidism but also in other situations, e.g. obesity, old age, multinodular goiter and depression. To elucidate the possible role of dopaminergic control of the TSH response to TRH in such patients, the oral TRH test (40 mg) was performed with and without simultaneous administration of metoclopramide (10 mg i.v.) in 20 patients known to have diminished or absent response to oral TRH (delta TSH < 1.0 mU/l). All patients had euthyroid basal levels of FT4-index and T3, and may thus be assumed to have "preclinical hyperthyroidism" (TSH suppression syndrome). In 11 patients the history suggested they were free of symptoms of mental depression, while 9 patients were considered by two independent examiners to have various degrees of depression. The TSH response to TRH in depressive patients was significantly increased when the dopamine-receptor-blocker metoclopramide (MCL) wad added. The delta TSH rose from 0.6 +/- 0.3 mU/l (SEM) without MCL to 8.8 +/- 1.8 mU/l with MCL (p < 0.002). In contrast, MCL failed to enhance the TSH response in non-depressive patients: the delta TSH was 0.7 +/- 0.3 mU/l without MCL, and with MCL 2.1 +/- 0.9 mU/l (n.s.). Thus the dopaminergic system appears to play a major role in modulating the sensitivity of the pituitary to TRH stimulation. In clinically doubtful situations, the combined metoclopramide-TRH test may be used to distinguish patients with a diminished or absent TSH response as a consequence of depression (central dopaminergic suppression) from patients with "preclinical hyperthyroidism" where the TSH response is suppressed by feedback control of TSH by thyroid hormones (thyroid autonomy).
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PMID:[Effect of the dopamin antagonist metoclopramide on the TSH response after oral TRH in the TSH suppression syndrome ("preclinical hyperthyroidism"). Preliminary report]. 677 75

17 obese women were examined, 8 of which were diabetic and 9 affected only by essential obesity. These patients, all of whom had become obese during adult life and 8 control subjects were tested for IRI, GH and PRL levels in basal conditions and after infusion of TRH. In the obese and diabetic women fasting GH values were normal while IRI levels were higher than those of the control subjects. In all cases neither IRI nor GH variations during TRH stimulation test. There was no difference in the plasma levels of PRL between the 3 groups when examined in basal conditions. After TRH the hormone increased considerably in all the subjects. In the obese and diabetic obese women the incremental area did not present different values from those observed in the control subjects. In conclusion in insulin-independent diabetes, as in essential obesity, the pharmacological stimulus did not show any evident alteration of the specific hypofisary receptorial system that regulates the secretion of PRL and GH.
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PMID:[Prolactin response to TRH in insulin-dependent diabetes mellitus]. 677 39

17 women affected by essential obesity were examined, 9 of whom had become obese as adults (group A) and 8 had been obese since childhood (group B). In group A, fasting and after TRH, the PRL presented higher plasmatic levels than those found in the controls. In group B the hormone showed basal values and global secretory areas higher than those observed in the controls and in group A, while incremental areas did not result different from those found in the other groups examined. In no case did IRI, GH and glycaemia undergo changes in relation to TRH. In conclusion we think that the behaviour of prolactin can be an important physiopathological characteristic, expression of the different neuroendocrine hypothalamic homeostasis existent in the heterogeneous obese population.
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PMID:[Prolactin secretion in patients with essential obesity]. 678 37

To investigate a possible hypothalamic alteration in obesity, we have studied the pattern of PRL secretion in response to insulin hypoglycemia, arginine infusion and TRH injection in 12 grossly obese patients and in 12 normal-weight controls. In the obese patients, PRL secretion was significantly lower than in normal subjects in response to insulin hypoglycemia and arginine infusion, while it was not significantly different from that in controls in response to TRH. The mean +/- SE values of the areas subtended by the PRL curves in the 3 above tests were 54.7 +/- 155.81 vs 3677.3 +/- 520.30 ng/2h, p less than 0,01, 210.3 +/- 148.93 vs 1034.8 +/- 203.15 ng/2h, p less than 0.05 and 1476.8 +/- 275.13 vs 2148.6 +/- 682.06 ng/2h, NS, respectively, in the obese and in controls. These results are compatible with the concept of impaired hypothalamic control of PRL secretion in obesity, although it is still unclear what role this may play in the pathogenesis of this disorder.
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PMID:Impaired prolactin secretion in obese patients. 679 62

Described here is a 27-year-old female, who had centripetal obesity, broad reddish-purple striae on the lower abdomen and hypertension. Serum cortisol levels, the results of a dexamethasone suppression test and an adrenal scintigram with 131I-19-iodocholesterol were all compatible with Cushing's syndrome due to an adrenal adenoma that secretes cortisol autonomously. This was confirmed by gross and microscopic examination of the removed adrenal tumor. In addition, the patient had markedly diminished T4 and T3 concentrations in serum. Basal TSH levels were not elevated and did not rise significantly after TRH injection. Serum T4 and T3 concentrations were elevated to the normal range when the hyperadrenocorticism was corrected. The results indicate that the patient had "'corticogenic hypothyroidism."
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PMID:Cushing's syndrome associated with corticogenic hypothyroidism: a case study. 730 57

The empty sella results from an extension of the subarachnoid space into an intrasellar position with subsequent remodeling of the sella turcica and the flattening of the pituitary gland. The sella turcica is usually enlarged causing the greatest diagnostic difficulty to distinguish it from a pituitary tumor. The most patients with this syndrome usually have normal pituitary function, while about 30% have varying degrees of hypopituitarism. The Authors describe a case report of a man with primary empty sella syndrome come to the medical observation for obesity and hyperglyccemia. The endocrine evaluation performed (TRH test, GN-RH test, T3, T4, FT3, FT4, Arginine test, metyrapone test) were normal. OGTT shows a maturity onset diabetes (glycemia = 160 mg%). This rare clinical association is not well understood. Probably this diabetes is to the interruption of the normal hypothalamo-pituitary neurovascular connection.
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PMID:[The primary empty sella syndrome. A case report study (author's transl)]. 747 Jan 79


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