S5726 Hepatic Infiltration and Failure by IgA Kappa Multiple Myeloma

Introduction: Multiple myeloma is a clonal plasma cell proliferative disorder in which unchecked monoclonal immunoglobulins lead to end-organ dysfunction, typically manifesting as hypercalcemia, renal dysfunction, anemia, and bony lesions. Extramedullary involvement of the liver is rare and does not have a typical manifestation as case reports range from asymptomatic transaminitis to acute liver failure, the latter of which we present here. Case Description/Methods: A 67-year-old man was admitted for persistent biliary leak from recent robotic cholecystectomy. He had previously undergone biliary stenting and biliary drain placement at outside hospital. Upon arrival, a repeat ERCP was performed without over leak visualized. However, over the course of one week, he started showing signs and symptoms of acute liver failure including rising liver function tests (LFTs) with unclear etiology, impaired synthetic function with international normalized ratio of 1.9, and persistent jaundice. He had >3 L/day of biliary drain output questionable for ascites and developed encephalopathy from progressive renal failure versus hepatorenal syndrome. Abdominal ultrasound showed no signs of cirrhosis or preexisting liver disease. Interestingly, subsequent workup showed a paraprotein gap and increased light chains which raised suspicion for multiple myeloma. An endoscopic retrograde cholangiopancreatography was repeated which affirmed no leak from biliary stump however concurrent liver biopsy showed hepatic involvement by plasma cell neoplasm. Results were consistent with hepatic infiltration by IgA-k multiple myeloma which was confirmed with bone marrow biopsy. Patient was started on Dara-CyBorD with response to treatment, however subsequent drug-induced liver injury (DILI) on repeat liver biopsy restricted his therapeutic options. Currently, he remains on chemotherapy with a close eye on liver function. Discussion: There are several dozen case reports of extramedullary hepatic involvement of multiple myeloma over the last 3 decades, ranging from LFT elevations to hepatic masses on imaging to fulminant hepatic failure. As in our case, an initial presentation on the severe end of the spectrum is rare. Histologic patterns include diffuse plasma cell infiltration, light chain deposition disease, and amyloidosis. As the number of reports rise, it is important to consider hepatic involvement to anticipate progression to hepatic failure, hepatotoxicity associated with chemotherapeutic drugs, and a poorer prognosis if involvement is confirmed.

Authors

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150364.30674.69
Primary Topic
Multiple Myeloma Research and Treatments
Type
article
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article

S5726 Hepatic Infiltration and Failure by IgA Kappa Multiple Myeloma

Andrew Dries, Rutvi Katariya
The American Journal of Gastroenterology
Multiple Myeloma Research and Treatments
article

S5726 Hepatic Infiltration and Failure by IgA Kappa Multiple Myeloma

Andrew Dries, Rutvi Katariya
article en

Abstract

Introduction: Multiple myeloma is a clonal plasma cell proliferative disorder in which unchecked monoclonal immunoglobulins lead to end-organ dysfunction, typically manifesting as hypercalcemia, renal dysfunction, anemia, and bony lesions. Extramedullary involvement of the liver is rare and does not have a typical manifestation as case reports range from asymptomatic transaminitis to acute liver failure, the latter of which we present here. Case Description/Methods: A 67-year-old man was admitted for persistent biliary leak from recent robotic cholecystectomy. He had previously undergone biliary stenting and biliary drain placement at outside hospital. Upon arrival, a repeat ERCP was performed without over leak visualized. However, over the course of one week, he started showing signs and symptoms of acute liver failure including rising liver function tests (LFTs) with unclear etiology, impaired synthetic function with international normalized ratio of 1.9, and persistent jaundice. He had >3 L/day of biliary drain output questionable for ascites and developed encephalopathy from progressive renal failure versus hepatorenal syndrome. Abdominal ultrasound showed no signs of cirrhosis or preexisting liver disease. Interestingly, subsequent workup showed a paraprotein gap and increased light chains which raised suspicion for multiple myeloma. An endoscopic retrograde cholangiopancreatography was repeated which affirmed no leak from biliary stump however concurrent liver biopsy showed hepatic involvement by plasma cell neoplasm. Results were consistent with hepatic infiltration by IgA-k multiple myeloma which was confirmed with bone marrow biopsy. Patient was started on Dara-CyBorD with response to treatment, however subsequent drug-induced liver injury (DILI) on repeat liver biopsy restricted his therapeutic options. Currently, he remains on chemotherapy with a close eye on liver function. Discussion: There are several dozen case reports of extramedullary hepatic involvement of multiple myeloma over the last 3 decades, ranging from LFT elevations to hepatic masses on imaging to fulminant hepatic failure. As in our case, an initial presentation on the severe end of the spectrum is rare. Histologic patterns include diffuse plasma cell infiltration, light chain deposition disease, and amyloidosis. As the number of reports rise, it is important to consider hepatic involvement to anticipate progression to hepatic failure, hepatotoxicity associated with chemotherapeutic drugs, and a poorer prognosis if involvement is confirmed.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 40%
Multiple Myeloma Research and Treatments
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