Abstract

Rhabdomyolysis is characterized by muscle necrosis and leakage of toxic intracellular contents into the circulatory system. It is most commonly caused by trauma, physical exertion, drugs, toxins, and a variety of infections; only rarely is it associated with acute human immunodeficiency virus (HIV) infection alone. The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening electrolyte imbalances and acute kidney injury. High HIV viral load is associated with higher muscle breakdown that increases the incidence of severe acute kidney injury and sometimes the need for renal replacement therapy. The introduction of highly active antiretroviral therapy (HAART) revolutionized the treatment of HIV infection and increased the life expectancy of such patients by suppressing viral replication. Myopathy is one of the neuromuscular manifestations of HIV. It can occur either as a result of a complication of HIV itself or as a result of medicines used to control HIV. Muscle involvement of HIV infection ranges from asymptomatic muscle enzyme elevation to severe, HIV-associated polymyositis or pyomyositis. Here we report a case of acute retroviral syndrome presenting as severe non-traumatic rhabdomyolysis.

Highlights

  • Rhabdomyolysis is characterized by muscle necrosis and leakage of toxic intracellular contents into the circulation

  • The concurrent risk factors of rhabdomyolysis include substance abuse, alcohol use, medication-related adverse effects such as the use of statins in combination with highly active antiretroviral therapy, opportunistic infections associated with human immunodeficiency virus (HIV), or co-infection with other viruses including hepatitis C [7,8,9]

  • The study showed that patients with a higher viral load were more likely to have an infectious etiology (p = 0.004); those with a suppressed viral load were more likely to have medications underlying the cause of their rhabdomyolysis (p < 0.001)

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Summary

Introduction

Rhabdomyolysis is characterized by muscle necrosis and leakage of toxic intracellular contents into the circulation. Increased myoglobin and creatine phosphokinase (CK) as a consequence of muscular cell death are the major laboratory findings [1] It is most commonly caused by trauma, physical exertion, drugs, toxins, and a variety of infections. A 24-year-old African American male with no significant past medical history presented to the emergency department with a five-day history of severe weakness, generalized muscle pains, and decreased urine output. He denied any trauma, exertional activity, or prolonged immobilization. About five days after the start of antiretroviral therapy, the patient’s symptoms and his CK level improved significantly (Figure 1) His urine output gradually increased and he was discharged home with scheduled outpatient dialysis.

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