Case Presentation: 80 y.o. female with a history significant for hypertension and hyperlipidemia who presented to the Emergency Department for abnormal blood work. Patient had been in her usual state of health but had noticed a dark color to her urine and a yellow tinge to her eyes.On review of her blood work she was found to have: severe acute kidney injury with a Creatinine of 10.62 and diffusely elevated liver enzymes with an ALP of 857, an AST to 738 and an ALT to 343. She was also found with a primarily conjugated hyperbilirubinemia with a direct bilirubin of 7.9 and a total bilirubin of 10.4. Finally our patient was noted to have an elevated creatine kinase to 10,711. The patient was initially treated for presumed rhabdomyolysis with aggressive IV fluids and worked up for obstructive jaundice. MRI abdomen ultimately showed a pancreatic head mass of 2.6 cm which was confirmed as pancreatic adenocarcinoma on biopsy. While her liver enzymes normalized after an ERCP and stent placement, the patient’s CK continued to rise despite fluids. Upon prompting the patient disclosed that she had noticed significant weakness in climbing the stairs to her apartment for a number of weeks due to bilateral thigh weakness.Given the concern for paraneoplastic myositis, an MRI of the lower extremities was conducted which showed areas of bilateral muscle signal hyper-intensity in the thigh area compatible with myositis. A muscle biopsy was inconclusive due to inaccessible muscle tissue due to excess fatty tissue. Our patient was started on steroids and had resolution of her AKI and CK and was discharged with close oncology follow-up.

Discussion: Adenocarcinomas have a close relationship with inflammatory myopathies making up about 70% of cases of paraneoplastic myopathies. However, diagnosing an inflammatory myositis can be difficult. A number of criterias have been utilized over the last few decades. While the Bohar and Peter criteria rely heavily on characteristic findings on muscle biopsy in order to make a diagnosis, the updated EULAR/ACR guidelines set parameters in cases that a biopsy is not possible. This made diagnosing our patient easier given that her muscle biopsy was inconclusive. While not pathognomonic for polymyositis, this finding can be a marker of long-standing inflammatory myopathy. A serologic work-up for inflammatory myopathy was also sent which were negative. This supported our assessment as there is an association between negative routine myositis panels and malignancy.We did consider a number of other etiologies for her symptoms. Commonly used medications and substances like statins, colchicine, glucocorticoids, antiretroviral therapies (ART) therapies, alcohol and cocaine are associated with myopathy. The only offending medication on the patient’s list was her statin which was discontinued on admission and she had no history of substance use. Given consistent clinical picture, concurrent malignancy, negative traditional serologies, and supporting MRI imaging the team elected to treat her with high dose steroids which led to improvement in her weakness, her CK and kidney function to her baseline.

Conclusions: Paraneoplastic myopathies are not uncommon in patients with malignancy and should be considered in any patient with cancer presenting with new musculoskeletal complaints. Diagnosis can be difficult without conclusive muscle biopsy but advancement in imaging, a concordant clinical picture, and negative traditional inflammatory serological testing can all help support the diagnosis.