HCC Associated with Polymyositis, Rhabdomyolysis, and Acute Renal Failure 893 for diagnosing the DM. Second, DM has been too rarely asso- ciated with HCC compared of its epidemic, particularly in Korea. Myoglobinemic ARF could be caused by non-traumatic skeletal muscle injury. Up to now, less than ten cases of the PM-induced myoglobinemic ARF have been reported in the literature. PM/DM could be presented as one of paraneoplas- tic manifestations, but only some cases of HCC-associated with PM/DM have been reported. This is a rare reported case of PM associated with HCC, present with fulminant rhab- domyolysis and ARF. Because of the rapidly deteriorating con- dition of the patient, it is difficult to determine whether PM occurred as a paraneoplastic syndrome or took place coinci- dentally with HCC in our case. A causal relationship between HCC and PM/DM was demonstrated in the case reported by Hasegawa et al. (3). Although the pathogenesis of PM/ DM has not been clarified, two reports suggested that HCV- induced autoantibodies or circulating immune complexes could contribute to the pathogenesis of PM/DM (11, 12). Hepatitis C virus was not detected in our case. Myoglobin- uria occurs not infrequently in patients with PM/DM, but it is rarely followed by ARF. About the pathophysiology of renal failure in rhabdomyolysis, Lewington et al. documented acute tubular necrosis and obstructive tubular cast of myo- globin in renal biopsy from the case of ARF which was attri- buted to rhabdomyolysis, secondary to PM (8). Both early hypocalcemic and late hypercalcemic phase were observed in this case. Either hyperphosphatemia-induced bone resistance to PTH or decreased levels of 1,25 dihydroxyvita- min D have been implicated as precipitating factors in the development of hypocalcemia. In the case of massive muscle necrosis and extensive calcification, the movement of calcium into necrotic muscle is regarded as a major contributory fac- tor. Remobilization of calcium from muscles has been thought to be a main mechanism for the development of subsequent hypercalcemia (13). Massive muscle calcification in ARF caused by non-trau- matic rhabdomyolysis has been rarely reported, whose mecha- nism has not been clarified yet. Coakley and colleagues (14) suggested that leakage of calcium into inflamed muscle cells where the phosphate concentration is high, leads to intracel- lular deposition of calcium phosphate. But Gray et al. (15) suggested that hyperphosphatemia, which is due to the release from damaged muscle cells, and the decreased renal clear- ance of phosphate are the main mechanisms for muscle cal- cification. Adams et al. (16) reported that muscle calcifica- tion could occasionally be seen, and appears as hypo-intense areas on MR imaging in patients with idiopathic inflamma- tory myopathies. To our knowledge, this is the first reported case of PM in which massive muscle calcification is proven pathologically. Akmal et al. (17) demonstrated that calcium deposits in dam- aged muscles occur during the oliguric phase of ARF due to rhabdomyolysis, and the calcification disappears with recovery of renal failure. Unfortunately, we did not follow up on mus- cle calcification after recovery from oliguric phase of ARF. Our case demonstrates that PM could be associated with HCC and instigate rhabdomyolysis leading to ARF. PM must be considered in the differential diagnosis of non-traumatic rhab- domyolysis and investigation for the associated malignancy, including HCC, should be included. REFERENCES 1. Yazici Y, Kagen LJ. The association of malignancy with myositis. Curr Opin Rheumatol 2000; 12: 498-500. 2. 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