Krishna S. Kasturi

Effect of Bariatric Surgery on Nonalcoholic Fatty Liver Disease: Systematic Review and Meta-Analysis

BACKGROUND & AIMS Weight loss in overweight or obese individuals results in marked improvement or resolution of hypertension, diabetes mellitus, and hyperlipidemia. However, the overall effect of weight loss on nonalcoholic fatty liver disease (NAFLD) remains unclear. This systematic review and meta-analysis is an effort to explore the effect of weight loss after bariatric surgical procedures on NAFLD. METHODS We performed an electronic literature search of published articles on bariatric surgery and liver histology since inception to September of 2007. Primary outcome measures were improvement and/or resolution in the 3 components of NAFLD (steatosis, steatohepatitis, and fibrosis) after bariatric surgery-induced weight loss. A pooled proportion of patients with improvement or resolution was calculated for steatosis, steatohepatitis, and fibrosis using a random effects model. Heterogeneity among the studies was assessed using the I(2) (inconsistency) statistic and subgroup analyses. RESULTS A total of 15 studies (766 paired liver biopsies) were selected for final data extraction. The percentage reduction in mean body mass index after bariatric surgeries ranged from 19.11 to 41.76. The pooled proportion of patients with improvement or resolution in steatosis was 91.6% (95% confidence interval [CI], 82.4%-97.6%), in steatohepatitis was 81.3% (95% CI, 61.9%-94.9%), in fibrosis was 65.5% (95% CI, 38.2%-88.1%), and for complete resolution of nonalcoholic steatohepatitis was 69.5 (95% CI, 42.4%-90.8%). CONCLUSIONS Steatosis, steatohepatitis, and fibrosis appear to improve or completely resolve in the majority of patients after bariatric surgery-induced weight loss.

Terlipressin therapy for reversal of type 1 hepatorenal syndrome: A meta-analysis of randomized controlled trials

Background and Aim:  Hepatorenal syndrome (HRS) is a serious complication of advanced liver disease and carries a poor prognosis. Recent trials have indicated that terlipressin may be effective in reversing HRS. Our aim was to evaluate the efficacy of terlipressin therapy in reversing type 1 HRS defined as a serum creatinine <1.5 mg/dL during treatment.

Effect of bisphosphonates on bone mineral density in liver transplant patients: a meta‐analysis and systematic review of randomized controlled trials

Bone mineral density (BMD) loss after liver transplantation (LT) results in considerable morbidity with the increased risk of fractures. Data on the efficacy of bisphosphonate use in post LT patients is scarce. This meta‐analysis aims to summarize the results from published randomized controlled trials (RCTs) on the topic of interest. Electronic databases were searched to identify relevant publications. A total of 157 articles were identified and reviewed. Individual authors were contacted from relevant RCTs to obtain individual patient data where necessary to uniformly quantify BMD values post LT pre‐ and post LT. A total of six RCTs were used for final data extraction. (i) Lumbar Spine: In 364 patients (six studies, 182 in intervention and control groups each), bisphosphonate therapy improved BMD by 0.03 g/cm2 (95% C.I. 0.01–0.05 g/cm2; P = 0.02) at 12 months post LT. (ii) Femoral neck: In 268 patients (four studies, 130 bisphosphonate, 138 control), bisphosphonate use did not result in a statistically significant change in BMD at the end of 1 year. None of the studies noted serious adverse effects related to bisphosphonate administration. Data on incident fractures could not be pooled because of heterogeneity. Bisphosphonate therapy during the first year in LT recipients appears to reduce accelerated bone loss and improve bone mineral density at the lumbar spine.

Neutropenic enterocolitis: An unusual complication of HCV combination therapy with PEG-IFN and ribavirin

Drug induced neutropenia as a consequence of intensive chemotherapy for hematological malignancies and solid tumors is known to be associated with severe, life-threatening infections such as neutropenic enterocolitis. However, the neutropenia associated with HCV combination therapy with Pegylated Interferon [PEG-IFN] and ribavirin is considered to be well tolerated in patients without other co-morbidities. We present a case of a severe gastrointestinal complication in a patient receiving HCV combination therapy and advocate caution in continuing therapy in patients with neutropenia, especially in the presence of underlying co-morbidities such as cirrhosis.

An Unusual Case of Ulcerative Duodenitis

Question: A 51-year-old Caucasian woman with a past medical history of gastroesophageal reflux disease presented to the emergency department with a 3-day history of worsening generalized abdominal pain, associated with nausea, non-bloody vomiting, 2–3 episodes of small volume hematochezia, and joint pains in hands and feet. Patient denied nonsteroid antiinflammatory or aspirin use, and recent alcohol intake, before such episodes. She had a normal screening colonoscopy 1 month ago. Two weeks before presentation, she was treated with a 1-week course of cephalexin for a urinary tract infection. Physical examination was significant for diffuse abdominal tenderness without peritoneal signs and scattered red macules on bilateral lower extremities. Admission laboratory test results were significant for leukocytosis (13,300/cmm), with left shift and bandemia, hemoglobin of 11 g/dL, and creatinine of 1.8 mg/dL. Urinalysis revealed 3 red blood cells (50–60 per high-powered field) and proteinuria (300 mg/dL). Abdominopelvic computed tomography was performed with findings suggestive of diffuse colitis and terminal ileitis and surrounding fat stranding. In view of her recent normal colonoscopy and antibiotic use before symptomatology, the patient was admitted, stool studies were sent to rule out infections, she was started on intravenous fluids and empiric metronidazole. The stool studies were negative for cultures, leukocytes, and Clostridium difficile toxin. She continued to have abdominal pain, nausea, vomiting, and episodes of hematochezia. The patient underwent an upper endoscopy and a colonoscopy for further diagnostic workup. The upper endoscopy was significant for diffuse mucosal edema, hemorrhage and ulceration starting from the postbulbar duodenum (Figure A, B, C). Colonoscopy revealed patchy erythema throughout the colon without gross ulceration. Biopsies ere obtained and sent to pathology and special staining. The day after endoscopy, the scant macular rash that was noted on initial valuation of the patient was noted to have evolved into a diffuse purplish, purpuric rash extending over bilateral lower extremities (Figure ). Scattered purpuric rash was also noted over abdomen and lower back. Biopsies of the skin rash were obtained and sent for ermatopathologic evaluation. Her renal function worsened further and serum creatinine increased to 3 mg/dL. What is the likely diagnosis based on the clinical presentation, skin findings, and upper endoscopic images? What specific stains ust be requested from the biopsy specimens to confirm the diagnosis? See the GASTROENTEROLOGY web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Conflicts of interest: The authors disclose no conflicts.

S1914 Metaanalysis of Comparison of Shunt Patency and Clinical Outcomes Between Bare & Polytetrafluoroethylene (Ptfe) Stent in Transjugular Intrahepatic Portosystemic Shunt (Tips)

A S L D A b st ra ct s and blood extravasation were the main histopathologic findings which had significantly increased following variceal obliteration. The morphometric study revealed significant increase (p<0.001) of the mean vascular area of ecstatic blood vessels in the gastric, duodenal and jejunal biopsies following variceal obliteration. Moreover, immunohistochemical expression of VEGF was, also, significantly increased (p<0.001) in the gastric, duodenal and jejunal biopsies after variceal obliteration. CONCLUSION: Portal hypertensive gastropathy and enteropathy are increased in frequency and severity after esophageal variceal obliteration.

Hepatobiliary and pancreatic: Portopulmonary hypertension with cirrhosis

A 44-year-old man was investigated because of orthopnea and progressive dyspnea on exertion over the preceding 6 months. He also complained of fatigue and weight loss. There was a history of intravenous drug use as a teenager. On physical examination, he had an elevated jugular venous pressure, a loud P2 and a pansystolic murmur over the left lower sternal border that was more prominent during inspiration. His spleen was enlarged but he did not have ascites or peripheral edema. Blood tests revealed a mild elevation of plasma bilirubin, elevated levels of liver enzymes and a low plasma albumin (28 g/l). He also had a low white cell count (2.9 ¥ 10/l) and a low platelet count (42 ¥ 10/l). He was positive for hepatitis C antibody. A chest radiograph (Fig. 1) showed markedly enlarged pulmonary arteries typical of severe pulmonary hypertension. A computed tomography scan of the chest (Fig. 2) showed dilatation of the main pulmonary artery trunk with a diameter of approximately 4 cm (arrow) as well as dilatation of the left and right main pulmonary arteries. The liver was also noted to be nodular and he had an enlarged spleen and enlarged collateral vessels, consistent with portal hypertension. An echocardiogram showed an elevated right ventricular systolic pressure estimated at 62 mmHg. At right heart catheterization, the mean pulmonary artery pressure was elevated at 55 mmHg. Portopulmonary hypertension is a rare manifestation of cirrhosis with an estimated prevalence of 0.25–4%. The pathogenesis of the syndrome remains unclear but it may develop when vasoactive molecules such as endothelin and serotonin bypass the liver because of portal hypertension and subsequently mediate vasoconstriction in the pulmonary circulation. In relation to management, recent trials of endothelin-1 receptor antagonists, phosphodiesterase V inhibitors and prostacyclin analogues have been of interest but, as yet, there are no consensus guidelines regarding optimal therapy. Without treatment, the median survival of patients with portopulmonary hypertension has been estimated at 2 years. Portopulmonary hypertension is a relative contraindication to liver transplantation because of reports of increased morbidity and mortality. The above patient was unusual in that his presenting symptoms were those of pulmonary hypertension rather than symptoms related to cirrhosis or portal hypertension.