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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared two subgroups of women of normal weight with bulimia nervosa: those with a history of anorexia nervosa and those without such a history. Those with a history of anorexia nervosa indicated a desired body weight significantly lower than those without the history. Those with a history of anorexia nervosa were more likely to abuse laxatives and less likely to self-induce vomiting. Both groups reported feeling fat and worrying a great deal about weight and shape issues.
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PMID:Bulimia nervosa with and without a history of anorexia nervosa. 231 84

Previous studies showed that symptoms of oesophageal motor disorders can be misinterpreted as indicating anorexia nervosa and that in primary anorexia nervosa gastric motility is frequently impaired. We investigated in 32 women with bulimia nervosa whether symptoms of oesophageal motor disorders could be obscured by or be mistaken as forming part of bulimic behaviour, and whether impaired gastric motility was frequent as well. Oesophageal motility was normal in 18 of 26 patients studied, another four had incomplete lower oesophageal sphincter relaxation. Two patients had vigorous achalasia and each one achalasia and diffuse oesophageal spasm, all of whom experienced two types of vomiting: one self-induced and one involuntary, in which the vomit was non-acidic and tasted as the preceding meal. Gastric emptying of a semisolid meal was studied in all patients except of the eight with oesophageal motor abnormalities. Emptying was significantly slower than in healthy controls and grossly delayed in nine of 24 patients. Antral contraction amplitudes were lower and increased less postcibally than in controls. In conclusion (i) bulimic behaviour can obscure symptoms of oesophageal motor disorders and (ii) gastric emptying is frequently delayed in bulimia nervosa.
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PMID:Oesophageal and gastric motor activity in patients with bulimia nervosa. 232 85

Patients who have bulimia nervosa and are overweight have received little attention in the medical literature. The authors identified 25 patients who weighed greater than or equal to 130% of their ideal body weight out of a series of 591 patients with bulimia nervosa. This subgroup was contrasted with a sample of 25 patients with bulimia nervosa who were 90% to 110% of their ideal body weight. Members of the overweight bulimia nervosa group were binge-eating and vomiting less frequently than the comparison group but were more likely to be abusing laxatives, and to report a history of self-injurious behavior and suicide attempt(s). Both groups reported frequent binge-eating.
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PMID:Bulimia nervosa in overweight individuals. 233 41

The related central nervous system peptides neuropeptide Y and peptide YY have been found to be among the most potent endogenous stimulants of feeding behavior. We measured these neuropeptides in cerebrospinal fluid to determine whether they contributed to the pathophysiologic characteristics of anorexia and bulimia nervosa. Cerebrospinal fluid neuropeptide Y concentrations were significantly elevated in underweight anorectic patients and in many of the anorectic patients studied at intervals after weight restoration. These levels normalized in long-term weight-restored anorectic patients who had a return of normal menstrual cycles. Increased neuropeptide Y activity may contribute to several characteristic disturbances in anorexia, including menstrual dysregulation. Cerebrospinal fluid peptide YY concentrations were significantly elevated in normal-weight bulimic patients abstinent from pathological eating behavior for a month compared with themselves when actively bingeing and vomiting or compared with healthy volunteers. Increased peptide YY activity may contribute to a drive to overfeed in normal-weight bulimic patients.
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PMID:Altered cerebrospinal fluid neuropeptide Y and peptide YY immunoreactivity in anorexia and bulimia nervosa. 235 Feb 7

Bulimia nervosa, an eating disorder now recognized with increasing frequency, is receiving growing attention because of purported complications. Recent claims of a high frequency of erosions, ulceration, and bleeding in the esophagus, ascribed to repeated, self-induced vomiting, prompted us to investigate by endoscopy the upper gastrointestinal mucosa in 37 consecutive patients with long-standing bulimia nervosa. The endoscopic appearance of esophageal and gastric mucosa was normal in 23 patients. Signs of mild esophagitis observed in eight patients were not related to the duration or severity of bulimic behavior or to symptoms of gastroesophageal reflux; two of these eight patients had sliding hiatal hernias. The remaining six patients were found to have superficial mucosal erythema in the stomach or duodenum, but none showed actual erosions, ulcers, or bleeding. Our observations suggest that, in contrast to reports by others, mucosal injury consequent to chronic, self-induced vomiting in patients with bulimia nervosa is relatively infrequent and limited.
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PMID:Upper gastrointestinal endoscopy findings in patients with long-standing bulimia nervosa. 259 94

In this reply to Leitenberg and Rosen (1989), we conclude that the evidence that response prevention of vomiting adds significantly to the efficacy of cognitive-behavioral treatment of bulimia nervosa is not strong. In this context and given the finding in our previous study (Agras, Schneider, Arnow, Raeburn, & Telch, 1989) that the addition of response prevention did not increase the efficacy of cognitive-behavioral treatment and may have reduced it, we believe that our cautionary note concerning the addition of response prevention to cognitive-behavioral treatment should stand.
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PMID:Cognitive-behavioral treatment with and without exposure plus response prevention in the treatment of bulimia nervosa: a reply to Leitenberg and Rosen. 260 Feb 51

Despite our strong belief in the utility of laboratory studies of eating behavior, we also note several caveats on the data thereby obtained. First, it must be assumed that subjects' behavior is influenced by the laboratory environment and is not identical to eating behavior in a "normal" setting. Second, not all bulimic subjects who were screened for these studies actually participated, so that it is possible that the sample of patients from whom we obtained data differed in some ways from a general clinical population of women with bulimia. Nonetheless, we believe that our data provide compelling evidence that the disturbed eating behavior characteristic of bulimia nervosa can be profitably studied in the laboratory. Even under structured laboratory conditions, most bulimic patients rated one of their multicourse meals as typical of a binge, and, during that meal, consumed a much larger amount of food and ate more rapidly than did controls who were asked to overeat. The significant correlations between the sizes of the multicourse and single-course binge meals and between the size of laboratory binge meals and the size of the "naturally occurring" binge meals reported to the dietician suggest that a reproducible phenomenon is being examined. The results of our studies suggest that the abnormalities of eating behavior in bulimia nervosa cannot be viewed simply as a disturbance of carbohydrate consumption or even as the episodic consumption of a certain type of food. Rather, eating behavior in this syndrome appears more generally disturbed. The most striking difference between the binge and the nonbinge meals of bulimic patients and between the binge eating of patients and the overeating of normal persons is the amount of food consumed, not the macronutrient composition of the meals. In addition, for all four meal types, the patients were hungrier after the end of the meal than were the controls, even though the patients' average caloric intakes were generally larger and their average hunger ratings before the meals did not differ from those of the controls. Certainly, self-induced vomiting may contribute to this abnormality, but it was also observed after nonbinge meals when vomiting did not occur. Together, these data are consistent with the notion that the essential appetitive abnormality in bulimia nervosa lies in the control of the amount of food consumed, not in the consumption of a particular macronutrient or type of food. Patients with bulimia nervosa appear less responsive than normal to the signals that lead to the termination of a meal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Eating behavior in bulimia. 263 74

Bulimia nervosa has been characterized by binge eating, which is often followed by either vomiting or laxative use. However, some bulimic individuals restrict caloric intake rather than purge as a means of controlling their weight. Treatment may include psychiatric evaluation, drug therapy, and nutrition counseling. This study evaluated the eating pattern of a bulimic woman from food records made before and while she was receiving nutrition counseling at an eating disorders clinic. Energy expenditure was also determined and examined in relation to patterns of eating behavior. The Harris-Benedict equation was used to estimate basal energy expenditure (BEE). Actual measured energy expenditure (MEE) was determined by indirect calorimetry. On initial assessment, this woman was eating 600 to 3,800 kcal/day, reflecting the range from a semi-fast to a binge day. At this time, her BEE was significantly higher than her MEE. Following modification of her eating pattern to three meals a day, providing approximately 1,200 kcal, there was a 50% increase in her MEE, which closely approximated her BEE. Modification of eating pattern appeared to be associated with a normalization of energy expenditure in this woman; however, each case must be considered individually. These results imply that certain eating patterns in bulimic individuals cause a decrease in energy expenditure that may resemble starvation.
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PMID:Energy expenditure and the abnormal eating pattern of a bulimic: a case report. 264 96

Women who are of normal weight and have bulimia nervosa have multiple neuroendocrine disturbances. The reasons for these neuroendocrine abnormalities are not known, but there are reasons to suspect that bingeing and vomiting behavior could be contributory. It is well known that food consumption in healthy volunteers increases plasma insulin, cortisol, and prolactin secretion and suppresses growth hormone secretion, whereas activation of the emetic reflex increases plasma arginine vasopressin (AVP) secretion. The purpose of this study was to investigate the effects of bingeing and vomiting on these hormones. In comparison with healthy control women consuming a large meal, bulimic patients, when bingeing and vomiting, had an exaggerated secretion of either the amount and/or the duration of insulin, cortisol, and prolactin. Vasopressin secretion was not increased during or after bingeing and vomiting, probably because bulimic subjects do not become nauseated. In addition, bulimic patients had significantly reduced baseline plasma prolactin and possibly elevated baseline cortisol compared with controls. In summary, this study supports the presence of neuroendocrine disturbances in bulimia and raises a question as to whether or not excessive and prolonged food consumption (and/or vomiting) are contributory.
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PMID:The effect of bingeing and vomiting on hormonal secretion. 264 57

In a 6-week, placebo-controlled, double-blind study of trazodone in 42 women with bulimia nervosa, trazodone was well tolerated and proved significantly superior to placebo in reducing the frequency of episodes of binge eating and vomiting. Nine- to 19-month follow-up of 36 study subjects revealed that 26 (72%) continued improved, with 18 (36%) in remission. Most remained on trazodone or another antidepressant at follow-up.
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PMID:Treatment of bulimia nervosa with trazodone: short-term response and long-term follow-up. 266 52


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