A case of granuloma faciale successfully treated with oral prednisone, tranilast and thalidomide

Granuloma faciale (GF) is an uncommon benign vascular inflammatory dermatosis with unclear etiology, usually occurring in middle-aged Caucasian men [1]. Clinically, the lesions of GF are characterized by single or multiple violaceous or reddish-brownish plaques, papules or nodules. Lesions are usually asymptomatic and grow slowly [2]. The typical histopathology of GF consists of mixed nodular inflammatory infiltration mainly composed of eosinophils and neutrophils in the dermis, and the “Grenz zone” in the superior dermis. In fresh lesions, there is observed leukocytoclastic vasculitis, and the old lesions show fibrosis and vascular proliferation [1]. Granuloma faciale is resistant to many treatments and prone to relapse. The typical therapies include topical, intralesional or systemic corticosteroid [3], dermabrasion [4], cryotherapy [5], laser treatments [6], and psoralen with ultraviolet A [7]. Other systemic treatments involve dapsone [3, 8], hydroxychloroquine [9] and clofazimine [10]. Here, we report a case of GF successfully treated with combined treatment of topical and systemic corticosteroids, tranilast and thalidomide.
A 58-year-old male patient was admitted to our hospital in June, 2015 with a 5- to 6-year history of facial and cheek itchy red plaques. Initially, the rash presented as ring-like erythema, gradually enlarging to form prominent nodular plaques with severe itching. This patient had no history of systemic disease or family history of genetic disease. There was no fever or trauma history before the onset and progression of the disease.
Systemic physical examination was normal. Skin lesions manifested dark-red plaques in irregular shapes scattering at the glabella and left cheek with a prominent edge. The middle area of partial lesions formed crusts and scaling. There was no skin atrophy or tenderness and the plaque was soft upon palpation (Figure 1).
There was no abnormality in the routine blood examination and the fungi microscopic detection. Histopathology features presented (Figure 2) hyperkeratosis with focal parakeratosis, hyperacanthosis and acanthosis with edema, liquefactive degeneration in some parts of the basal layer, mild edema in the superficial dermis, dilation and hyperemia of blood vessels, diffused infiltration of eosinophils, neutrophils, lymphocytes and histiocytes in the dermis and subcutaneous fat tissue, accompanied by hyperplasia of collagen. Infiltration of inflammatory cells was not involved...


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