br Discussion There have been only cases

Discussion There have been only 12 cases of ticlopidine-induced lupus and only two cases of ticlopidine-induced SCLE reported in the literature (Table 1). The time from ticlopidine exposure to the onset of drug-induced lupus varied from 1 week to 4 years. Most patients started to feel better after discontinuing ticlopidine for several weeks and completely recovered after several months. ANAs and antihistone nonreceptor tyrosine kinase are a common finding in drug-induced lupus and are detected in almost all ticlopidine-induced systemic lupus cases. ANAs and Ro/SS-A autoantibodies were detected in both cases of ticlopidine-induced SCLE. The case of ticlopidine-induced SCLE reported in Poland shares many similar findings with our patient, including old age (age >70 years), the presence of anti-Ro/SS-A autoantibodies, interface dermatitis, and the resolution of cutaneous lesions soon after discontinuing ticlopidine. There is no significant difference between drug-induced and non-drug-induced SCLE based on clinical, histopathological, or immunopathological features. Both present with annular/papulosquamous lesions occurring mainly in sun-exposed areas, interface dermatitis with perivascular lymphocytes infiltration, and detectable ANA, anti-Ro/SS-A (a positive result is obtained in more than 80% of cases), or occasionally anti-La/SS-B autoantibodies. Attempting to distinguish drug-induced from non-drug-induced SCLE by tissue eosinophilia is not reliable or feasible. One clue for a physician to consider is that drug-induced SCLE often affects older individuals presenting with SCLE for the first time, particularly those being treated with antihypertensive or antifungal agents. Although the golden standard for a definite diagnosis is a rechallenge test, it is not ethical in most situations. Therefore, a diagnosis can also be made if a complete recovery is achieved after halting the suspected medication. The pathogenesis underlying drug-induced SCLE is unclear, but is probably multifactorial and complex. Reed et al proposed possible mechanisms that included enhancing Ro/SS-A antigen expression, enhancing epidermal cytotoxicity through direct phototoxicity, or enhancing anti-Ro/SS-A antibody production. In the review by Lowe et al and the study by Sontheimer et al, many drugs that trigger SCLE were argued to do so by inducing a photosensitivity state. There has been no report that ticlopidine could cause a photosensitive reaction but its chemical analog, the thienopyridine (clopidogrel), has been reported to induce photosensitive lichenoid eruption.
A 60-year-old woman with a medical history of infiltrative ductal carcinoma of the right breast underwent breast-conserving surgery and axillary lymph node dissection, followed by adjuvant chemotherapy, hormone therapy, and radiotherapy (conventional radiotherapy, 25 fractions for a total dose of 5000 cGy). Six years after treatment, asymptomatic skin eruptions on the right side of the chest and axilla were observed for 4 weeks. The patient was referred to the dermatology department for suspected cutaneous metastases. Physical examination revealed multiple discrete papules, clear fluid-containing vesicles, and lesions with a mild erythematous base on the right side of the chest. A grayish, rubbery but compressible cystic nodule, 1.5 cm in diameter, was observed near the right axillary fossa (). No regional lymphedema or significant sclerotic change of the skin was noted. Excisional biopsy of the 1.5-cm cystic nodule was performed. Histopathological analysis revealed diffuse anastomotic vessels and dilation of the vascular space, mostly in the deep dermis (A), with concomitant dissection of collagen bundles in some areas (B). In the subcutis, more dilated vascular channels with stromal projection were observed (C). The endothelial cells were plump, discontinuous in a single layer, without cytologic atypia (D). Immunohistochemistry revealed positive staining for CD31, positive staining for CD34 (E), and negative staining for smooth muscle actin (F). A postradiation lymphatic type atypical vascular lesion (AVL) was diagnosed.