Pepsin and bile acid concentrations in sputum of mustard gas exposed patients

Gastro-esophageal reflux has been suggested to be associated with several pulmonary complications such as asthma, and post-transplant bronchiolitis obliterans [BO]. Pepsin or bile salts in the sputum is shown to be an optimal molecular marker of gastric contents macro/micro aspiration. In this study, we investigated sputum pepsin as a marker of micro-aspiration in sulfur mustard [SM] exposed cases compared to healthy controls. In a case controlled study, 26 cases with BO and 12 matched healthy controls were recruited and all cases were symptomatic and their exposure to SM was previously documented during Iran-Iraq conflict. Pepsin levels in sputum and total bile acids were measured using enzymatic assay. The severity of respiratory disorder was categorized based upon the spirometric values. The average concentration of pepsin in sputum was higher in the case group [0.29 +/- 0.23] compared with healthy subjects [0.13 +/- 0.07; P +/- 0.003]. Moreover, the average concentration of bile acids in the sputum cases was not significantly different in comparison to the controls [P = 0.5]. Higher pepsin concentrations in sputum of SM exposed patients compared with healthy control subjects indicate the occurrence of significantly more gastric micro-aspiration in SM exposed patients

Diagnostic methods of active pulmonary TB

Tuberculosis is considered a major cause of morbidity and mortality worldwide. According to the WHO report 9.4 million individuals were suffering from active TB in 2009 [1]. Diagnostic methods for active pulmonary TB include: clinical suspicion, tuberculin skin test, acid fast bacilli stain, cultures for maycobacterium, and in recent years NNA [nucleid acid amplification]. An ideal test for pulmonary active tuberculosis should be easily performed with rapid results, it should have high sensitivity and specificity, low cost,technically easy to operate and reproducible results in a variety of settings, have the possibility of drug-susceptibility testing and could distinguish Mycobacterium tuberculosis from other mycobacteria. Direct smear sputum microscopy is the primary method for diagnosing pulmonary tuberculosis but it lacks enough sensitivity and only about 44% of all new cases are detected by this method [2]. Culture technique is still seen as the gold standard for active TB. Although, the sensitivity and specificity of culture is high, this method is slow and time consuming and needs special laboratory equipments [3,4,5]. It not only provides the detection of various mycobacterial species but also the examination of drug sensitivity. It also provides the examination of genotype for epidemiological purposes if needed. Nucleic acid amplification tests [NAATs] can be performed in one day. But NAAT are not [fully] standardized and the diagnostic accuracy is highly heterogeneous, and need experienced personnel and expensive equipments

Hepatitis C and pulmonary fibrosis

Hepatitis C virus [HCV] is a hepatotropic and lymphotropic virus that causes hepatic and extrahepatic disease. Emerging clinical data suggest that chronic HCV infection can lead to many direct and indirect effects on the lung. This article discusses evidence on the relationship between HCV infection and pulmonary fibrosis to increase knowledge on this topic among clinicians and scientists and highlights the need for further study. We searched the MEDLINE, ISI WEB OF KNOWLEDGE, OVID, ELSEVIER, and MDCONSULT databases and top respiratory journals, such as the American Journal of Respiratory and Critical Care, Chest, and Thorax for articles in English using the following keywords: hepatitis C, HCV infection, IPF, pulmonary fibrosis, and interstitial pneumonitis. We reviewed the reference lists of all identified studies. The evidence for a pathogenetic link between pulmonary fibrosis and HCV is: the higher frequency of HCV markers in IPF patients, an increase in lymphocyte and neutrophil numbers in bronchoalveolar lavage of chronic HCV infection patients, and the development of IPF in HCV-related chronic hepatitis that is treated with interferon. There is a discrepancy between studies on the frequency of HCV in IPF patients, which might be attributed to geographical differences of in the prevalence of HCV infection, selection bias in choosing the control group, and the HCV genome. BAL studies in HCV infection are associated with increased counts of lymphocytes and neutrophils in BAL fluid. These studies show that HCV infection is associated with nonspecific pulmonary inflammatory reactions that are not compatible with IPF but that it can lead to pulmonary fibrosis. The other factor is interferon therapy. Interstitial pneumonia and sarcoidosis are well-documented complications of IFN therapy. More extensive cohort studies should be conducted to confirm an actual causal relationship between HCV infection and pulmonary fibrosis