[Treatment of early post resection syndrome (dumping syndrome)].
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Dumping syndrome commonly occurs after gastrectomy. The late dumping, which is one of the dumping syndromes, is due to postprandial hypoglycaemia caused by an excessive insulin secretion after a sharp rise in plasma glucose. Several treatments, including operation, dietary fibre and somatostatin, have been attempted to relieve dumping symptoms. These treatments take effect through modulation of plasma insulin and glucose levels, but their efficacy is still under consideration. Alpha-glucosidase inhibitor attenuates the postprandial increase of plasma glucose levels and is widely used for treatment of non-insulin-dependent diabetes mellitus (NIDDM). The acute effect of alpha-glucosidase inhibitor on late dumping syndrome has been reported by some studies with test meals. The purpose of this study was to evaluate a long-term effect of alpha-glucosidase inhibitor treatment with ordinary meals in late dumping patients with NIDDM because administration of alpha-glucosidase inhibitor is only ethically allowed for diabetic patients in Japan. Six late dumping patients with NIDDM were orally administered alpha-glucosidase inhibitor, acarbose (50 or 100 mg), three times a day before each meal for 1 month. Diurnal changes of plasma glucose, insulin and pancreatic glucagon levels were compared before and after the alpha-glucosidase inhibitor treatment. All patients had late dumping-related symptoms, such as weakness, palpitation and dizziness before the induction of alpha-glucosidase inhibitor treatment. Patients suffered from a rapid fall in plasma glucose levels from hyperglycaemia at the same time as dumping symptoms. These late dumping-related symptoms disappeared and a rapid change of plasma glucose and insulin levels were attenuated after the alpha-glucosidase inhibitor treatment. These data suggest a long-term therapeutic efficacy of alpha-glucosidase inhibitor for late dumping patients.
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Although most patients have a satisfactory permanent result following partial gastrectomy for peptic ulcer, some have severe and occasionally disabling postprandial distress, due mainly to the postgastrectomy dumping syndrome. Despite 50 years of extensive research the etiology of this syndrome is not fully understood, although recent evidence suggests that this is, at least in part, a chemically mediated phenomenon due to release of humoral factor(s) from the intestinal mucosa during stimulation by hyperosmotic material.Animal experiments which have yielded evidence in support of the humoral theory have been reported by several workers, but this communication is the first in which experimentally induced dumping has been reported in man before and after portal systemic shunt. The symptoms elicited add further support to the hypothesis that a humoral factor is responsible for initiation of the dumping syndrome.
The dumping syndrome following gastric surgery for peptic ulcer disease can cause severe morbidity. In this study the benefit of interposition of an antiperistaltic jejunal loop to reverse peristalsis and delay gastric emptying was assessed in four patients with severe symptoms by performing gastric emptying studies pre-operatively, and at 6 months and 24 months following surgery. Gastric emptying was delayed at 6 months but by 2 years had returned to pre-operative values. Patients' symptoms were improved at 6 months and remained so despite the deterioration in gastric emptying. This surgical procedure is of some value to patients with severe symptoms due to the dumping syndrome.
The dumping syndrome consists of early postprandial abdominal and vasomotor symptoms, resulting from osmotic fluid shifts and release of vasoactive neurotransmitters, and late symptoms secondary to reactive hypoglycemia. Effective relief of symptoms of dumping syndrome can be achieved with dietary modifications to minimize ingestion of simple carbohydrates and to exclude fluid intake during ingestion of the solid portion of the meal. More severely affected individuals may respond to agents such as pectin and guar, which increase the viscosity of intraluminal contents, or to drugs such as the alpha-glucosidase inhibitor acarbose, which blunts the rapid absorption of glucose, and the somatostatin analog octreotide, which alters gut transit and impairs release of vasoactive mediators into the bloodstream.
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A dumping provocation test using 50% of glucose solution labeled with Indium 115 m, was performed on 146 occasions pre- and postoperatively in 85 patients. Dumping elicited by the test was defined by the symptoms produced by the test and various objective measures of dumping. The influence of various factors other than the type of operation on the occurrence of dumping has been studied in detail. The incidence of dumping symptoms induced by the test has shown no significant correlation with age, sex, weight, height, smoking habits, race, dose of hypertonic glucose, and the time elapsed since surgery. However, a significant relationship has been observed between the duration of ulcer symptoms before operation and the occurrence of dumping symptoms induced by the test. The test not only reproduced the symptoms patients had reported after eating ordinary foods, it also helped in eliminating patients with borderline symptoms as our objective measures collectively differentiated three patients from those with the dumping syndrome.
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In patients after gastric surgery, early dumping symptoms can be provoked by oral glucose challenge. Octreotide effectively prevents the occurrence of dumping symptoms. We have studied plasma renin activity (PRA), aldosterone and atrial natriuretic peptide (ANP) concentrations in nine patients with early dumping, 10 surgical control subjects and nine healthy control subjects after an oral glucose challenge preceded by either placebo or 25 micrograms of octreotide subcutaneously (s.c.). In the dumping group, basal PRA was significantly (P < 0.01) higher (3.9 +/- 0.6 micrograms L-1 h-1) than in either surgical or healthy control subjects (1.1 +/- 0.3 micrograms L-1 h-1 and 1.1 +/- 0.2 micrograms L-1 h-1 respectively) and showed a significant rise after glucose ingestion to 5.4 +/- 0.9 micrograms L-1 h-1 that did not occur in control subjects. Aldosterone concentration showed a concomitant rise. In dumping patients, plasma ANP decreased after glucose ingestion from 31 +/- 6 ngL-1 to 21 +/- 5 ngL-1 (P < 0.05). This decrease did not occur in control subjects. Early dumping is associated with an activation of the renin-aldosterone axis and a decrease in plasma ANP, reflecting a hypovolaemic state. Octreotide prevents the occurrence of these changes.
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Dumping syndrome developed in seven children after gastric surgery, (Nissen fundoplication in six, Whipple procedure in one). The patients ranged from age 10 months to 13 years, and four of the seven were neurologically impaired. The diagnosis was made by demonstrating an abnormal response to an orally administered glucose challenge. The pediatric literature records only eight cases, but we believe that dumping syndrome is more common in children than once believed. Dietary management can often dramatically diminish the associated symptoms.
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