Correspondence Address:
Ipek Gungor Dogan
Department of Neurology, Sancaktepe Sehit Prof. Dr. Ilhan Varank Training and Research Hospital, Istanbul
Turkey

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Leukocytoclastic vasculitis (LCV) is small-vessel vasculitis involving arterioles, capillaries, and postcapillary venules. It is histopathologically characterized by an inflammatory infiltrate consisting of neutrophils with fibrinoid necrosis and nuclear debris referred to as “leukocytoclasia.”[1] The microscopic changes seen in LCV are not specific to any disease entity; thus, this kind of histopathologic picture may occur in various types of small-vessel vasculitis affecting the skin and internal organs. However, because of the dominancy of single-organ skin-limited presentations, the name LCV is more commonly used synonymously for cutaneous small-vessel vasculitis and cutaneous leukocytoclastic angiitis.[2]

LCV usually presents as palpable purpura, symmetrically distributed on the lower extremities, with or without systemic involvement.[2],[3] It may be either idiopathic or associated with an underlying pathology such as systemic diseases, medications, infections, or malignancy. In medication-induced LCV, antibiotics and nonsteroidal anti-inflammatory drugs are the most common triggers.[3] In recent years, however, with increased use, biologic agents have taken their place in the literature as new suspects in the etiology of LCV.[4] Among these publications, very few rituximab-induced LCV cases stand out.[5],[6],[7],[8],[9]

Here, we report the case of a 28-year-old woman with a 3-year history of generalized myasthenia gravis (MG) presenting with LCV developing shortly after rituximab infusion.

A 28-year-old woman, with a history of fluctuating weakness and diplopia following the postpartum period, was diagnosed as having anti-acetylcholine receptor antibody-positive MG at the age of 25 years. Her past disease-modifying treatment record included prednisolone (PLN), intravenous immunoglobulins (IVIG), and mycophenolate mofetil (MMF). In the early period, treatment response to PLN was good, but she soon developed marked iatrogenic Cushing's syndrome. IVIG failed to improve her condition without PLN. Recently, MMF was stopped after 15 months due to a lack of benefits. Rituximab therapy was considered after all these treatment attempts. Ten days after the first i.v. infusion of 1000-mg rituximab, skin lesions suddenly appeared on the lower extremities of her body, which were compatible with nonblanching purpuric lesions [Figure 1]a. Her vital parameters were within normal range, and systemic examination revealed no abnormalities. Laboratory tests performed to assess any organ involvement or related systemic diseases were all normal. A skin biopsy was performed, and the histopathologic findings revealed LCV [Figure 2]a and [Figure 2]b.{Figure 1}{Figure 2}

Based on the temporal association between the rituximab infusion and skin lesions and the clinicohistopathologic findings, a diagnosis of rituximab-induced LCV was made. Rituximab therapy was discontinued. Due to severe arthralgia accompanying purpuric lesions, a short-term oral steroid regimen was planned in addition to topical corticosteroids. In 2 weeks, both her skin lesions and arthralgia showed regression, and no recurrence was observed during a 3-month follow-up period [Figure 1]b.

 Discussion

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