Calcium Deficiency Is Associated with Small Intestinal Bacterial Overgrowth after Roux-en-Y Gastric Bypass Surgery

Abstract

Purpose: We have shown that after Roux-en-Y gastric bypass surgery (GBS), patients frequently have elevated serum folate levels, a marker of small intestinal bacterial overgrowth (SIBO). Gastric pouch achlorhydria after GBS may lead to SIBO. Calcium deficiency with subsequent hyperparathyroidism and decreased bone mineral density has been reported after GBS. We hypothesize that by altering gut ecology, GBS induces calcium deficiency. Methods: This is a retrospective chart review of 452 patients who underwent Roux-en-Y gastric bypass surgery from 1999–2005. Of these patients, 154 had determination of serum folate, serum calcium, and 24 hour urinary calcium levels. Baseline patient demographics and characteristics included age, sex, and BMI. Glucose-hydrogen breath testing (HBT) had been performed in 43 patients (abnormal test was: hydrogen concentration >15 ppm over baseline fasting value or fasting hydrogen level >10 ppm). Results: In 129 female and 25 male patients, average age was 42 years (21 to 63 years) with BMI range of 40 to 80 kg/m2. Among 43 patients who underwent HBT, 42 had an abnormal breath test. Of these 42 patients, 38 also had elevated serum folate (90% sensitivity for elevated serum folate as a predictor of SIBO). Of 42 patients with abnormal HBT, 30 had low 24 hour urinary calcium (Chi-squared 2 × 2: P < .01). In the154 patients, 48 patients had normal serum folate levels of whom 38 had normal urinary calcium; in 106 patients with elevated serum folate, 80 had low 24 hour urinary calcium (Chi-squared 2 × 2: P < .001). Corrected serum calcium was within the normal range in all patients. Conclusion: Using HBT as the gold standard, almost all GBS patients who were tested had abnormal HBT, supporting the belief that SIBO is common after GBS. Elevated serum folate has a high sensitivity for detecting SIBO. Serum calcium determination is not accurate in predicting calcium metabolism in these patients. This study supports our hypothesis that by altering gut ecology, GBS induces calcium deficiency. Calcium malabsorption and secondary hyperparathyroidism may increase the risk for developing osteopenia, osteoporosis, and ultimately osteomalacia. Further studies of calcium metabolism after treatment of SIBO may support a treatment option for these patients.