Determinants of delayed gastric emptying in anorexia nervosa and bulimia nervosa.

Abstract

SUMMARY Gastric emptying was measured using a gamma camera in 22 patients with anorexia nervosa, in 10 patients of normal or high weight with bulimia nervosa and in 10 controls. Patients with anorexia nervosa were tested (1) while underweight and selecting their own diet (10 patients); (2) underweight, but receiving an adequate diet on an inpatient unit (refeeding diet) (12 patients); and (3) under refeeding diet conditions after weight gain (eight patients). Three meals, each labelled with technetium 99m-sulphur colloid, 3.7 MBq were used: (1) a mixed solid meal containing labelled poached egg; (2) 200 ml d-glucose solution, 0.5 kcal/ml, and (3) 200 ml physiological saline. Only gastric emptying rates of the solid meal and glucose solution were significantly delayed. Gastric emptying of saline was normal. The gastric disturbance was confined to patients with anorexia nervosa selecting their own diet. Patients receiving adequate nutrition on the ward had normal gastric emptying and weight gain in this group had no significant effect on emptying. Slow emptying was observed in patients who maintained a low weight solely by food restriction as well as in patients whose anorexia nervosa was complicated by episodes of bulimia. Thus, slow gastric emptying occurred when the quantity of food reaching the duodenum was sufficiently reduced to result in severe weight loss. Moreover, abnormal gastric emptying was seen only after the two meals that contained calories and were hypertonic to plasma, either of which properties could mediate the disturbance. Gastric emptying in bulimia nervosa was normal. Slow gastric emptying could exacerbate undereating in starving patients with anorexia nervosa by enhancing satiety.Gastric distension is a potent inhibitor of feeding, and the demonstration of delayed gastric emptying in patients with anorexia nervosa`15 suggests that gastric retention might contribute to the maintenance of undereating in this condition. The mechanisms underlying delayed emptying, and whether it is a primary disorder or secondary to other disturbances are, however, unknown and we have investigated gastric emptying of various meals in anorexic patients at different stages of nutritional treatment in an attempt to identify the determinants of delayed gastric emptying in anorexia nervosa. In the closely related condition, bulimia nervosa,6 patients succumb to episodes of massive overeating, suggesting a failure of satiety. Because an acceleration of gastric emptying has been proposed as a factor mediating overeating in morbid obesity7 we studied

Primary anorexia nervosa: Gastric emptying and antral motor activity in 53 patients

“…The results of the present study confirm the reported high incidence of delayed gastric emptying (Dubois et al, 1979;Holt et al, 1981;McCallum et al, 1985;Stacher et al, 1986Stacher et al, , 1987aAbell et al, 1987;Rigaud et al, 1987;Robinson et al, 1988) and reduced antral motor activity (Abell et al, 1987;Stacher et al, 198713) in patients with PAN. The mechanisms underlying these changes are still unclear.…”

“…In chronically starved prisoners of war (Markowski, 1947), neglected children (Gloebl, Capitano, & Kirkpatrick, 1976;Franken, Fox, Smith, & Smith, 1978), PAN patients (Russell, 1966;Scobie, 1973;Jennings & Klidjian, 1974), but also in healthy volunteers participating in starvation experiments (Keys et al, 1950), acute gastric distension was observed upon the ingestion of large quantities of food. This distension might, as well as the delay in gastric emptying (Dubois et al, 1979;Holt et al, 1981;McCallum et al, 1985;Stacher et al, 1986Stacher et al, , 1987aAbell et al, 1987;Rigaud et al, 1987;Robinson et al, 1988) and the reduced antral motor activity (Stacher et al, 1986;Abell et al, 1987) observed in PAN, primarily result from muscular decompensation. When the distension progresses, venous occlusion, infarction, and rupture may occur (Evans, 1968;Saul, Dekker, & Watson, 1981;Abdu, Garritano, & Culver, 1987).…”

Nitric Oxide as an Endogenous Peripheral Modulator of Visceral Sensory Neuronal Function

“…Nausea and vomiting are linked to activation of vagal afferents (Andrews and Sanger, 2002;Blackshaw and Gebhart, 2002). Eating disorders are associated with abnormal responses to luminal contact with a meal (Robinson et al, 1988), and may involve altered nitrergic function (Morley et al, 1995).…”

A controlled trial of cisapride in anorexia nervosa

“…The rate of improvement varies, one study finding normal emptying after only 2 weeks (although this was not a serial study; Robinson et al, 1988), while we found that 50% of patients failed to normalize after a month (Szmukler et al, 1990).…”