3-50 mg/dL), Model for End-Stage Liver Disease score = 184 ± 7

3-5.0 mg/dL), Model for End-Stage Liver Disease score = 18.4 ± 7.0, and Child score = 9.1 ± 2.0]. None had severe hyponatremia manifesting as neurological complications. We did not find any decrease in the serum sodium level on day 1 (133.2 ± 5.6 mmol/L, P = 0.22); instead, we found increases in the serum sodium level on day 2 (133.9 ±

5.0 mmol/L, P = 0.02), day 3 (134.1 ± 5.0 mmol/L, P = 0.01), day 4 (134.6 ± 6.5 mmol/L, P = 0.03), and day 5 (135.2 ± 5.7 mmol/L, P = 0.007). However, we stress that albumin was given to 34 of our 47 patients (72%) because of either a low central venous pressure or an increase (>0.3 mg/dL) in the serum creatinine level from the baseline. Even a shorter course of terlipressin has been found to have equal efficacy.4 In fact, terlipressin even improved the serum sodium Cytoskeletal Signaling inhibitor level when it was given with albumin to patients with hepatorenal syndrome and severe liver dysfunction.5 Solà et al. did not mention how many patients received albumin in the group with a ≥5 mmol/L decrease in the serum sodium level. Although we do respect the observations made by the Spanish group, we emphasize that before its conclusions

are accepted, more prospective studies should be undertaken in patients with AVB. Praveen Sharma M.D., D.M.*, Shweta Singh M.D.*, Shiv Kumar Sarin M.D., D.M.*, * Institute of Liver and Biliary Sciences, Vasant Kunj, New Delhi, learn more India. “
“A woman, aged 74, was admitted to hospital with a 2-week history of upper abdominal pain and recurrent vomiting. She also described significant weight loss. Her medical problems included diabetes mellitus, cardiomyopathy and hypothyroidism. A previous upper abdominal ultrasound study had shown stones in the gallbladder. Mild tenderness was noted on palpation over the upper

abdomen. At endoscopy, she had gastric erosions and a dark filling-defect in the duodenal cap that prevented passage of the endoscope into the second part of the duodenum. A repeat ultrasound study failed to identify the gallbladder but there were check two hyperechoic foci with posterior acoustic shadowing in the upper abdomen. A barium study (Figure 1) showed a large filling-defect in the duodenal cap (thick arrow), the extraluminal passage of contrast from the duodenal bulb (intermediate arrow) and a calcified shadow to the right of the spine (thin arrow). An abdominal computed tomography (CT) scan (Figure 2) showed a calculus, 4 cm in diameter, in the duodenal cap, a second calculus, 3 cm in diameter, in a thick-walled gallbladder (thin arrow) and a fistulous tract between the duodenum and the gallbladder (intermediate arrow). A diagnosis of Bouveret’s syndrome was made and the patient was treated by cholecystectomy, removal of the duodenal calculus and a duodenal repair. There were no post-operative complications. The migration of gallstones from the gallbladder into the gastrointestinal tract has been recognized for over 100 years.

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