Background Deficiencies in vitamins A, D and E have been linked to night blindness, bone health, and post-liver transplant reperfusion injury. Aims To determine the prevalence and predictive factors of fat soluble vitamin deficiencies in liver transplantation candidates. Methods We reviewed medical records of liver transplantation candidates at our center from 1/2008–9/2011. Etiology of cirrhosis, MELD scores, Child Pugh class, BMI, vitamin A, vitamin E, and vitamin 25-OH-D levels were recorded. Patients were excluded for incomplete laboratory data, short gut syndrome, celiac disease, pancreatic insufficiency, or prior liver transplantation. Results Sixty three patients were included. The most common etiologies of liver disease were alcohol (23), hepatitis C (19), and NASH (5). Vitamin A and D deficiency was noted in 69.8% and 80.9%, respectively. Only 3.2% of patients were vitamin E deficient. There were no documented cases of night blindness. Of 55 patients with bone density measurements, 25 had osteopenia and 10 had osteoporosis. Four patients had vertebral fractures. There was one case of post-transplant reperfusion injury in a patient with vitamin E deficiency. In a multivariate analysis, there were no statistically significant predictors for vitamin D deficiency. Child Pugh class (OR=6.84 {1.52–30.86};p = 0.012), elevated total bilirubin (OR=44.23{5.02–389.41}; p < .001), and elevated BMI (OR=1.17{1.00–1.36};p = 0.045) were found to be predictors of vitamin A deficiency. Conclusions The majority of liver disease patients evaluated for liver transplantation at our center had vitamin A and D deficiency. Presence or absence of cholestatic liver disease did not predict the deficiency, whereas Child Pugh class, bilirubin level, and elevated BMI predicted vitamin A deficiency.

Background & Aims Normal responses of the upper esophageal sphincter (UES) and esophageal body to liquid reflux events prevent esophagopharyngeal reflux and its complications, but abnormal responses have not been characterized. We investigated whether patients with supra-esophageal reflux disease (SERD) have impaired UES and esophageal body responses to simulated reflux events. Methods We performed a prospective study of 25 patients with SERD (19–82 y old, 13 female) and complaints of regurgitation and supra-esophageal manifestations of reflux. We also included 10 patients with gastroesophageal reflux disease (GERD; 32–60 y old, 7 female) without troublesome regurgitation and supra-esophageal symptoms and 24 healthy asymptomatic individuals (controls; 19–49 y old, 13 female). UES and esophageal body pressure responses, along with luminal distribution of infusate during esophageal rapid and slow infusion of air or liquid, were monitored by concurrent high-resolution manometry and intraluminal impedance. Results A significantly smaller proportion of patients with SERD had UES contractile reflexes in response to slow esophageal infusion of acid than controls or patients with GERD. Only patients with SERD had abnormal UES relaxation responses to rapid distension with saline. Diminished esophageal peristaltic contractions resulted in esophageal stasis in patients with GERD or SERD. Conclusions Patients with SERD and complaints of regurgitation have impaired UES and esophageal responses to simulated liquid reflux events. These patterns could predispose them to esophagopharyngeal reflux.

In this large survey of GIs and surgeons, physician specialty was strongly associated with accurate polyp characterization and a recommendation for endoscopic resection of complex polyps. Surgeons were most likely to recommend surgical resection of complex nonmalignant colorectal polyps compared with specialists in complex polypectomy who were the least likely. Therefore, collaboration with specialists in complex polypectomy may be helpful in determining the appropriate management of complex colon polyps. Further teaching is needed among all specialists to improve accurate communication and ensure optimal management of these lesions.

Although there is growing awareness of celiac disease, the delay in diagnosis for patients without gastrointestinal symptoms remains prolonged, with an average delay of 3.5 years.

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