An 85-year-old hypertensive woman was started on amoxicillin for a dental abscess. Two days later she developed nausea and vomiting with dull pain over the left upper abdomen, later involving the right side as well. On examination she was febrile with severe tenderness over both hypochondria with no palpable hepatosplenomegaly.Her laboratory investigations showed a leukocyte count of 15.5 × 109/L/mm3 (normal range, 3.5–10.5 × 109/L). Liver function tests showed normal bilirubin levels with aspartate aminotransferase levels of 2001 U/L (normal range, 8–43), alanine aminotransferase levels of 2333 U/L (normal range, 9–29), and alkaline phosphatase levels of 157 U/L (normal range, 55–142). Hepatitis serologies were negative. An axial image from a computerized tomography scan (Figure A) in the portal venous phase (long arrow) shows thrombus in the splenic vein, the 2 short arrows show thrombus in the segmental branches of the right portal vein. There is extensive splenic infarction. In the coronal image (Figure B), a portal venous phase scan shows extensive splenic vein thrombus (long arrows), thrombus in the segmental branch of the right portal vein (short arrow), extensive splenic infarct, and a large area of low attenuation in the superior portion of the right hepatic lobe that could represent perfusion abnormality, fatty infiltration, or evolving infarct. An axial view of a computerized tomography scan of the liver 5 months later showed a small wedge-shaped area of low attenuation in the right hepatic lobe with volume loss and overlying capsular retraction, consistent with infarct (Figure C).A thrombophilia screen was negative. A work-up for intra-abdominal malignancy also was negative. Common causes for hepatic infarction are post–liver transplant, hepatic artery embolization, vasculitis, and thrombophilia. She developed mesenteric ischemia 14 months after the initial episode, which required emergency laparotomy. Her international normalized ratio was subtherapeutic at this time. An 85-year-old hypertensive woman was started on amoxicillin for a dental abscess. Two days later she developed nausea and vomiting with dull pain over the left upper abdomen, later involving the right side as well. On examination she was febrile with severe tenderness over both hypochondria with no palpable hepatosplenomegaly. Her laboratory investigations showed a leukocyte count of 15.5 × 109/L/mm3 (normal range, 3.5–10.5 × 109/L). Liver function tests showed normal bilirubin levels with aspartate aminotransferase levels of 2001 U/L (normal range, 8–43), alanine aminotransferase levels of 2333 U/L (normal range, 9–29), and alkaline phosphatase levels of 157 U/L (normal range, 55–142). Hepatitis serologies were negative. An axial image from a computerized tomography scan (Figure A) in the portal venous phase (long arrow) shows thrombus in the splenic vein, the 2 short arrows show thrombus in the segmental branches of the right portal vein. There is extensive splenic infarction. In the coronal image (Figure B), a portal venous phase scan shows extensive splenic vein thrombus (long arrows), thrombus in the segmental branch of the right portal vein (short arrow), extensive splenic infarct, and a large area of low attenuation in the superior portion of the right hepatic lobe that could represent perfusion abnormality, fatty infiltration, or evolving infarct. An axial view of a computerized tomography scan of the liver 5 months later showed a small wedge-shaped area of low attenuation in the right hepatic lobe with volume loss and overlying capsular retraction, consistent with infarct (Figure C). A thrombophilia screen was negative. A work-up for intra-abdominal malignancy also was negative. Common causes for hepatic infarction are post–liver transplant, hepatic artery embolization, vasculitis, and thrombophilia. She developed mesenteric ischemia 14 months after the initial episode, which required emergency laparotomy. Her international normalized ratio was subtherapeutic at this time. Improving Clinical Trial Efficiency in GastroenterologyGastroenterologyVol. 157Issue 3PreviewWe read with interest the recent article by Harris and Howden, “Innovative Trial Designs in GI Drug Development: Why Trials Succeed and Fail,”1 Given the rich pipeline of next-generation therapies across multiple disciplines of gastroenterology, we are pleased to see this dialogue on critical, although often neglected topics, in clinical trial design. Many agents that seem to be promising in preclinical studies fail to show efficacy in human trials, and Harris and Howden discuss several concepts that may improve trial success rates, including integrated phase and adaptive enrichment designs, early assessment of pharmacodynamic effects with biomarker and target engagement, objective disease evaluation by endoscopy and histology, and prospective, randomized, open-label blinded end point studies. Full-Text PDF
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Oct 18, 2024
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