Steatorrhea and Hyperoxaluria in Severely Obese Patients Before and After Roux-en-Y Gastric Bypass.

BACKGROUND AND AIMS: Hyperoxaluria after Roux-en-Y gastric bypass (RYGB) is generally attributed to fat malabsorption. If hyperoxaluria is indeed caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrhea should correlate. Severely obese patients, prior to bypass, ingest excess dietary fat that can produce hyperphagic steatorrhea. The primary objective of the study was to determine whether urine oxalate excretion correlates with elements of fat balance in severely obese patients before and after RYGB. METHODS: Fat balance and urine oxalate excretion were measured simultaneously in 26 severely obese patients before and 1 year after RYGB, while patients consumed their usual diet. At these time points, stool and urine samples were collected. Steatorrhea and hyperoxaluria were defined as fecal fat >7 g/day and urine oxalate >40 mg/day. Differences were evaluated using paired 2-tailed t tests. RESULTS: Prior to RYGB, 12 of 26 patients had mild to moderate steatorrhea. Average urine oxalate excretion was 61 mg/day; there was no correlation between fecal fat and urine oxalate excretion. After RYGB, 24 of 26 patients had steatorrhea and urine oxalate excretion averaged 69 mg/day, with a positive correlation between fecal fat and urine oxalate excretions (r = 0.71, P < .001). For each 10 g/day increase in fecal fat output, fecal water excretion increased only 46 mL/day. CONCLUSIONS: Steatorrhea and hyperoxaluria were common in obese patients before bypass, but hyperoxaluria was not caused by excess unabsorbed fatty acids. Hyperphagia, obesity, or metabolic syndrome could have produced this previously unrecognized hyperoxaluric state by stimulating absorption or endogenous synthesis of oxalate. Hyperoxaluria after RYGB correlated with steatorrhea and was presumably caused by excess fatty acids in the intestinal lumen. Because post-bypass steatorrhea caused little increase in fecal water excretion, most patients with steatorrhea did not consider themselves to have diarrhea. Before and after RYGB, high oxalate intake contributed to the severity of hyperoxaluria.

Disseminated aspergillosis following infliximab therapy in an immunosuppressed patient with Crohn's disease and chronic hepatitis C: a case study and review of the literature.

A 55-year-old white woman with a greater than 25-year history of Crohn's disease developed disseminated aspergillosis following combination therapy with Methylprednisolone, azathioprine, and infliximab. The patient was hospitalized 11 days after initiation of infliximab for respiratory symptoms and developed respiratory failure, coma, and died. Postmortem examination revealed disseminated Aspergillus fumigatus involving multiple organs. This case demonstrates that combined treatment with infliximab, methylprednisone, and azathioprine may induce severe immunosuppression and depressed cellular immunity, leading to severe opportunistic infections. Given the increasing use of antitumor necrosis factor agents, physicians should be aware of the risk of opportunistic infections and be vigilant about diagnosing and aggressively treating these infections to reduce the risk of disseminated disease.

Intestinal perforation caused by insertion of a nasogastric tube late after gastric bypass.

A 57-year-old woman, who had undergone Roux-en-Y gastric bypass surgery 9 years earlier, was admitted to the intensive care unit because of pneumonia. Despite antibiotic therapy, she died 40 days later, apparently because of sepsis and organ failure related to the pneumonia. However, the patient's family requested an autopsy, which revealed that her death was due to perforation of the Roux limb of her gastric bypass, which had resulted in severe peritonitis. The perforation was caused by a nasogastric tube inserted for enteral nutrition. We discuss ways nasogastric tubes might be inserted more safely after gastric bypass, the response of Baylor University Medical Center at Dallas to this complication, and the role of autopsy in improving the quality of hospital care.

Stimulated active potassium secretion in a patient with colonic pseudo-obstruction: a new mechanism of secretory diarrhea.

BACKGROUND & AIMS: Secretory diarrhea is caused by inhibition of intestinal active sodium absorption and stimulation of active chloride secretion. The resulting increase in fecal sodium salts causes an isotonic increase in fecal water output. Abnormalities in potassium transport are not known to be a cause of secretory diarrhea. The aim of our report is to describe a patient with secretory diarrhea that was mediated by excess intestinal secretion of potassium. METHODS: A 78-year-old woman developed colonic pseudo-obstruction, complicated by severe diarrhea and hypokalemia. Her stools were collected quantitatively on 11 occasions and analyzed for electrolyte concentrations. Rectosigmoid potential difference was measured. RESULTS: The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low sodium concentration (4-15 mEq/L). Stool potassium losses were as high as 256 mEq/day (normal, 9 mEq/day), and fecal sodium losses were never higher than 13 mEq/day. Potential difference between colonic lumen and a peripheral reference electrode was -14 mV (lumen side negative). CONCLUSIONS: Fecal potassium salts were the exclusive driving force for severe secretory diarrhea in a patient with colonic pseudo-obstruction. The high fecal output of potassium was due to stimulation of active colonic potassium secretion, possibly because of changes in autonomic nervous system activity and distention of the colon in association with colonic pseudo-obstruction. The extremely low fecal excretion of sodium indicates that active sodium absorption was not inhibited. This case study reveals an ion transport mechanism of secretory diarrhea that has not been previously appreciated.