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An Unusual Case of Cirrhosis

DOI: 10.1155/2014/670176

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Abstract:

49-year-old white female with remote h/o sarcoidosis was referred to GI when her liver was noted to be nodular. Physical examination revealed normal vital signs and no icterus, spider nevi, clubbing, ascites, hepatosplenomegaly, or ankle edema. LFTs, hepatitis serologies, ANA, AMA, ASMA, Ferritin, Ceruloplasmin, and α1-AT, level were unremarkable. Liver biopsy showed cirrhosis. She developed worsening of baseline SOB and was hospitalized. She was eventually diagnosed with constrictive pericarditis. A diagnosis of cardiac cirrhosis was made. 1. Introduction Constrictive pericarditis is a rare but severely disabling consequence of the chronic inflammation of the pericardium, leading to an impaired filling of the ventricles and reduced ventricular function [1]. The timely diagnosis of a cardiac etiology of liver dysfunction is important because such dysfunction is potentially reversible if the underlying cardiac disease is treated before the development of frank cirrhosis [2, 3]. Below, we present a case of a 49-year-old female who was incidentally found to have cirrhosis. Initial workup was negative. Thoracic imaging showed pericardial calcifications which ultimately led to the diagnosis of constrictive pericarditis. We will briefly discuss the literature on cardiac causes of liver cirrhosis. 2. Case Report 49-year-oold white female with remote h/o sarcoidosis was referred to GI when her liver was noted to be nodular during laparoscopy for an ovarian cyst. She denied fatigue, vomiting-up blood, abdominal distension and pain, ankle swelling, itching, yellow discoloration of skin and eyes, and episodes of confusion or sleepiness. She denied alcohol abuse. Physical examination revealed normal vital signs and no icterus, spider nevi, clubbing, ascites, hepatosplenomegaly, or ankle edema. LFTs revealed mild elevation in alkaline phosphatase and PT was slightly prolonged. CBC showed mild thrombocytopenia. Hepatitis serologies, ANA, AMA, ASMA, Ferritin, Ceruloplasmin, and α1-AT, level were unremarkable. A liver biopsy was done. It confirmed cirrhosis. Biopsy did not show any granulomas but showed sinusoidal dilatation which prompted a referral to cardiology. ECHO showed enlarged IVC and was otherwise unremarkable. A left and right heart catheterization was done. LHC showed normal coronaries and RHC showed RAP of 12?mm?Hg, PAP of 32/15 (mean 21) mm?Hg, PAWP of 18?mm?Hg, LVEDP of 18?mm?Hg, and CO of 5.2?L/min. She developed worsening shortness of breath and was referred to pulmonary medicine. PFTs showed mild restriction but CXR was unrevealing. CTPA ruled out PE

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