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.

Oesophageal carcinoma mimicking a submucosal lesion: A case report.

BACKGROUND: Oesophageal cancer is the fourth most common cause of cancer-related deaths in India. Esophageal squamous cell carcinomas (ESCCs) arise from the epithelial layer, and commonly present as polypoidal, ulcerative or ulceroproliferative growth in the oesophageal lumen. In contrast, oesophageal submucosal tumours are a distinct group of tumours arising from the mesenchyme (examples include leiomyoma, fibrovasculoma, lipoma, granular cell tumour or carcinoid), and mostly do not breach the mucosa. Oesophageal submucosal tumours are a distinct group of tumours arising from the mesenchyme, and mostly do not breach the mucosa. Complete intramural growth of an advanced primary ESCC is an exceedingly rare presentation, with only six cases reported in the literature thus far. We herein report a case of primary ESCC with complete intramural invasion that endoscopically mimics a submucosal lesion. CASE SUMMARY: A 50 year old male presented with a progressive mechanical type of dysphagia for one month. His history was significant, including squamous cell carcinoma of the tongue that was treated with surgery and chemoradiation 1 year prior. Upper gastrointestinal endoscopy revealed a large, hemispherical lesion with normal-appearing overlying mucosa about 4 cm × 5 cm in size extending from 30-34 cm from incisors. The patient underwent endoscopic ultrasound (EUS), and a fine­needle biopsy was performed, which was suggestive for squamous cell carcinoma. We herein report a case of primary ESCC with complete intramural invasion, endoscopically mimicking a submucosal lesion. The diagnosis could be established only by a EUS-guided biopsy. CONCLUSION: This case report highlights that intramural ESCC may look like a submucosal lesion in endoscopy, and EUS biopsy is needed for final diagnosis.