Nancy Gupta

Gastrointestinal complications associated with catheter ablation for atrial fibrillation

Atrial fibrillation is the most common arrhythmia in the United States. With the ageing population, the incidence and prevalence of atrial fibrillation are on the rise. Catheter ablation of atrial fibrillation is a widely accepted treatment modality in patients with drug refractory symptomatic paroxysmal or persistent atrial fibrillation. The close proximity to the left atrium posterior wall makes the thermosensitive esophagus a potential site of injury during catheter ablation of AF leading to various gastrointestinal complications. The major gastrointestinal complications associated with catheter ablation include atrioesophageal fistula, gastroparesis, esophageal thermal lesions and esophageal ulcers. Multiple studies, case reports and series have described these complications with various catheter ablation techniques such as radiofrequency, cryoenergy and high frequency focused ultrasound energy ablation. This review addresses the gastrointestinal complications after AF ablation procedures and aims to provide the clinicians with an overview of clinical presentation, etiology, pathogenesis, prevention and management of these conditions.

The management of eosinophilic gastroenteritis

Abstract Eosinophilic gastroenteritis (EG) is a rare disorder characterized by eosinophilic infiltration of the gastrointestinal tract. No medication at present is approved by the Food and drug administration of United States for the treatment of EG. The rarity of the disease limits our experience with the different management options. It also limits the ability to conduct randomized controlled trials that could clearly delineate the efficacy of new therapeutic agents. This review assesses the various management options that have been tried on patients with EG.

Gastrointestinal Bleeding Secondary to Calciphylaxis.

Patient: Female, 66 Final Diagnosis: Calciphylaxis Symptoms: Gastrointesinal haemorrhage Medication: None Clinical Procedure: Hemodialysis • blood transfusions Specialty: Gastroenterology and Hepatology Objective: Rare disease Background: Calciphylaxis is associated with a high mortality that approaches 80%. The diagnosis is usually made when obvious skin lesions (painful violaceous mottling of the skin) are present. However, visceral involvement is rare. We present a case of calciphylaxis leading to lower gastrointestinal (GI) bleeding and rectal ulceration of the GI mucosa. Case Report: A 66-year-old woman with past medical history of diabetes mellitus, hypertension, end-stage renal disease (ESRD), recently diagnosed ovarian cancer, and on hemodialysis (HD) presented with painful black necrotic eschar on both legs. The radiograph of the legs demonstrated extensive calcification of the lower extremity arteries. The hospital course was complicated with lower GI bleeding. A CT scan of the abdomen revealed severe circumferential calcification of the abdominal aorta, celiac artery, and superior and inferior mesenteric arteries and their branches. Colonoscopy revealed severe rectal necrosis. She was deemed to be a poor surgical candidate due to comorbidities and presence of extensive vascular calcifications. Recurrent episodes of profuse GI bleeding were managed conservatively with blood transfusion as needed. Following her diagnosis of calciphylaxis, supplementation with vitamin D and calcium containing phosphate binders was stopped. She was started on daily hemodialysis with low calcium dialysate bath as well as intravenous sodium thiosulphate. The clinical condition of the patient deteriorated. The patient died secondary to multiorgan failure. Conclusions: Calciphylaxis leading to intestinal ischemia/perforation should be considered in the differential diagnosis in ESRD on HD presenting with abdominal pain or GI bleeding.

Incidence and Predictors of Readmissions in Acute Pancreatitis: A Nationwide Analysis

Objectives Acute pancreatitis (AP) is a common cause for hospitalization, and readmission is common, with variable associated risk factors for readmission. Here, we assessed the incidence and risk factors for readmission in AP in a large national database. Methods We analyzed data from the National Readmission Database during the year 2013. Index admissions with a primary discharge diagnosis of AP using the International Classification of Diseases, Ninth Revision, Clinical Modification were identified from January to November to identify 30-day readmission rates. Demographic, hospital, and clinical diagnoses were included in multivariate regression analysis to identify readmission risk factors. Results We identified 243,816 index AP discharges with 39,623 (16.2%) readmitted within 30 days. The most common reason for readmission was recurrent AP (41.5%). Increased odds of all-cause readmission were associated with younger age, nonhome discharge, increasing Charlson Comorbidity Index, and increased length of stay. Cholecystectomy during index admission was associated with reduced all-cause and recurrent AP readmissions (odds ratios of 0.5, and 0.35, respectively). Conclusions Readmission for AP is common, most often due to recurrent AP. Multiple factors, including cholecystectomy, during index admission, are associated with significantly reduced odds of all-cause and recurrent AP readmissions.

Bilirubin in coronary artery disease: Cytotoxic or protective?

Bilirubin has traditionally been considered a cytotoxic waste product. However, recent studies have shown bilirubin to have anti-oxidant, anti-inflammatory, vasodilatory, anti-apoptotic and anti-proliferative functions. These properties potentially confer bilirubin a new role of protection especially in coronary artery disease (CAD), which is a low grade inflammatory process exacerbated by oxidative stress. In fact, recent literature reports an inverse relationship between serum concentration of bilirubin and the presence of CAD. In this article, we review the current literature exploring the association between levels of bilirubin and risk of CAD. We conclude that current evidence is inconclusive regarding the protective effect of bilirubin on CAD. A causal relationship between low serum bilirubin level and increased risk of CAD is not currently established.

Coronary Artery Disease in Patients With Disorders of Bilirubin Excretion

We aimed to determine the predictors of coronary artery disease (CAD) in patients with abnormal bilirubin excretion, that is, Gilbert syndrome, Crigler–Najjar syndrome, Dubin–Johnson syndrome, and Rotor syndrome. We analyzed data from the Healthcare Cost and Utilization Project (HCUP) of the Agency for Healthcare Research and Quality, Rockville, MD for the period 2009 to 2010. All patients ≥18 years of age with a primary diagnosis of “disorders of bilirubin excretion” [International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9CM) code 277.4] were included in the study. Primary outcome was to determine predictors of CAD in adult patients diagnosed with abnormal bilirubin excretion. We identified a total of 12,423 adult patients with bilirubin excretion disorder hospitalized during 2009–2010 (0.03% of all inpatient admissions). CAD was seen in 18% of patients, with a higher prevalence in men (21% in men vs. 13% in women, P < 0.0001). In multivariate logistic regression adjusted for demographic and traditional risk factors, hypertension [odds ratio (OR): 1.74; 95% confidence interval (CI), 1.33–2.27, P < 0.001], hyperlipidemia (OR: 2.49; 95% CI, 1.95–3.18, P < 0.001), diabetes (OR: 1.46; 95% CI, 1.12–1.91, P = 0.01), and age (OR: 1.05; 95% CI, 1.04–1.06, P < 0.001) were found to be independent predictors of CAD in adult patients with abnormal bilirubin excretion. Female sex (OR: 0.49; 95% CI, 0.36–0.65, P < 0.001) demonstrated an inverse association in predicting CAD. There was increased prevalence of CAD in our patient population with increased prevalence of cardiovascular risk factors. Age, diabetes mellitus, hypertension, and hyperlipidemia were found to be independent predictors of CAD.

Autoimmune Hepatitis in Association With Sofosbuvir.

Sofosbuvir in combination with ribavirin was approved by the Food and Drug Administration as a treatment option for hepatitis C (HepC) in 2013. We describe a case of autoimmune hepatitis triggered in a patient on therapy with sofosbuvir and ribavirin. A 65-year-old woman with a medical history of diabetes mellitus, hypertension, and HepC (genotype 2) underwent pretreatment liver biopsy in May 2012, which demonstrated mild chronic active hepatitis with focal piece-meal necrosis and mild stage 1 periportal fibrosis with no increased iron deposition. No features of autoimmune hepatitis were seen on biopsy. The patient was administered 400 milligrams (mg) sofosbuvir and weight-based 1000 mg ribavirin for a planned duration of 12 weeks. Liver function tests (LFTs) initially improved on therapy; however, 3 weeks after the treatment initiation, the patient started complaining of weakness and fatigue. Repeat tests revealed elevated LFTs. Autoimmune titers were positive for antinuclear antibody, anti-smooth muscle antibody with elevated immunoglobulin (IgG), and serum gamma globulin levels. Repeat liver biopsy in June 2014 showed markedly distorted architecture secondary to formation of nodules completely enclosed by fibrous septa and areas of confluent necrosis with mild to moderate chronic inflammation consisting mainly of lymphocytes and plasma cells along with moderate to severe interface hepatitis. Ballooning degeneration of hepatocytes, with rosette formation possibly associated with regenerative activity was seen, consistent with superimposed autoimmune hepatitis. Based on laboratory and biopsy findings, diagnosis of drug-induced autoimmune hepatitis was made, and the treatment for HepC with sofosbuvir and ribavirin was discontinued. The patient was subsequently administered prednisolone with improvement in LFTs. We describe a patient with autoimmune hepatitis after initiation of sofosbuvir and ribavirin. To our knowledge, this complication has never been reported before in association with sofosbuvir. The most frequent adverse events noticed with this combination regimen have been headache, anemia, fatigue, and nausea.