A Rare Cause of Esophageal Dysphagia - Secondary Esophageal Tuberculosis.

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. It continues to be one of the most common causes of death in adults across all countries. It is found to be relatively lower in North America. When aerosol droplets that contain Mycobacterium tuberculosis are inhaled, it can deposit in the respiratory tract, particularly in the patient's lungs. Following this deposition, one of the four outcomes can take place. These include clearance of the organism immediately, primary disease, latent infection, and reactivation disease. Unhindered bacterial growth after primary infection can lead to a hematogenous spread of bacilli to produce disseminated TB. Esophageal involvement causing esophageal TB can be primary or secondary esophageal TB. We present a unique case of secondary esophageal TB with symptoms of dysphagia and odynophagia with primary TB focus on the lung. Computed tomography (CT) of the chest noted diffuse bilateral miliary lung disease. TB QuantiFERON gold and sputum culture were positive for TB. Mycobacterial culture for identification with high-performance liquid chromatography showed isoniazid-resistant TB. The patient was started on antitubercular therapy with rifampin, ethambutol, moxifloxacin, and pyrazinamide for a total of nine months. Esophagogastroduodenoscopy (EGD) reported severe ulcerations of the oropharynx and focal ulceration in the proximal to the mid esophagus. Histopathology revealed active ulcerative and granulomatous esophagitis with mycobacterial organisms. After EGD she was started on a full liquid diet and advanced as tolerated. After discharge, she followed with the Health Department and had three negative sputum cultures after the completion of therapy.

Primary prophylaxis of variceal bleeding.

Gastroesophageal varices are present in almost half of patients with cirrhosis at the time of initial diagnosis. Variceal bleeding occurs in 25% to 35% of patients with cirrhosis. Effective and timely care can prevent variceal bleeding (primary prophylaxis). For example, clinical studies demonstrate that both beta-blockers and endoscopic variceal ligation are effective in preventing a first episode of variceal bleeding. The major challenge is to screen patients in a timely manner and institute a form of therapy that has the highest chance of success in terms of patient compliance and effectiveness.

Secular trends in the incidence of cholangiocarcinoma in the USA and the impact of misclassification.

BACKGROUND AND AIMS: It has been reported that the incidence of intrahepatic cholangiocarcinoma (ICC) has increased in the USA, while extrahepatic cholangiocarcinoma (ECC) has decreased or remained stable. However, neither the recent trends nor the effects of the misclassification of Klatskin tumors are known. METHODS: Using the Surveillance, Epidemiology, and End Results program databases, we calculated the average annual age-adjusted incidence rates (AA-IRs) of ICC and ECC in 4-year time periods (1992-1995, 1996-1999, 2000-2003, 2004-2007). These AA-IRs were calculated with misclassified as well as correctly classified Klatskin tumors. AA-IRs were also calculated based on age, sex, and race. Multivariable Poisson regression models were used to evaluate the secular trends of ICC and ECC. RESULTS: The AA-IR of ICC was 0.92 in 1992-1995 and 0.93 in 2004-2007, while the AA-IR of ECC increased from 0.70 in 1992-1995 to 0.95 in 2004-2007. There was no significant trend in AA-IR of ICC (p = 0.07), while there was a significant increase in ECC across the 4-year time periods (p < 0.001). Klatskin tumors comprised 6.7% of CCs with approximately 90 and 45% misclassified as ICC during 1992-2000 and 2001-2007, respectively. Adjusted Poisson models showed no significant differences in the temporal trend of ICC or ECC due to misclassification of Klatskin tumors. CONCLUSIONS: The incidence of ICC has remained stable between 1992 and 2007 with only slight fluctuations, while the incidence of ECC has been increasing. Misclassification of Klatskin tumors does not appear to play a significant role in the trends of CCs.

HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV.

UNLABELLED: Data show that viral genotype 1 may increase the risk of cirrhosis and hepatocellular carcinoma (HCC) compared to genotype 2 in patients with chronic hepatitis C virus (HCV) infection. However, the effect of HCV genotype 3 on cirrhosis and HCC risk is uncertain. We identified patients with active HCV infection, confirmed by positive polymerase chain reaction (PCR) and a known HCV genotype, from the VA HCV Clinical Case Registry between 2000 and 2009. We examined the effect of HCV genotype on the risk of cirrhosis and HCC in a Cox proportional hazards model adjusting for patients' age, period of service (World War I/II, Vietnam era, post-Vietnam era), race, gender, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment receipt. Of the 110,484 patients with active HCV viremia, 88,348 (79.9%) had genotype 1, 13,077 (11.8%) genotype 2, 8,337 (7.5%) genotype 3, and 1,082 (0.9%) patients had genotype 4 infection. Despite being younger, patients with genotype 3 had a higher risk of developing cirrhosis (unadjusted hazard ratio [HR] = 1.40, 95% confidence interval [CI] = 1.32-1.50) and HCC (unadjusted HR = 1.66, 95% CI = 1.48-1.85) than HCV genotype 1 patients. After adjustment for prespecified demographic, clinical, and antiviral treatment factors, the risk of cirrhosis and HCC was 31% (adjusted HR = 1.31, 95% CI = 1.22-1.39) and 80% (adjusted HR = 1.80, 95% CI = 1.61-2.03) higher in patients with genotype 3 compared to genotype 1 infected patients. CONCLUSION: HCV genotype 3 is associated with a significantly increased risk of developing cirrhosis and HCC compared to HCV genotype 1. This association is independent of patients' age, diabetes, body mass index, or antiviral treatment.

An overview of emerging therapies for the treatment of chronic hepatitis C.

Advances in our understanding of the HCV lifecycle and refinement of in vitro methods to select candidate compounds with anti-HCV activity have led to development of DAA agents and other novel antiviral therapies capable of increasing the curative SVR rates in patients with CHC. The use of the liner protease inhibitors telaprevir and boceprevir, in combination with Peg-IFN-a and ribavirin has become the new SOC for treatment of CHC genotype 1. Rapid development of new protease inhibitors, NI and NNI NS5B polymerase inhibitors, NS5A inhibitors, Peg-IFN-l, cyclophilin inhibitors, caspase inhibitors, and therapeutic vaccines promises to provide even safer and more effective therapy. Combination therapies with 2 or more oral agents may permit elimination of Peg-IFN-a in the near future. Introduction of DAA therapies will confront physicians and patients with regimens of increased complexity, a greater need for compliance, and the necessity of monitoring for virological resistance. Patients with CHC should continue to consider participation in clinical trials of new therapies to accelerate progress.

Liver transplantation in autoimmune liver diseases.

Liver transplantation is indicated for terminal phases of autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis. Indications for transplantation in autoimmune liver diseases are similar to those used in other acute or chronic liver diseases. Therapeutic advances have reduced the need for transplantation for autoimmune hepatitis and primary biliary cirrhosis but not for primary sclerosing cholangitis. Overall, outcomes of transplantation for autoimmune liver diseases are excellent. However, recurrence of autoimmune liver diseases in the allograft has variable impacts on graft and patient survivals. Treatment of recurrent diseases requires changes in immunosuppression or addition of ursodeoxycholic acid. Among autoimmune liver diseases, only autoimmune hepatitis occurs de novo in recipients transplanted for other diseases. Patients transplanted for autoimmune hepatitis or primary sclerosing cholangitis are at risk for reactivation or de novo onset of ulcerative colitis. Better understanding of the pathogenesis of recurrent autoimmune liver diseases is needed to devise effective means of prevention and treatment.

An overview of emerging therapies for the treatment of chronic hepatitis C.

Chronic hepatitis C (CHC) is a leading cause of chronic hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma (HCC) worldwide. Currently, pegylated interferon (Peg-IFN) and ribavirin therapy achieve curative responses in 40% to 80% of patients, depending on genotype. Recognition of new therapeutic targets for HCV therapy has led to development of novel therapies. The purpose of this review is to summarize the status of novel therapeutics for CHC that promise to increase the safety and efficacy of therapy.