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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women with long-lasting anorexia nervosa often display osteopenia. Furthermore, we have observed additional marked loss of bone mass under tube feeding in underweight anorexia patients. Such loss of bone substances can lead to spontaneous fractures. Therefore, we investigated in this study whether this undesirable effect of tube-feeding might be prevented by administration of bisphosphonates (Didronel), a substance that inhibits the activity of osteoclasts. Bone density was assessed by a high-precision, low dose, quantitative computed tomography of the distal radius and the distal tibia. A group of 6 anorexia patients (tube feeding with an initial underweight of 74.9 +/- 10.3% of ideal weight, mean +/- SD) treated with bisphosphonates showed only slight loss of trabecular bone (0.8 +/- 0.2%, mean +/- SEM) after 2 months of observation, whereas in 2 control groups a marked diminution of trabecular bone was observed (4.4 +/- 0.7% and 7.6 +/- 1.1% respectively, p less than 0.001 for each comparison). Cortical bone was unchanged throughout. Treatment with bisphosphonates provides effective prevention of bone loss observed in tube-feeding.
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PMID:[Loss of bone mass in patients with anorexia on tube feeding and its prevention with biphosphonates]. 156 19

The presence of hypothalamic disturbances affecting GH secretion in anorexia nervosa has been suggested, although a normal GH response to GH-releasing hormone (GHRH) administration has been shown in these patients. The present study was performed to investigate the role of acetylcholine in regulating GH secretion by using pirenzepine, which selectively blocks muscarinic cholinergic receptors. Paired tests were performed in nine anorexia nervosa patients (age +/- SEM, 19.1 +/- 1.2 yr; percent ideal body weight, -32.7 +/- 2.2%) and in six normal controls (20.1 +/- 0.3 yr; -3.1 +/- 1.8%). GHRH-(1-44) (1 microgram/kg) was infused iv with and without pirenzepine pretreatment (0.6 mg/kg, iv). Basal levels of GH were not different in anorexia nervosa compared to normal controls, whereas, somatomedin-C levels were significantly lower in anorexia nervosa patients. However, after pirenzepine administration, the GHRH-stimulated GH responses were completely blocked in normal controls, but not in anorexia nervosa patients. These results suggested that altered muscarinic cholinergic mechanism are involved in the modulation of GH secretion in patients with anorexia nervosa.
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PMID:Effect of cholinergic muscarinic receptor blockade on human growth hormone (GH)-releasing hormone-(1-44)-induced GH secretion in anorexia nervosa. 210 28

The aim of this study was to test the hypothesis that low serum T3 concentrations may promote an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa. Eight anorexic women and two anorexic men, ages 15-25 years, with low free T3 circulating levels (mean +/- SEM = 2.8 +/- 0.3 pmol/l) were studied. A TRH test (200 micrograms IV) was carried out under basal conditions and repeated following treatment with oral T3 (1.5 micrograms/kg BW/day) for eight days. Following T3 administration, GH levels dropped significantly from a baseline of 7.1 +/- 1.3 micrograms/l to 3.1 +/- 0.7 micrograms/l (p less than 0.02), as did GH peak responses to TRH (9.0 +/- 1.0 micrograms/l vs 4.4 +/- 0.8 micrograms/l, p less than 0.01). ANOVA and analysis of area under the curve (AUC) confirmed that after T3 treatment there was a significant reduction in TRH-induced GH release in these patients (GH AUC: 902 +/- 132 micrograms/l vs. 456 +/- 91 micrograms/l, p less than 0.02). TSH responses to TRH, which were normal prior to T3 treatment, completely disappeared following it, and PRL responses to TRH also were diminished. Although our experimental approach does not permit a conclusion that low T3 levels were the primary reason for these changes, the data support the theory that low T3 circulating levels may facilitate abnormal GH secretion and the GH-releasing activity of intravenous TRH.
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PMID:Triiodothyronine administration reduces serum growth hormone levels and growth hormone responses to thyrotropin-releasing hormone in patients with anorexia nervosa. 212 17

Patients with anorexia nervosa occasionally suffer from hypoglycemic comas. We investigated the role of human pancreatic polypeptide (HPP) in insulin-induced hypoglycemia (0.1 U/kg of regular insulin). Ten female patients with anorexia nervosa (20.7 +/- 2.0 years, mean +/- SEM; 34.9 +/- 1.7 kg, mean +/- SEM) and 8 age-matched female controls (20.9 +/- 0.6 years, 51.5 +/- 0.8 kg) were tested. In the patients with anorexia nervosa, testing was performed before and after the restoration of body weight (45.0 +/- 0.8 kg). There was no significant difference in glucose nadir between patients with anorexia nervosa and the control subjects. However, glucose recovery from nadir was delayed in patients with anorexia nervosa. In anorexia nervosa patients, the plasma pancreatic glucagon responses to insulin-induced hypoglycemia did not differ from those of the controls. Results also showed, however, that HPP responses to insulin-induced hypoglycemia were significantly higher in patients with anorexia nervosa than in controls (p less than 0.01). The increased HPP responses were still present after the restoration of body weight in anorexia nervosa patients. A complete body weight recovery or a longer period of time may be required to normalize the HPP response to insulin-induced hypoglycemia in patients with anorexia nervosa, after the restoration of body weight.
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PMID:Human pancreatic polypeptide responsiveness to insulin-induced hypoglycemia in anorexia nervosa. 227 11

A dual radioisotope technique was used to measure gastric emptying of a mixed liquid and solid meal in 11 patients with bulimia nervosa, and was compared with 10 patients with anorexia nervosa and a sex-matched control population. The relationship of body weight and gastrointestinal symptoms to gastric emptying was also examined. Gastric emptying of solids in patients with bulimia nervosa was similar to that in controls (gastric T1/2 131 +/- 15 min vs 119 +/- 7 min; mean +/- SEM). In contrast, patients with anorexia nervosa had overall delayed emptying (182 +/- 31 min; p less than 0.05); six patients had normal emptying of the solid components of the meal and four had markedly delayed emptying. Gastric emptying of liquids was similar in the bulimics and controls (gastric T1/2 48 +/- 5 min and 49 +/- 4 min, respectively), whereas the anorexics tended to have prolonged gastric emptying (65 +/- 11 min, p = NS). There was no correlation between body weight, gastrointestinal symptoms, and gastric emptying in either group. These findings suggest that gastrointestinal symptoms are unreliable indicators of gastric emptying in patients with eating disorders, and that gastric emptying studies should be performed in such patients before treatment with prokinetic agents is considered.
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PMID:Gastric emptying in patients with bulimia nervosa and anorexia nervosa. 229 62

In rats allowed to eat for only 2 h per day, gastric emptying of three different meals [poached egg white, glucose (0.5 kcal/ml) and physiological saline, each labelled with 60 MBq of technetium-99m tin colloid visualized using a gamma camera] was markedly slowed 8 h after the last meal. Mean body weight in rats on the restricted feeding schedule was 80% of the weight of free-feeding controls. Gastric emptying curves for all three meals in controls were best described using loge transformed counts. Other models used were linear and square root. For each of the three meals, the percentage remaining in the stomach at 120 min was estimated using linear regression of gastric contents, transformed if necessary to yield the best curve against time. At 120 min, % gastric contents (mean +/- SEM) were 19.5 +/- 5.6 (egg), 15.5 +/- 6.27 (glucose) and 27.1 +/- 7.48 (saline) in control rats. After 4 months restriction, the corresponding figures were 75.2 +/- 4.04, 81.5 +/- 4.75 and 70.3 +/- 5.83. After 3 months of free feeding, emptying rates of the three meals were not significantly different from control values. We conclude that dietary restriction causes profound changes in gastric emptying by unknown mechanisms which may be operating in patients with anorexia nervosa.
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PMID:Dietary restriction delays gastric emptying in rats. 236 15

Anorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age-matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1-29 (1 microgram/kg i.v.) induced a GH peak (mean +/- SEM) of 28.2 +/- 5.1 ng/ml (GH ng/ml x 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH-stimulated GH peak in the control women (28.1 +/- 10.0 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 +/- 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen-treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen-treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH-induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.
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PMID:Growth hormone and prolactin secretion after growth hormone-releasing hormone administration, in anorexia nervosa patients, normal controls and tamoxifen-pretreated volunteers. 289 60

This study was designed to compare the dietary intakes of patients with anorexia nervosa and normal controls. Twenty-four patients hospitalized for treatment of anorexia nervosa were compared with 10 normal controls. Patients ate a self-selected diet and maintained their admission weight to within 1.0 kg during this period (19 +/- 3 days). Food chosen by each subject was weighed before and after meals, and intake was determined to be the difference. Intakes of food energy, protein, fat, and carbohydrate were calculated. Patients were closely monitored to ensure that no disposal of food occurred. Patients with anorexia nervosa had a mean daily energy intake of 1,017 +/- 54 kcal (mean +/- SEM), significantly lower than the mean energy intake for controls (1,651 +/- 108 kcal). Similarly, mean intakes of macronutrients (41 +/- 4 gm protein, 34 +/- 2 gm fat, and 136 +/- 9 gm carbohydrate) were significantly lower for patients than for controls (68.5 +/- gm protein, 65 +/- 6 gm fat, and 204 +/- 13 gm carbohydrate). However, when protein, fat, and carbohydrate were assessed as a percent of total calories, there were no significant differences between patients and controls. There were also no significant differences in calories consumed per kilogram body weight. Underweight patients with anorexia nervosa who maintain their weight on an unrestricted hospital diet have energy intake per kilogram body weight and dietary macronutrient content indistinguishable from those of normal women.
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PMID:Energy intake and dietary macronutrient content in women with anorexia nervosa and volunteers. 290 92

Adrenal androgen secretion is decreased in patients with anorexia nervosa. To assess the reversibility of the decreased secretion with recovery of body weight, we measured ACTH-stimulated adrenal androgen levels at different stages of recovery. Basal plasma GH and somatomedin-C levels also were measured, because both have been proposed as potential stimuli for adrenal androgen secretion. When studied at low body weight [58 +/- 3% (+/- SEM) ideal BW], women with anorexia nervosa had decreased ACTH-stimulated levels of dehydroepiandrosterone (DHA), DHA sulfate (DHAS), and androstenedione and decreased DHA to cortisol, DHAS to cortisol, and androstenedione to cortisol ratios compared to normal women. Women who had recently completed a refeeding program (within 2-4 weeks, 81 +/- 2% ideal BW) had an increased somatomedin-C level compared to low weight patients, but similar ACTH-stimulated adrenal androgen levels. Long term weight-recovered women (86 +/- 4% ideal BW, recovery for more than 6 months, with resumption of menses), however, had significant increases in ACTH-stimulated DHA and DHAS levels and DHA to cortisol and DHAS to cortisol ratios, and their hormone levels and ratios were not different from those in normal women. GH levels fell during weight recovery, although the values in the three patient groups did not differ significantly. We conclude that the recovery of adrenal androgen secretion while GH levels were falling provides evidence against a direct effect of GH as a stimulus for adrenal androgen secretion. The recovery of somatomedin-C before the recovery of adrenal androgens, however, and the positive correlation between plasma somatomedin-C and the integrated level of plasma DHAS (r = 0.50; P less than 0.02) are consistent with the hypothesis that somatomedin-C is a stimulus for adrenal androgen secretion.
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PMID:Adrenocorticotropin-stimulated adrenal androgen secretion in anorexia nervosa: impaired secretion at low weight with normalization after long-term weight recovery. 299 44

Pituitary-adrenocortical responses to the iv injection of 100 micrograms synthetic ovine corticotropin-releasing hormone (CRH) were studied in 13 patients with anorexia nervosa, and the concentrations of immunoreactive CRH in cerebrospinal fluid were measured in 7 of them. Mean basal levels of plasma ACTH and cortisol were 32 +/- 5 pg/ml (+/- SEM) and 21.1 +/- 1.5 micrograms/dl, respectively. The latter value was significantly higher than that in age-matched normal women (P less than 0.005). The mean increments of plasma ACTH and cortisol in response to CRH injection in those 13 patients were 21 +/- 5 pg/ml and 5.3 +/- 1.7 micrograms/dl, respectively, significantly lower than those in normal women (58 +/- 6 pg/ml and 15.3 +/- 7.7 micrograms/dl, respectively; P less than 0.005). When 4 patients were reexamined after weight gains of between 3 and 22 kg, their responses to the CRH injection increased. The mean concentration of immunoreactive CRH in the cerebrospinal fluid of seven patients was 30.8 +/- 3.9 pg/ml (+/- SEM), which was higher than the value of 18.4 +/- 1.1 pg/ml (P less than 0.005) in control subjects with cervical spondylosis. These findings suggest the possibility that hypersecretion of CRH may occur in patients with anorexia nervosa.
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PMID:The responses of plasma adrenocorticotropin and cortisol to corticotropin-releasing hormone (CRH) and cerebrospinal fluid immunoreactive CRH in anorexia nervosa patients. 300 Nov 25


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