Introduction
Vasculitis, defined as the inflammation of blood vessels, can be due to primary or secondary causes. Primary vasculitis results from an isolated inflammatory attack upon the blood vessels, and secondary vasculitis is due to an underlying health condition, but the clinical presentation between them is similar (1). Such a presentation can include localized or systemic signs and symptoms such as purpura, petechiae, fever, malaise, arthralgias/arthritis, peripheral blood eosinophilia, and any other organ involvement(2). Once determining the type and cause behind the vasculitis, it is crucial to decide on the extent of the vasculitis. This means assessing the vasculitis location and size, which can help in confirming the diagnosis. (3)
Once the diagnosis is determined, we can move to management and treatment. These can vary based on the type, cause, and degree of vasculitis. In our case, vasculitis was secondary to atorvastatin, and the treatment consisted of stopping the drug and taking moderate dose steroids for a short period.
Drug-induced vasculitis often leads to ANCA-associated vasculitis, and the offending agents that have been implicated include hydralazine, PTU, montelukast, and others.
Drug-induced vasculitis can appear similar to primary vasculitis, so it can be hard to distinguish; furthermore, no specific test can confirm the causative drugs. One method to orient the diagnosis is the increase in ANCA levels, which can be assessed with high titers of anti-myeloperoxidase. (4) This noticeable increase also disappears with the removal of the drugs. (5)
Although not as commonly noted in the literature, one offending agent is a statin, given the rarity of its occurrence or underdiagnosis. Statins are widely used for the treatment of dyslipidemia. However, the adverse effects are mainly myopathy and muscle weakness when reported. (6)