Hepatic Involvement in Systemic Sarcoidosis.

BACKGROUND Sarcoidosis is a systemic disease that can affect any organ, including the liver. It is manifested by the presence of non-caseating granulomas within involved organs, most commonly the pulmonary, lymphatic, and hepatic system. Unlike pulmonary or lymphatic involvement, hepatic involvement is usually asymptomatic and it is underdiagnosed. Here, we report a case of a patient with a history of pulmonary sarcoidosis who developed hepatic sarcoidosis. CASE REPORT 68-year-old female with pulmonary sarcoidosis with a 2-week history of severe abdominal pain and epigastric tenderness presented to our center. Abdominal magnetic resonance imaging (MRI) demonstrated mild hepatic fibrosis and cirrhosis. A thorough workup was performed including a liver biopsy which showed chronic non-necrotizing granulomas consistent with sarcoidosis. She was started on prednisone and subsequently improved. The patient was symptom-free on follow-up 1 month later. CONCLUSIONS The majority of patients with hepatic sarcoidosis are usually asymptomatic, with only 5-30% presenting with abdominal pain, jaundice, nausea, vomiting, and hepatosplenomegaly. In rare cases, hepatic sarcoidosis can lead to cholestasis, portal hypertension, cirrhosis, or Budd-Chiari syndrome. Treatment with steroids is the mainstay of therapy; however, in severe cases, patients may require liver transplantation. This case report demonstrates that hepatic sarcoidosis is a serious condition, and if not treated, can lead to portal hypertension and cirrhosis. In patients with sarcoidosis, early detection and longitudinal follow-up is important in preventing overt liver failure.

Early Versus Delayed Feeding in Patients With Acute Pancreatitis: A Systematic Review.

BACKGROUND: Acute pancreatitis is among the most common and costly reasons for hospitalization in the United States. Bowel rest, pain control, and intravenous fluids are the cornerstones of treatment, but early feeding might also be beneficial. PURPOSE: To compare length of hospital stay, mortality, and readmission in adults hospitalized with pancreatitis who received early versus delayed feeding. DATA SOURCES: MEDLINE via Ovid, EMBASE, the Cochrane Library, CINAHL, and Web of Science through January 2017. STUDY SELECTION: Two authors independently reviewed and selected studies if they were randomized clinical trials, included adults hospitalized with acute pancreatitis, and compared early versus delayed feeding (≤48 vs. >48 hours after hospitalization). DATA EXTRACTION: Two investigators independently extracted study data and rated risk of bias using the Cochrane Collaboration tool. DATA SYNTHESIS: Eleven randomized trials (8 peer-reviewed publications, 3 abstract-only presentations) that included 948 patients were eligible. Seven trials (3 with low risk of bias) enrolled patients with mild to moderate pancreatitis. Four trials (1 with low risk of bias) included patients with predicted severe pancreatitis. Routes used for early feeding included oral (4 studies), nasogastric (2 studies), nasojejunal (4 studies), and oral or nasoenteric (1 study). Among patients with mild to moderate pancreatitis, early feeding was associated with reduced length of stay in 4 of 7 studies (including 2 of 3 with low risk of bias). Other outcomes were heterogeneous and variably reported, but no study showed an increase in adverse events with early feeding. Among patients with severe pancreatitis, limited evidence revealed no statistically significant difference in outcomes between early and delayed feeding. LIMITATION: Heterogeneity of feeding protocols and outcomes, scant data, and unclear or high risk of bias in several studies. CONCLUSION: Limited data suggest that early feeding in patients with acute pancreatitis does not seem to increase adverse events and, for patients with mild to moderate pancreatitis, may reduce length of hospital stay. PRIMARY FUNDING SOURCE: None. (PROSPERO: CRD42015016193).

Cold snare piecemeal resection of colonic and duodenal polyps ≥1 cm.

BACKGROUND: Endoscopic removal of duodenal and colorectal adenomas is currently considered to be the standard of care for prevention of adenocarcinoma. The use of cautery carries a risk of delayed bleeding, post-polypectomy syndrome, and perforation. We examined the safety and feasibility of removing colonic and duodenal polyps ≥ 1 cm using a piecemeal cold snare polypectomy technique. PATIENTS: The study included 15 patients with duodenal polyps ≥ 1 cm and 15 patients with colonic polyps ≥ 1 cm. MAIN OUTCOME MEASUREMENTS: Bleeding, perforation, abdominal pain, or hospitalization occurring within 2 weeks of polypectomy. RESULTS: Between 24 August 2011 and 29 April 2013, 15 patients had removal of duodenal polyps ≥ 1 cm. Mean patient age was 64 years and 9/15 patients were male. The mean polyp size was 24 mm (10 - 60 mm). All polyps were removed with a cold snare and some required cold biopsy forceps. One patient required hospitalization for gastrointestinal blood loss 7 days post-polypectomy; this patient was using Coumadin. Between 27 February 2012 and 30 May 2013, 15 patients underwent resection of a ≥ 1 cm colonic polyp. Mean patient age was 68 years and 9/15 were male. The mean polyp size was 20 mm (10 - 45 mm). All polyps were primarily removed with a cold snare. None of the patients required hemostatic clips for control of immediate bleeding. One patient presented to the emergency department with abdominal pain 1 day after initial endoscopy. CT scan showed no abnormalities and the patient was discharged. CONCLUSIONS: Cold snare polypectomy for large duodenal and colonic polyps is technically feasible and may have a favorable safety profile compared to standard electrocautery-based endoscopic resection. Comparative trials are required to determine the relative safety and efficacy of cold snare techniques for complete and durable resection of large polyps compared to standard hot snare methods.

The incidence and predictors of lupus-like reaction in patients with IBD treated with anti-TNF therapies.

BACKGROUND: The incidence of lupus-like reactions (LLRs) in patients with inflammatory bowel disease (IBD) treated with anti-tumor necrosis factor (ATNF) has not been well defined. We aimed to characterize the features and predictors associated with LLR. METHODS: We studied a cohort of adult patients with IBD treated with ATNF by a single specialist during 2009. Patients with LLR were characterized and compared with those without LLR for possible predictors. RESULTS: Twenty of 289 patients (6.9%) had LLR (19.9 cases per 1000 patient-years). Female gender and IBD-unclassified were more prevalent in the LLR group (85% versus 54%, P = 0.009; and 15% versus 2.2%, P = 0.018, respectively), with a hazard ratio of 3.89 (95% confidence interval = 1.12-13.55; P = 0.033) and 7.38 (95% confidence interval = 1.93-28.23; P = 0.003), respectively. ATNF duration was shorter in the LLR group (median, 1 year [interquartile range, 0-3] versus 3 years [interquartile range, 1-6.5], P = 0.005). Arthropathy was universal, followed by fatigue and dermatitis (30% each). Antinuclear antibodies were universally positive, and 16 of 20 had anti-double-stranded DNA. ATNF was discontinued in all; 8 patients required corticosteroids and 1 required hydroxychloroquine followed by complete clinical resolution (mean 7.9 ± 5.9 months). Antinuclear antibodies reverted or normalized in 7 of 16 patients (44%). Fourteen patients (70%) were switched to a second ATNF, 2 with concomitant immunomodulators, and 12 as monotherapy. One patient on ATNF monotherapy developed a second LLR and was successfully switched to a third ATNF. CONCLUSION: LLRs secondary to ATNFs are more frequent than previously reported, more common in women and IBD-unclassified. It is reversible with cessation of the culprit agent and steroids. Switching to an alternative ATNF rarely results in recurrence.

Low-dose smoking resumption in ex-smokers with refractory ulcerative colitis.

BACKGROUND AND AIM: Ulcerative colitis (UC) is primarily a disease of non-smokers. Ex-smokers may have a more refractory disease course and anecdotal evidence in non-controlled clinical trials have suggested that smoking resumption, or the administration of nicotine, may ameliorate signs and symptoms of UC in ex-smokers. We report outcomes of ex-smokers with refractory UC who resumed low-dose cigarette smoking. METHODS: 17 ex-smokers with refractory UC were identified. Clinical remission was defined as a disease activity index score of 0. RESULTS: Two out of 17 patients refused the recommendation to resume smoking. Of the 15 patients who resumed smoking, the mean daily number of cigarettes was 8.6. Fourteen out of those 15 patients who resumed smoking were able to maintain prolonged clinical remission off steroids. One out of the 15 patients failed to improve and required oral steroids. Another patient was compelled to quit smoking since he became addicted. His disease flared after maintaining a prolonged remission of 3 years and he eventually underwent surgery. Three out of these 15 patients switched from cigarettes smoking to nicotine compounds and continued to maintain remission. CONCLUSION: Resumption of low dose smoking in a selected group of ex-smokers with refractory UC may ameliorate signs and symptoms. Quality of life, medication side effects, and smoking risk factors should all be considered and discussed with patients. Smokers should be meticulously followed for compliance with "low-dose" regimen and all associated smoking risks.

Gene-environment interactions in a mutant mouse kindred with native airway constrictor hyperresponsiveness.

We mutagenized male BTBR mice with N-ethyl-N-nitrosourea and screened 1315 of their G3 offspring for airway hyperresponsiveness. A phenovariant G3 mouse with exaggerated methacholine bronchoconstrictor response was identified and his progeny bred in a nonspecific-pathogen-free (SPF) facility where sentinels tested positive for minute virus of mice and mouse parvovirus and where softwood bedding was used. The mutant phenotype was inherited through G11 as a single autosomal semidominant mutation with marked gender restriction, with males exhibiting almost full penetrance and very few females phenotypically abnormal. Between G11 and G12, facility infection eradication was undertaken and bedding was changed to hardwood. We could no longer detect airway hyperresponsiveness in more than 37 G12 offspring of 26 hyperresponsive G11 males. Also, we could not identify the mutant phenotype among offspring of hyperresponsive G8-G10 sires rederived into an SPF facility despite 21 attempts. These two observations suggest that both genetic and environmental factors were needed for phenotype expression. We suspect that rederivation into an SPF facility or altered exposure to pathogens or other unidentified substances modified environmental interactions with the mutant allele, and so resulted in disappearance of the hyperresponsive phenotype. Our experience suggests that future searches for genes that confer susceptibility for airway hyperresponsiveness might not be able to identify some genes that confer susceptibility if the searches are performed in SPF facilities. Experimenters are advised to arrange for multigeneration constancy of mouse care in order to clone mutant genes. Indeed, we were not able to map the mutation before losing the phenotype.