S5716 The Silent Infiltrator: Sarcoidosis Progressing to Cirrhosis

Introduction: Although hepatic involvement is a known manifestation of sarcoidosis, progression to cirrhosis is uncommon. Hepatic involvement—defined by abnormal liver enzymes, imaging findings, or histopathology—is seen in approximately 6%–30% of systemic sarcoidosis cases, though most are asymptomatic or non-progressive. Clinically significant complications, such as cirrhosis and portal hypertension, occur in a minority of patients. The pathogenesis is thought to involve chronic granulomatous inflammation, granulomatous phlebitis, and secondary ischemic injury. When cirrhosis develops, it carries substantial morbidity and mortality, with gastrointestinal bleeding and hepatic failure being common. Treatments like TIPS and variceal banding have shown limited efficacy in these cases. We present a case of hepatic sarcoidosis progressing to end-stage liver disease, emphasizing this rare but serious complication. Case Description/Methods: A 43-year-old African American woman initially presented to the hospital with complaints of progressive dysphagia, weight loss, chronic cough, and low-grade fevers. Lab work was significant for an elevated aspartate aminotransferase at 57 U/L, international normalized ratio of 1.2, and hemoglobin of 8.4 g/dL. Computed tomography Chest revealed mediastinal lymphadenopathy, bilateral ground-glass opacities, and hepatomegaly. Bronchoscopy with lymph node biopsy showed non-caseating granulomas consistent with stage I–II pulmonary sarcoidosis. A liver biopsy also demonstrated non-caseating granulomas, confirming hepatic involvement. She was diagnosed with sarcoidosis and started on prednisone 40 mg daily, with close outpatient follow-up. Seven years later, she returned with abdominal pain and swelling. She was diagnosed with cirrhosis and admitted for evaluation, including paracentesis and thoracentesis. Records from a recent outside hospital confirmed prior esophageal variceal banding. Imaging showed bilateral pleural effusions, mild pericardial effusion, and cirrhotic liver morphology on ultrasound. Findings consistent with decompensated liver disease secondary to hepatic sarcoidosis. Discussion: This case highlights how chronic liver involvement in sarcoidosis can quietly advance to fibrosis and, ultimately, cirrhosis—even in the absence of clear symptoms. In patients without common risk factors for liver disease, sarcoidosis should remain on the differential. Timely recognition, consistent follow-up, and early management may help slow progression and improve patient outcomes in this uncommon yet significant complication.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001150324.50364.cf
Primary Topic
Sarcoidosis and Beryllium Toxicity Research
Type
article
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0.00
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article

S5716 The Silent Infiltrator: Sarcoidosis Progressing to Cirrhosis

Pramod Reddy, Samir Sunil Parekh, Yasasvhinie Santharam, A. P. K. Reddy et al.
The American Journal of Gastroenterology
Sarcoidosis and Beryllium Toxicity Research
article

S5716 The Silent Infiltrator: Sarcoidosis Progressing to Cirrhosis

Pramod Reddy, Samir Sunil Parekh, Yasasvhinie Santharam, A. P. K. Reddy, Nadim Qadir, Gerardo Diaz Garcia
article en

Abstract

Introduction: Although hepatic involvement is a known manifestation of sarcoidosis, progression to cirrhosis is uncommon. Hepatic involvement—defined by abnormal liver enzymes, imaging findings, or histopathology—is seen in approximately 6%–30% of systemic sarcoidosis cases, though most are asymptomatic or non-progressive. Clinically significant complications, such as cirrhosis and portal hypertension, occur in a minority of patients. The pathogenesis is thought to involve chronic granulomatous inflammation, granulomatous phlebitis, and secondary ischemic injury. When cirrhosis develops, it carries substantial morbidity and mortality, with gastrointestinal bleeding and hepatic failure being common. Treatments like TIPS and variceal banding have shown limited efficacy in these cases. We present a case of hepatic sarcoidosis progressing to end-stage liver disease, emphasizing this rare but serious complication. Case Description/Methods: A 43-year-old African American woman initially presented to the hospital with complaints of progressive dysphagia, weight loss, chronic cough, and low-grade fevers. Lab work was significant for an elevated aspartate aminotransferase at 57 U/L, international normalized ratio of 1.2, and hemoglobin of 8.4 g/dL. Computed tomography Chest revealed mediastinal lymphadenopathy, bilateral ground-glass opacities, and hepatomegaly. Bronchoscopy with lymph node biopsy showed non-caseating granulomas consistent with stage I–II pulmonary sarcoidosis. A liver biopsy also demonstrated non-caseating granulomas, confirming hepatic involvement. She was diagnosed with sarcoidosis and started on prednisone 40 mg daily, with close outpatient follow-up. Seven years later, she returned with abdominal pain and swelling. She was diagnosed with cirrhosis and admitted for evaluation, including paracentesis and thoracentesis. Records from a recent outside hospital confirmed prior esophageal variceal banding. Imaging showed bilateral pleural effusions, mild pericardial effusion, and cirrhotic liver morphology on ultrasound. Findings consistent with decompensated liver disease secondary to hepatic sarcoidosis. Discussion: This case highlights how chronic liver involvement in sarcoidosis can quietly advance to fibrosis and, ultimately, cirrhosis—even in the absence of clear symptoms. In patients without common risk factors for liver disease, sarcoidosis should remain on the differential. Timely recognition, consistent follow-up, and early management may help slow progression and improve patient outcomes in this uncommon yet significant complication.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 51%
Sarcoidosis and Beryllium Toxicity Research
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