Dumping syndrome (DS) has been reported as a postoperative complication of Nissen fundoplication. Typically, children with DS may have early postprandial hyperglycemia (PPH) within 60 minutes of feeding, followed by late hypoglycemia 1 to 4 hours later. The physiopathologic mechanisms of DS are poorly understood: A possible explanation is that DS results from a precipitous emptying of hyperosmolar carbohydrate-containing solutions into the small bowel with subsequent rapid glucose absorption and hyperglycemia followed by reactive hypoglycemia (1). Dietary strategies based on frequent feeding with complex carbohydrates and fat emulsion can ameliorate symptoms (2,3), but this approach is not always foolproof. Limited evidence in the literature reports the efficacy of acarbose for children who are unresponsive to feeding manipulations (4). As a matter of fact, only 8 cases are reported, with an acarbose dosage varying from 25 mg to a maximum of 50 mg (4).
We report 8 cases of children between the ages of 7 and 24 months with DS. In all but 1 DS was diagnosed after fundoplication surgery; in 1 case it followed a continuous enteral feeding in a child with Haddad syndrome. Three of 7 patients have undergone Nissen fundoplication for gastroesophageal reflux disease due to esophageal atresia. All of the children were symptomatic and the diagnosis was confirmed by oral glucose tolerance test or glycemic controls after bolus feeding. Nutritional manipulations were attempted in all of the cases and failed to control symptoms in 4 of 8 (50%). Acarbose treatment was started in the other 4 children with an initial dose of 25 mg per feeding. The dose was increased in increments of 25 mg per feeding until postprandial serum glucose was stable. In 3 of 4 cases the final dose reached to achieve the desired effect was higher than previously reported: respectively, 75 mg in 2 cases and 100 mg in another one (Table 1). Acarbose was well tolerated in all of the patients, with no side effects.
To the best of our knowledge, this is the second largest series in the literature about acarbose efficacy and the only one showing efficacy and safety of higher dosages. Furthermore, DS has been reported in Haddad syndrome only once (1), and our report further emphasizes the importance of dysregulation of autonomic control in this disease.
The issue of feeding children with DS not responding to dietary treatment can be a critical and challenging one, mainly because many of these patients have a history of poor growth, feeding difficulties, and sometimes distressed families. We believe that the possibility of an efficacious treatment deserves to be reiterated, highlighting at the same time the efficacy of higher than previously reported dosages.
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