Reversal of megaduodenum and duodenal dysmotility associated with improvement in nutritional status in primary anorexia nervosa.

Anorexia nervosa is considered one type of eating disorder that may result in severe malnutrition. Patients with this disorder commonly complain of postprandial nausea, abdominal pain, and distension. We describe the radiologic and motility abnormalities associated with anorexia nervosa in a 21-year-old female. Barium gastrointestinal series demonstrated marked dilation of the duodenum, with prolongation of intestinal transit. A 4-hr fasting gastroduodenal motility study showed no propagating migrating motor complexes (MMC). Prolonged, but nonpropagating, bursts of high-amplitude phasic and tonic contractions were seen in the duodenum. In contrast, antral contractions were of low amplitude and esophageal motor function was normal. Metoclopramide and edrophonium caused an increase in gastroduodenal motor activity, but increased contractions were not associated with symptoms. Following a renutrition program that raised the patient's weight from 64 to 80% of her ideal body weight, the radiographic abnormalities and gastrointestinal dysmotility resolved completely. These observations suggest that anorexia-associated gastrointestinal motor dysfunctions are a consequence, not the cause of the generalized protein-calorie malnutrition associated with anorexia nervosa. The facts that motility in different parts of the gut is affected to different degrees and that gastric and duodenal muscle responds normally to exogenous stimulation argue against a generalized myogenic dysfunction and, rather, point to a reversible dysfunction of neural regulation.