We describe a 79-year-old gentleman with a longstanding history of chronic lymphocytic leukaemia who presented with subacute onset of cholestatic jaundice. Comprehensive review of the patient's data and medications failed to reveal any obvious causes. Exhaustive testing including abdominal CT and magnetic resonance cholangiopancreatography failed to reveal any obstruction. A liver biopsy demonstrated scattered non-caseating granulomas. The patient was diagnosed with granulomatous hepatitis and treated with oral steroids and eventually improved. It was thought to be due to paraneoplastic cholestasis as an extrahepatic manifestation of non-Hodgkin's lymphoma.
e22184 Background: Heparin induced thrombocytopenia (HIT) is known to be caused by the presence of PF 4 antibody. Tumors exert immunomodulatory effects on the host immune response, including development of antibodies. Our aim was to analyze the presence of HIT in cancer patients and determine if HIT Ab is an adverse risk factor in patients with cancer. Methods: Patients with suspected HIT were selected. A case – control study was designed with 1:1 age and gender matched controls. We used chi – square analysis to compare proportions and Cox proportional hazard model to detect various predictors. Time to survival analysis was performed using Kaplan – Meier method. Results: Of 600 patients, 300 (63±15 years, women 48.8%) had a mean 4T pre – probability score of 4 ± 1.6. There were 132 cancers in both groups. 65 of these (49.2%) were in patients with probable HIT. The numbers of carcinomas and sarcomas were not significantly different between the two groups. There were no significant differences between the two groups when comparing the number of cancer diagnoses or the particular types of cancer diagnosed. The mean time to detection of cancer was within 9 ± 23 months for patients with HIT Ab versus 31 ± 54 months in cancer patients without HIT Ab (p <0.0001). In addition, there was a greater number of patients with at least 2 primary cancers among the HIT Ab positive group (p = 0.003). No predictive relationship between the type of cancer and the presence of HIT Ab was found (p >0.05). Patients with advanced cancer (stage 3 or 4) were also more likely to be HIT Ab positive (HR 3.61; 95% CI 1.31 – 10.11, p = 0.013). Cancer patients with HIT Ab were more likely to have venous thromboembolism as compared to cancer patients without HIT Ab (7.7% vs. 4.7, p = 0.0001). Kaplan – Meier’s showed worse mortality for cancer patients with HIT Ab than patients without the HIT Ab (Breslow statistic = 0.04). Conclusions: Among our cohort with suspected HIT, cancer was a common finding. Patients with HIT antibody positivity were more likely to have a new cancer diagnosis within 1 year of a positive result. These patients were also more likely to have thromboembolic complications and worsened mortality. These findings require further study, but perhaps suggest that the presence of HIT Ab should trigger earlier surveillance for cancer.
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