Relapsed nodular lymphocyte-predominant Hodgkin lymphoma presenting as severe paraneoplastic hepatitis: a case report.

BACKGROUND: Hematological malignancies are an infrequent but important cause of liver dysfunction. There are several mechanisms by which this can occur, including direct malignant infiltration of the hepatic parenchyma and/or vasculature, vanishing bile duct syndrome, and paraneoplastic hepatitis. Paraneoplastic hepatitis is an extremely rare mechanism by which a hematological malignancy can cause liver dysfunction, and we present the first case, to our knowledge, of paraneoplastic hepatitis caused by nodular lymphocyte-predominant Hodgkin lymphoma in the literature. CASE PRESENTATION: A 28-year-old Caucasian male presented with 3 weeks of fatigue, epigastric pain, and jaundice. His medical history was significant for early stage nodular lymphocyte-predominant Hodgkin lymphoma in the cervical region in remission for 5 years after primary treatment with involved-field radiotherapy. Liver biochemistry was normal at the time of treatment for lymphoma and there was no known liver disease before the current presentation. On physical examination, there was scleral icterus and ecchymoses, but no evidence of hepatic encephalopathy, other stigmata of chronic liver disease, or lymphadenopathy. A computed tomography scan of his neck, chest, abdomen, and pelvis showed heterogeneous enhancement of the liver, multiple enlarged upper abdominal lymph nodes, and an enlarged spleen with multiple rounded lesions. Portal and hepatic veins were patent. Initial workup for viral, autoimmune-, toxin-, and medication-related hepatitis was negative. A transjugular liver biopsy was performed with histology showing a predominantly T-cell mediated hepatitis with very extensive multiacinar hepatic necrosis, but no evidence of lymphoma within the liver. Retroperitoneal lymph node biopsy revealed nodular lymphocyte-predominant Hodgkin lymphoma. The patient's symptoms, bilirubin, and transaminases improved significantly after treatment with oral prednisolone and a staged introduction of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy. CONCLUSIONS: Nodular lymphocyte-predominant Hodgkin lymphoma may cause paraneoplastic hepatitis. Physicians should be aware of the possibility of this life-threatening presentation and the importance of early liver biopsy and treatment before acute liver failure occurs. Interestingly, paraneoplastic hepatitis did not occur when nodular lymphocyte-predominant Hodgkin lymphoma was first diagnosed and confined to the cervical region, but was the presenting feature of the recurrence below the diaphragm.

Post-Endoscopy Upper Gastrointestinal Cancer Rate in a Tertiary Referral Centre: An Australian Data Linkage Analysis.

OBJECTIVE: High-quality gastroscopy is critical for early diagnosis of upper gastrointestinal cancers (UGCs), and assessment of missed cancers may serve as a key quality metric. Using a prospective gastroscopy database and data linkage with the Queensland Cancer Registry, we assessed the risk of developing UGC within 3 years of a cancer-negative gastroscopy at an Australian tertiary centre. Additional aims were to identify factors predictive of missed cancer, perform root cause analyses for missed cancers and assess overall survival. DESIGN/METHOD: We identified patients who were diagnosed with UGC within 3 years of undergoing gastroscopy between 2011 and 2016. Non-mucosal cancers, cancers distal to duodenum and patients undergoing surveillance were excluded. Cases diagnosed within 6 months of gastroscopy were defined as detected cancers, while those developing within 6-36 months were defined as missed cancers. Post-endoscopy UGC rate (PEUGIC-3Y) was calculated as ratio of missed over total cancers detected. Demographic, clinical, endoscopic and histologic variables were analysed. RESULTS: A total of 17,131 gastroscopies were performed for 10,393 patients during the study period. One hundred and twenty-six UGCs were diagnosed, including 120 detected UGCs and 6 missed UGCs. The overall PEUGIC-3Y rate was 4.8% (95% CI 2.1-10.4). The missed UGCs included 3 gastric adenocarcinomas, 2 gastro-oesophageal junction adenocarcinomas and 1 oesophageal squamous cell carcinoma. At the preceding 'cancer-negative gastroscopy', no macroscopic abnormalities were detected at the site of future UGC in 5/6 patients. A UGC developed in 2/6 patients despite an apparent adequate examination at index gastroscopy. Age, sex, indication for endoscopy and cancer location or histology were not predictive of missed cases, and survival was comparable between groups. CONCLUSION: We demonstrate that the PEUGIC-3Y rate was 4.8% (95% CI 2.1-10.4). The majority of missed cases were adenocarcinomas of the gastro-oesophageal junction or stomach and developed in segments which were found to be normal at index gastroscopy, highlighting the challenges in detecting subtle mucosal lesions in the upper gastrointestinal tract. While overall survival between patients with detected and post-gastroscopy cancers was comparable, these ultimately represent potential missed opportunities for diagnosing an early cancer and underscore the need for quality improvement in gastroscopy.