Recombinant granulocyte colony-stimulating factor (rG-CSF) is a myeloid growth factor that is widely used in haematology to recover neutropenia secondary to myelosuppressive chemotherapy. Leukocytoclastic vasculitis is an acknowledged side effect of the above therapy. Its pathogenesis involves many mechanisms that collectively induce an increase in neutrophil function and a subsequent release of cytokines. Here, we report a case of leukocytoclastic vasculitis proven by skin biopsy, following the use of rG-CSF in a heart transplant patient with leukopenia secondary to immunosuppressive therapy. 1. Introduction Vasculitis is an inflammation of the blood vessel wall that leads to various clinical manifestations, depending on which organ system is involved. Cutaneous vasculitis is a histopathologic entity that is characterized by neutrophilic transmural inflammation of the vessel wall and is associated with fibrinoid necrosis, which is also termed leukocytoclastic vasculitis. Vasculitis has a wide spectrum of severity, ranging from skin-limited disease to life-threatening systemic involvement [1]. rG-CSF (filgrastim) is a myeloid growth factor produced by monocytes, macrophages, fibroblasts, and endothelial cells. The clinical use of rG-CSF includes recovery from neutropenia in patients receiving myelosuppressive chemotherapy for solid as well as hematologic malignancies; management of neutropenia deriving from other causes such as AIDS, genetic disorders in granulocyte production and, mobilization of peripheral blood progenitor cells [2, 3]. Some side effects have been reported for rG-CSF treatment: they are usually mild and they include bone pain, headache, and fatigue [3, 4]. Below, we report a case of leukocytoclastic vasculitis that occurred during rG-CSF treatment in a heart transplant patient. 2. Case Report A 35-year-old man was admitted to our hospital because of leukopenia and anaemia. The patient had undergone heart transplantation (H-Tx) two months previously on account of dilated cardiomyopathy. After H-Tx, immunosuppression consisted in rabbit antithymocyte globulin (RATG) for three days (in doses that were regularly adjusted on the basis of absolute CD3+ T lymphocytes count), cyclosporine A, azathioprine, and steroids. No acute rejection episodes or infectious or autoimmune diseases were observed during followup. At admission, the patient was on cyclosporin A (CyA:？trough levels: 200？ g/l), azathioprine (AZA: 100？mg/d), and steroids (5？mg/d). Laboratory data showed WBC /mcl, neutrophils /mcl, Hb g/dL, and platelets /mcl. Renal, hepatic, and
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