Rodenticide ingestion is an important cause of acute hepatotoxicity in Tamil Nadu, southern India.

BACKGROUND AND AIM: Though rodenticidal hepatotoxicity is reported from India, there is no systematic study to assess its magnitude. This study aimed to assess exposure to rodenticide as a risk factor for acute hepatotoxicity in Tamil Nadu, India. METHODS: We retrospectively analyzed acute hepatotoxicity caused by ingestion of hepatotoxin or potentially hepatotoxic drug overdose across 15 hospitals in 6 districts of Tamil Nadu from 1 January 2019 to 30 June 2019. Study exclusion criteria were idiosyncratic drug-induced liver injury and chronic liver diseases. RESULTS: Of the 702 patients, 685 gave history of consuming rodenticide; hepatotoxicity in the other patients resulted from paracetamol overdose (n=10) and due to other drugs (n=7); 97% patients had a suicidal intent. Of 671 patients with complete data, ratio of number of patients with hepatotoxicity due to rodenticide to paracetamol overdose was 450:6 (i.e. 75:1). The 451 rodenticidal hepatotoxicity patients (255 males, 75% were 15-34 years old) underwent conservative management (n=396), plasma exchange (n=54) and plasma exchange followed by liver transplant (n=1); 159 patients (35%) had poor outcome (131 died, 28 discharged in moribund state). Based on our observations, we estimate a case burden of 1584 rodenticidal hepatotoxicity patients (95% CI: 265-6119) with poor outcome in 554 patients in Tamil Nadu from January 2019 to June 2019. Population attributable risk for rodenticide as cause of hepatotoxicity was 22.7%. CONCLUSION: Rodenticide ingestion was an important cause of acute hepatotoxicity in Tamil Nadu. Most patients were young and one-third had poor outcome. Public health interventions are needed to address this.

CagA and VacA genes of Helicobacter pylori and their clinical relevance.

CONTEXT: : Helicobacter pylori is associated with the development of a variety of gastroduodenal diseases which varies with ethnicity and the type of strains that infect the population. AIMS: This study aims to evaluate the prevalence of H. pylori cagA and vacA genotypes in our region and to determine their relationship to the severity of the lesions that they cause. SETTINGS AND DESIGN: : This study was an observational cross-sectional study. SUBJECTS AND METHODS: DNA was extracted from 165 gastric biopsies from patients evaluated for dyspepsia. PCR was used to detect cagA and vacA (s1, s2, m1, m2) genes of H. pylori. Statistical analysis of associations was performed between endoscopy findings and virulence genes. STATISTICAL ANALYSIS USED: Pearson Chi-square test and Fischer's exact test. RESULTS: The prevalence of H. pylori infection was 37% and the dominant genotypes was vacA s1 cagA-positive strain (54.1%) in this study. The vacAs1 subtype was found in all patients with peptic ulcer disease (PUD). The entire normal study group had VacA s2 variant only. This clearly shows that vacA s1 is a significant virulence marker and patients harboring s1 strains are more prone to develop ulcers (P = 0.007). There was a significant association of cagA with s1 strain rather than s2. Variation in VacA m genotype did not seem to have any association with disease status. There was a statistically significant association between the presence of cagA gene and PUD rather than the nonulcer dyspepsia (P = 0.027). CONCLUSION: The predominant genotype in our population was cagA positive vacA s1, which was found to be significantly associated with patients with gastric diseases, especially PUD. VacA s1 can serve as a single best virulence marker of the disease manifestation.