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

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55

To evaluate whether the PRL, TSH and gonadotropin secretion is altered in conditions with elevated body mass index, 7 patients with central Cushing's disease before and after transsphenoidal surgery, 7 untreated patients with Cushing's syndrome caused by adrenal adenoma, 17 simplex obese (obese) women and 9 non-obese controls (all females, aged 18-45 years) were tested with TRH (200 micrograms i.v. bolus) and GnRH (100 micrograms i.v. bolus) and the hormone responses were measured. There were no differences in the basal pituitary hormone secretion among the groups. In obese subjects the PRL response was reduced as compared to untreated patients with corticotrop pituitary adenoma. No significant differences of TSH release could be observed among the groups, whereas serum total T4 levels were higher in obesity than in patients with hypercorticism either caused by pituitary or adrenal Cushing's syndrome. No differences were found in the LH response, but the stimulated FSH release was lower in obesity, in patients with central Cushing's disease after transsphenoidal surgery and in patients with primary Cushing's syndrome as compared to the normal controls.
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PMID:[Anterior pituitary responsiveness in central Cushing disease and in Cushing syndrome caused by adrenal cortex tumors, as well as in simple obesity]. 786 32

Secondary causes of hyperlipidemia are important to recognize. In fact, hyperlipidemia may be a clue to the presence of an underlying systemic disorder. It may greatly heighten the risk of atherosclerosis with a raised LDL-c, triglyceride-rich lipoprotein excess, and increased lipoprotein(a) as well as lowered HDL-c. The search for secondary causes may provide a clue as to why patients with primary lipid disorders suddenly develop worsening lipid profiles. The point is a crucial one because some acquired causes of hyperlipidemia, such as alcohol, estrogens, steroids, or pregnancy, when superimposed on a primary familial form of hypertriglyceridemia can result in a saturated removal system and a buildup of chylomicrons, which can lead to life-threatening pancreatitis. A convenient way to remember secondary causes is to think of the four D's of diet, drugs, disorders of metabolism, and diseases. Although diets rich in saturated fats and cholesterol are a common cause of the mild hypercholesterolemia seen in our society, alcohol excess and weight gain can explain much of the tendency toward hypertriglyceridemia. Interestingly anorexia nervosa has long been associated with severe but reversible hypercholesterolemia. Several classes of drugs need to be considered as common causes of altered lipid profiles. Glucocorticoids and estrogens elevate triglycerides and raise levels of HDL-c. Anabolic steroids taken orally markedly reduce levels of HDL-c in contrast to injectable testosterone, which does not adversely affect the LDL-to-HDL ratio. Oral contraceptives affect atherosclerotic risk depending on the kind and doses of progestin/estrogen. In those with an underlying primary hypertriglyceridemia and associated obesity, estrogenic medications can depress triglyceride removal mechanisms, leading to the chylomicronemia syndrome and pancreatitis. Antihypertensives have variable effects on lipids and lipoproteins. Although short-term thiazide usage raises cholesterol, triglycerides, and LDL-c, long-term usage is not necessarily associated with significant alterations in lipid levels. Alpha blockers may cause an increase in HDL-c, whereas beta blockers raise triglycerides and lower HDL-c. Sympatholytics, angiotensin converting enzyme inhibitors, and calcium channel blockers are essentially lipid neutral. Retinoids can be associated with increased LDL-to-HDL ratios and occasionally striking elevations in triglycerides. Cyclosporine raises LDL-c and lipoprotein(a). Classes of drugs that may raise HDL-c include cimetidine, antiepileptic drugs, and tamoxifen, but the effect may be seen primarily in women. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered. A thyroxine and TSH level should be obtained on all new cases of clinically important hyperlipidemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Secondary causes of hyperlipidemia. 828 27

Neonatal administration of MSG leads to a syndrome of endocrine dysfunction characterised by reduced growth, obesity and hypogonadism. The aim of the present investigation was to gain information on the structure and function of the pituitary-thyroid axis in MSG-treated rats. Neonatal Wistar rats received an s.c. MSG (4 mg/g body weight) or hyperosmotic saline (controls) on days 2, 4, 6, 8 and 10 of life. Histological and morphometrical studies were carried out on the thyroids of rats during the 4th month of life. Plasma TSH, T3, and T4 were measured by RIA kits. MSG-treated rats showed stunted growth, obesity and decreased pituitary weight. MSG administration resulted in increases in thyroid weight, absolute volumes of epithelium, colloid and stroma, and blood T3 level while T4 level remained unchanged. In enlarged thyroid gland, percentage fractions occupied by epithelium, colloid and stroma were similar to those observed in control rats. The results obtained suggest that the rat hypothalamic centres involved in regulation of the pituitary-thyroid axis are slightly affected by neonatal MSG treatment.
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PMID:Effects of neonatal treatment with MSG (monosodium glutamate) on hypothalamo-pituitary-thyroid axis in adult male rats. 830 23

Thyrotropin releasing hormone (TRH) administration is known to induce a greater TSH response in normal subjects than in obese subjects. In obesity even GH and PRL response to various stimuli are blunted, presumably because of an augmented somatostatinergic tone in obese subjects. Further studies have shown that pyridostigmine (Pyr), an acetylcholinesterase inhibitor, is capable of augmenting GH in obesity by means of somatostatin inhibition. In order to evaluate the possible interference of an increased somatostatinergic tone on TSH secretion, we studied the TSH response to a TRH bolus in 5 obese children with or without a pyr pretreatment. Similarly, we tested a group of 10 obese adult subjects, with TRH alone or TRH plus pyr administration, 30 min or 60 min before TRH. All subjects had a body weight of 30-50% greater than I.B.W. Our data show that a pretreatment with pyr, 60 min before TRH administration, significantly augments the TSH response in adult obese subjects but not in children; the modality of pyr administration seems to be crucial to evidenciate such an alteration since the pyr pretreatment is not effective when administered 30 min before TRH. The absence of this pyr effect in obese children induces to hypothesize that somatostatinergic tone is differentially modulated in children vs adult obese subjects.
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PMID:Pyridostigmine effects on TSH response to TRH in adult and children obese subjects. 834 46

A 16-year-old Brazilian girl presented with severe growth retardation (-6.3 SDS), obesity, delayed pubertal development, facial dysmorphia, dry skin, and borderline low intelligence (IQ 89). Endocrinological evaluation showed primary hypothyroidism (no uptake of iodine-131 of the right thyroid lobe). Basal and stimulated gonadotropins were increased and ultrasonography revealed hypoplastic ovaries. The karyotype of peripheral lymphocytes was 46,X,i(Xq). The GH response in euthyroid condition after stimulation with GHRH and insulin was diminished. MRI of the pituitary region showed a suprasellar mass (12 x 15 mm) which was removed by transsphenoidal surgery because of extension to the optic chiasm. Histological examinations revealed regular pituitary tissue with hyperplasia of TSH- and FSH-producing cells. Thyroxine treatment was adjusted and GH was given. We conclude that the suprasellar mass was the consequence of long-lasting hypothalamic overstimulation with TRH and LHRH, due to gonadal and thyroid insufficiency.
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PMID:Pituitary hyperplasia in a girl with gonadal dysgenesis and primary hypothyroidism. 905 Sep 52

The effects of changing body size, energy intake and substrate oxidation on serum T4, FT4, T3, FT3 and TSH were investigated in ten morbidly obese subjects (4 men/6 women; age: 37 +/- 6 years; BMI: 53.8 +/- 6.5 kg/m2; mean +/- SD) who had undergone a surgical bilio-pancreatic by-pass in order to reduce their body weight. The starting value of serum FT3 was inversely related to the BMI (r = -0.63; p < 0.05). After 1-3 months, all the subjects were losing weight and their intake of carbohydrates was almost negligible; at this time a significant reduction of T3 (-14.6%; p < 0.0001), T4 (-19.5%; p < 0.0001), and FT3 (-10.5%; p < 0.001) was observed. Nine to 16 months after surgery, all the subjects were still losing weight, although there was no carbohydrate restriction; T3, T4, and FT3 were lower than prior to surgery but were beginning to increase. Finally, after 36-42 months the body weight of all the patients had been stable for at least the previous six months (final BMI: 32.9 +/- 4.1) and their body composition, as assessed by bio-impedance, was almost normal; only the concentrations of FT3 proved to be significantly lower than the basal value (-11.2%; p < 0.03). The change in FT3 proved to be independently influenced by the degree of fat malabsorption but not by changes in any of the physical characteristics considered. All values were always in the normal range; FT4 and TSH did not change significantly during the whole period of study. The final concentrations of TSH proved to be independently related to the postabsorptive protein oxidation (g/24h) (TSH = 2.37-0.018* protein oxidation). These results would suggest that nutritional factors have some influence on the blood levels of thyroid hormones, especially of FT3, while the removal of obesity does not seem to have any independent effect in the long-run.
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PMID:Influences of obesity and weight loss on thyroid hormones. A 3-3.5-year follow-up study on obese subjects with surgical bilio-pancreatic by-pass. 925 7

The degree of thyroid impairment and the effects on growth have not been investigated in children with Cushing's disease. We followed the thyroid function of 24 children and adolescents (12 males and 12 females) with CD (age, 12.9 +/- 3.2 years; mean +/- SD), who were successfully treated by transsphenoidal surgery. Patients were evaluated before, and 3, 6, and 12 months after TSS. Analysis of variance and linear correlation were performed between thyroid function tests and body weight and mass index and bone age. Preoperative free thyroxine levels (1.37 +/- 0.03 ng/dl) were significantly higher than those at 3 months (1.17 +/- 0.05 ng/dl, p < 0.05), but similar to those at 6 and 12 months postoperatively. Preoperative T3 (114.2 +/- 7.7 ng/dl) and TSH (1.36 +/- 0.2 IU/ml) were significantly lower than the postoperative values at 3 (158.9 +/- 6.8 and 2.3 +/- 0.3, respectively), 6 (159.1 +/- 10.8 and 2.5 +/- 0.3, respectively), and 12 months (136 +/- 6.5 and 2.2 +/- 0.3, respectively) (all p < 0.05). One patient had frank hypothyroidism (fT4 < 1 ng/dl) before surgery. Five additional patients had secondary hypothyroidism in the immediate postsurgical period; two of them had normal thyroid function 2 and 3 years postoperatively. One patient has remained hypothyroid for more than 5 years since surgery. No significant correlation was found between thyroid function and body weight, BMI, or BA. We conclude that hypothyroidism was an infrequent complication of CD and TSS. Mild suppression of thyroid function occurs in most children and adolescents with CD before and in the first few months after TSS, but it fully resolves after 6 months and does not correlate with the growth delay and obesity of these patients.
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PMID:Thyroid function in children with Cushing's disease before and after transsphenoidal surgery. 942 98

Metabolic and endocrine abnormalities secondary to hyperprolactinemia, such as hypogonadism and hyperandrogenicity, may be involved in the excessive body weight gain induced by antipsychotic drugs in women. The present study was conducted in healthy premenopausal women, in order to detect an endocrine imbalance secondary to antipsychotic drug administration, which, if sustained in the long term, might be involved in the development of obesity. After a control menstrual cycle, sulpiride (200 mg/day) or placebo was nonblindly administered for 28 days; blood lipids and the serum levels of the following hormones which are involved in body weight regulation were assessed at days 3, 10, 20 and 26 of the cycle: prolactin (PRL), 17-beta estradiol (E2), progesterone (P4), follicle stimulating hormone (FSH), luteinizing hormone (LH), free testosterone (T5), dehydroepiandrosterone sulfate (DHEAS), cortisol, tyrotropic hormone (TSH), tetraiodothyroxine (T4), and the areas under the insulin and glucose tolerance curve. During sulpiride administration, the following changes were observed when compared to placebo administration: PRL levels were significantly increased; E2 levels were significantly reduced at days 10 and 20; P4 levels were significantly reduced at day 20, and the area under the glucose tolerance curve was significantly increased. The other variables were not significantly affected. The body weight gain was higher during sulpiride than during placebo administration, but it did not reach statistical significance, perhaps because the period of treatment was too short. The decrease in the serum levels of E2 during sulpiride administration is probably secondary to hyperprolactinemia. It affects the E2/T5 ratio in the direction of increasing the androgenic activity, as observed in women with well-established obesity. This effect, along with a genetic predisposition, increased appetite, hypoactivity and ignorance of proper dietary habits, may explain the excessive weight gain and obesity observed in women during chronic treatment with sulpiride and other antipsychotic agents.
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PMID:Effects of the antipsychotic drug sulpiride on reproductive hormones in healthy premenopausal women: relationship with body weight regulation. 944 48

Chronic feeding of dehydroepiandrosterone (DHEA) and its sulfated metabolite, dehydroepiandrosterone sulfate (DHEAS), has previously been reported to decrease hyperglycemia, obesity, cancer, and autoantibody generation in a number of animal models and to increase muscle mass and physiological and psychological well-being in elderly humans, although these latter studies remain controversial. The present study was carried out to determine whether large amounts of DHEAS given orally would prevent the occurrence of spontaneous and iodine-induced autoimmune lymphocytic thyroiditis (LT) and/or spontaneous insulin-dependent diabetes mellitus (DM) in male and female BB/Wor rats. DHEAS was administered by gavage (44 mg/rat/day) or in the chow (133 mg/rat/day) to LT- and DM-prone rats from 30 to 120 days of life; some of these rats also received iodine in the drinking water to enhance the incidence and intensity of LT. Onset of DM requiring protamine zinc insulin and its maintenance dose were assessed. Rats were killed at 90 or 120 days of age and blood, thyroid, adrenals, pancreases, testes, and ovaries were removed. Serum glucose, DHEA, DHEAS, thyroxine (T4), tri-iodothyronine (T3) and thyrotropin (TSH) concentrations were measured in all rats in both experiments. Serum DHEAS concentrations were 10-fold higher in the rats given the steroid by gavage or in the diet compared with levels in control rats. DHEAS administered over a prolonged period of time had no significant effect on body weight, incidence and severity of DM, incidence and intensity of spontaneous and iodine-induced LT, and thyroid, pancreas and testes weights but did significantly decrease adrenal and ovarian weights. Serum T4, T3, and TSH concentrations were similar in control and DHEAS-treated rats. In conclusion, DHEAS did not prevent the occurrence of iodine-induced or spontaneous autoimmune LT or spontaneous DM in the BB/Wor rat, at variance with its reported immunosuppressive effects in other animal models.
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PMID:Dehydroepiandrosterone sulfate does not prevent spontaneous and iodine-induced lymphocytic thyroiditis and diabetes mellitus in the BB/Wor rat. 967 43


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