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)