Journal of the Formosan Medical Association (2014) 113, 137e138

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Acute rhabdomyolysis and chylous ascites in a patient with cirrhosis and malignant hepatic tumor Sarantuya Gidaagaya a,b, Jui-Ting Hu b,c, Ding-Shinn Chen d, Sien-Sing Yang b,c,* a

Department of Gastroenterology, Health Science University of Mongolia, Ulaanbaatar, Mongolia Liver Unit, Cathay General Hospital and Medical Faculty, Taipei, Taiwan c Medical Faculty, Fu-Jen Catholic University, Taipei, Taiwan d Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan b

Received 8 July 2011; received in revised form 22 July 2011; accepted 30 July 2011

A 73-year-old woman was admitted for chronic hepatitis B with cirrhosis and hepatocellular carcinoma. She denied recent usage of alcohol, drugs, or herbs. There was no recent incident of trauma, exertion, fever, or sepsis. She developed decompensated cirrhosis, ascites, and esophageal varices with albumin 3 g/dL, aspartate aminotransferase 250 IU/L, alanine aminotransferase 222 IU/L, total bilirubin 2.2 mg/dL, direct bilirubin 0.7 mg/dL, international normalized ratio for prothrombin time 1.71, creatinine 0.74 mg/dL, sodium 138 mmol/L, potassium 3.6 mmol/L, hepatitis B virus deoxyribonucleic acid 5.4  106 IU/mL, and alpha-fetoprotein 656 ng/mL. Both hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were detected to be positive. Telbivudine was prescribed on admission. Abdominal sonography, computed tomography, and magnetic resonance imaging confirmed the presence of two ill-defined tumors (5.8  5.2 and 3.3  2.8 cm2 in size) at the right liver and several retroperitoneal lymphadenopathies; the inferior vena cava was invaded by tumorous tissue with complete thrombosis. Conflicts of interest: The authors have no conflicts of interest relevant to this article. * Corresponding author. Liver Unit, Cathay General Hospital Medical Center, No. 280, Sec. 4, Jen-Ai Road, Taipei 10630, Taiwan. E-mail address: [email protected] (S.-S. Yang).

Liver histology could not be obtained due to massive ascites and coagulopathy. On the 11th day, the patient developed weakness and myalgia on her lower limbs. Acute idiopathic rhabdomyolysis was confirmed by the laboratory data of creatine phosphokinase (CPK) 3554 IU/L, CPK-MB 137.5 ng/mL, Troponin-I 0.04 ng/mL, myoglobin 2415 ng/mL, and lactate dehydrogenase 1326 IU/L. Acute renal failure was prevented by intensive hydration, urine alkalization and diuresis. On the 17th day, CPK was at 1831 IU/L and creatinine at 0.77 mg/dL despite continuous telbivudine use. Telbivudine has been reported to cause rhabdomyolysis at 11e21 months of treatment1 and was thus unlikely to be the cause of rhabdomyolysis in this patient. The patient developed chylous ascites with ascitic triglyceride level of 335 mg/dL on the 22nd day. The cultures of ascitic fluids, blood, and urine showed no bacterial growth. The ascitic fluid showed no atypical cell, and the adenosine deaminase was 2 U/L. The chylous ascites, which might have been caused by hepatocellular carcinoma with retroperitoneal lymphadenopathies, responded poorly to the low-fat diet with medium-chain triglyceride and diuretics. Because of deteriorating hepatic failure, the patient expired on the 30th day. To our knowledge, this is the first reported case of combined rhabdomyolysis and chylous ascites in a patient

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138 with cirrhosis and hepatocellular carcinoma. In cirrhotic patients, the incidence of idiopathic rhabdomyolysis was 1.8%, and the mortality rate ranged from 32.2% to 42.1%, depending on the patients’ underlying liver function.2 Rhabdomyolysis should be suspected in patients of decompensated cirrhosis with muscular symptoms such as weakness and myalgia.3 Early recognition and treatment may prevent acute renal failure. Chylous ascites occurs in 0.5e1.3% of cirrhotic patients.4 Portal hypertension with excessive lymph flow of up to 20 L/d would cause dilatation and rupture of lymphatic channels. Chylous ascites can be used to predict unfavorable outcome in patients with decompensated liver cirrhosis and hepatic malignancy. Methods of management of chylous ascites includes portosystemic shunt, transjugular intrahepatic portosystemic shunt, and octreotide with total parenteral nutrition.5

S. Gidaagaya et al.

References 1. Lai CL, Gane E, Liaw YF, Hsu CW, Thongsawat S, Wang Y, et al. Telbivudine versus lamivudine in patients with chronic hepatitis B. N Engl J Med 2007;357:2576e8. 2. Baek JE, Park DJ, Kim HJ, Lee JD, Chang SH. The clinical characteristic of rhabdomyolysis in patients with liver cirrhosis. J Clin Gastroenterol 2007;41:317e21. 3. Lee OJ, Yoon JH, Lee EJ, Kim HJ, Kim TH. Acute myopathy associated with liver cirrhosis. World J Gastroenterol 2006;12: 2254e8. 4. Cardenas A, Chopra S. Clinical review: chylous ascites. Am J Gastroenterol 2002;97:1896e900. 5. Zhou DX, Zhou HB, Wang Q, Zou SS, Wang H, Hu HP. The effectiveness of the treatment of octreotide on chylous ascites after liver cirrhosis. Dig Dis Sci 2009;54:1783e8.

Acute rhabdomyolysis and chylous ascites in a patient with cirrhosis and malignant hepatic tumor.

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