ELECTRONIC CLINICAL CHALLENGES AND IMAGES IN GI An Unexpected Cause of an Infiltrative Liver Mass Vivian Ng,1 Tram T. Tran,2 and Vinay Sundaram2 1
Department of Medicine, Division of Gastroenterology, University of California at Los Angeles Medical School, Los Angeles; and 2Department of Gastroenterology and Hepatology and Comprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, California
Question: A 73-year-old man with history of obesity, diabetes, and recently diagnosed cryptogenic cirrhosis is admitted to the hospital for progressively worsening ascites and altered mental status. He had been living in El Salvador for the past 6 years and had recently returned to the United States. The patient denies significant alcohol use but had a history of obesity throughout his adult life, with a body mass index of >40 kg/m2. The patient’s home medications included Furosemide, spironolactone, and metformin. He reported frequent ingestion of the herb Chipilin (Crotalaria longirostrata). Physical examination revealed icteric sclera, moderate abdominal distention without tenderness, and asterixis. Laboratory studies demonstrated an alanine aminotransferase of 100 U/L, aspartate aminotransferase of 139 U/L, alkaline phosphatase of 138 U/L, total bilirubin of 16.0 mg/dL, albumin of 3.1 g/dL, platelet count of 99,000/UL, and International Normalized Ratio of 2.6. Hepatitis B and C serologies were negative and alpha-fetoprotein level was normal. Magnetic resonance imaging revealed hepatomegaly with a nodular liver contour and without fatty infiltration of the liver. Additionally, diffuse, heterogeneous signal intensity was seen primarily in the right hepatic lobe, with heterogeneous enhancement and washout pattern, suggestive of an infiltrative malignancy (Figure A). The hepatic veins and portal veins were patent (Figure B). A targeted, computed tomography–guided liver biopsy was performed (Figure C, D). Based on the clinical scenario, imaging, and pathologic findings, what is the diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2014.03.038
Gastroenterology 2014;147:e12–e13
ELECTRONIC CLINICAL CHALLENGES AND IMAGES IN GI Answer to the Clinical Challenges and Images in GI Question: Image 6: Sinusoidal Obstructive Syndrome Liver biopsy demonstrated changes consistent with hepatic outflow obstruction, including partial central vein obstruction from organizing thrombi (Figure C) and sinusoidal congestion and dilatation with hepatocyte dropout in zone 3 (Figure D). The findings were consistent with sinusoidal obstructive syndrome (SOS). No evidence of malignancy was found on biopsy. The significant degree of hepatic congestion secondary to the venous outflow obstruction can lead to the infiltrative picture seen on imaging.1 Once the patient was diagnosed with SOS, he was placed on anticoagulation. However, he developed acute renal failure during his hospital course, and per the patient and his family’s wishes, he decided not to undergo dialysis and instead undergo comfort measures only. He died shortly afterward. SOS is a form of acute hepatic injury secondary circulatory to obstruction at the sinusoidal level, often occurring concurrently with central vein obstruction. Associated clinical features include hyperbilirubinemia, ascites, weight gain, and hepatomegaly. Although most commonly seen as a complication from myeloablative conditioning regimens before hematopoietic stem cell transplantation, ingestion of food containing pyrrolizidine alkaloids may also lead to SOS. The patient’s family reported that the patient frequently ingested Chipilin (Crotalaria longirostrata), a plant containing pyrrolizidine alkaloids. Consumption of large amounts of this plant can cause acute SOS, and chronic ingestion of lower doses can lead to a subacute presentation of SOS.2
References 1. 2.
Mortelé KJ, Van Vlierberghe H, Wiesner W, et al. Hepatic veno-occlusive disease: MRI findings. Abdom Imaging 2002; 27:523–526. DeLeve LD, Shulman HM, McDonald GB. Toxic injury to hepatic sinusoids: sinusoidal obstruction syndrome (venoocclusive disease). Semin Liver Dis 2002;22:27–42.
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Department of Medicine, Division of Gastroenterology, University of California at Los Angeles Medical School, Los Angeles; and 2Department of Gastroenterology and Hepatology and Comprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, California
Question: A 73-year-old man with history of obesity, diabetes, and recently diagnosed cryptogenic cirrhosis is admitted to the hospital for progressively worsening ascites and altered mental status. He had been living in El Salvador for the past 6 years and had recently returned to the United States. The patient denies significant alcohol use but had a history of obesity throughout his adult life, with a body mass index of >40 kg/m2. The patient’s home medications included Furosemide, spironolactone, and metformin. He reported frequent ingestion of the herb Chipilin (Crotalaria longirostrata). Physical examination revealed icteric sclera, moderate abdominal distention without tenderness, and asterixis. Laboratory studies demonstrated an alanine aminotransferase of 100 U/L, aspartate aminotransferase of 139 U/L, alkaline phosphatase of 138 U/L, total bilirubin of 16.0 mg/dL, albumin of 3.1 g/dL, platelet count of 99,000/UL, and International Normalized Ratio of 2.6. Hepatitis B and C serologies were negative and alpha-fetoprotein level was normal. Magnetic resonance imaging revealed hepatomegaly with a nodular liver contour and without fatty infiltration of the liver. Additionally, diffuse, heterogeneous signal intensity was seen primarily in the right hepatic lobe, with heterogeneous enhancement and washout pattern, suggestive of an infiltrative malignancy (Figure A). The hepatic veins and portal veins were patent (Figure B). A targeted, computed tomography–guided liver biopsy was performed (Figure C, D). Based on the clinical scenario, imaging, and pathologic findings, what is the diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.
Conflicts of interest The authors disclose no conflicts. © 2014 by the AGA Institute 0016-5085/$36.00 http://dx.doi.org/10.1053/j.gastro.2014.03.038
Gastroenterology 2014;147:e12–e13
ELECTRONIC CLINICAL CHALLENGES AND IMAGES IN GI Answer to the Clinical Challenges and Images in GI Question: Image 6: Sinusoidal Obstructive Syndrome Liver biopsy demonstrated changes consistent with hepatic outflow obstruction, including partial central vein obstruction from organizing thrombi (Figure C) and sinusoidal congestion and dilatation with hepatocyte dropout in zone 3 (Figure D). The findings were consistent with sinusoidal obstructive syndrome (SOS). No evidence of malignancy was found on biopsy. The significant degree of hepatic congestion secondary to the venous outflow obstruction can lead to the infiltrative picture seen on imaging.1 Once the patient was diagnosed with SOS, he was placed on anticoagulation. However, he developed acute renal failure during his hospital course, and per the patient and his family’s wishes, he decided not to undergo dialysis and instead undergo comfort measures only. He died shortly afterward. SOS is a form of acute hepatic injury secondary circulatory to obstruction at the sinusoidal level, often occurring concurrently with central vein obstruction. Associated clinical features include hyperbilirubinemia, ascites, weight gain, and hepatomegaly. Although most commonly seen as a complication from myeloablative conditioning regimens before hematopoietic stem cell transplantation, ingestion of food containing pyrrolizidine alkaloids may also lead to SOS. The patient’s family reported that the patient frequently ingested Chipilin (Crotalaria longirostrata), a plant containing pyrrolizidine alkaloids. Consumption of large amounts of this plant can cause acute SOS, and chronic ingestion of lower doses can lead to a subacute presentation of SOS.2
References 1. 2.
Mortelé KJ, Van Vlierberghe H, Wiesner W, et al. Hepatic veno-occlusive disease: MRI findings. Abdom Imaging 2002; 27:523–526. DeLeve LD, Shulman HM, McDonald GB. Toxic injury to hepatic sinusoids: sinusoidal obstruction syndrome (venoocclusive disease). Semin Liver Dis 2002;22:27–42.
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