Abstract

It is difficult to imagine that the morbidly obese patient suffers from nutritional deficiencies. Nonetheless, severe obesity can lead to hepatic steatosis and cirrhosis, which may significantly alter protein synthesis and immune response. Early surgical therapy for morbidly obese patients involved creating a short gut by performing a jejunoileal bypass. Many of these patients developed malabsorption and blind‐loop syndrome, with significant metabolic abnormalities, and some died.1 Recently, the vertical‐banded gastric bypass has been shown to be effective in morbidly obese patients, not only by reducing the volume of food eaten, but also by discouraging the consumption of concentrated sweets by causing dumping. A small upper‐gastric pouch is created that is completely excluded from the distal stomach and duodenum. A Roux‐en‐Y limb of jejunum is then anastomosed to this pouch to restore intestinal continuity.2 Although weight loss is significant, many of these patients develop pernicious anemia. It is unclear whether this is caused by a lack of intrinsic factor from the stomach itself, inasmuch as the large parietal cell mass remains intact, or by hypoacidity of the proximal pouch. Pernicious anemia is seen in other states of hypoacidity, which are recreated by these small pouches.Ten patients who had undergone vertical Roux‐en‐Y gastric bypass were compared with 15 healthy volunteers. Gastric tubes were positioned in the stomach or proximal pouch to assess acid production. The patients underwent a Schilling test using either free or food‐bound 57Co‐labeled cyanocobalamin (Vitamin B12). Twenty‐four hours later, urine was collected, and the percentage of labeled B12 that was detected represented gastrointestinal tract absorption.Acid secretion from the proximal gastric pouch was markedly less than the acid output in the total stomach of age‐matched hospital controls (0 ± 0 vs 5 ± 0.7 mEq/h; p <.001). This may explain the incidental fmding of few anastomotic gastrojejunal ulcers. Crystalline Vitamin B12 absorption was normal in both groups, suggesting that intrinsic factor continued to be produced and bound with the B12 in the jejunum before its absorption. However, when food‐bound Vitamin B12 was given, uptake was significantly decreased in the bypass patients (0.8% ± 0.2% vs 3.7% ± 0.5%; p <.01).

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