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    • As for the acantholysis the patient had

    2018-10-29

    As for the acantholysis, the patient had negative direct immunofluorescence and indirect immunofluorescence studies, which exclude autoimmune bullous diseases. In addition to keratinocyte injury induced shedding, exfoliative toxin A produced by targets desmoglein 1 and may cause acantholysis. Moreover, in a previous report, two out of 10 patients treated with cetuximab, an EGFR antibody, were noticed to have intraepidermal acantholysis with mild perifolliculitis 4 days and 8 days after treatment, respectively. Neither Candida nor bacteria were found in culture at the onset of these lesions. Therefore, EGFR inhibition might also contribute to acantholysis. Controversially, EGFR overactivation could cause loss of cell adhesion in tumor Go 6976 and EGFR inhibition was reported to promote desmosome assembly and strengthen intercellular adhesion in squamous cell carcinoma cells. However, the effects of EGFR inhibition on intercellular adhesion of keratinocytes, instead of tumor cells, remained unclear. Further studies may be needed.
    Lichen planus (LP) is a common chronic inflammatory mucocutaneous condition of unknown origin that usually affects middle-aged patients. Nail involvement occurs in 10% of patients, with permanent damage to at least one nail occurring in ∼4% of patients. The nails may also be affected in the absence of cutaneous symptoms. Herein we report a case of a patient with nail LP who was refractory to topical and intralesional corticosteroids but was treated successfully with topical tacrolimus. A 17-year-old girl was referred from a local clinic for onychodystrophy of fingernails with poor response to topical agents. The nail lesions had occurred and progressed for 2 months. The patient denied any trauma to, or contact history for, the affected areas. Physical examination revealed soft, thin, splitting, brittle nails, including swelling with erythematous change without cutical involvement of the proximal nail folds and onycholysis, on the second and forth fingers of the left hand and the fifth finger of the right hand. Asymptomatic slightly raised whitish plaques were noted over the bilateral buccal mucosa (). No other skin lesions were found. A nail matrix biopsy was suggested, but the patient refused due to concerns over possible nail deformity after the biopsy. Some recent studies have suggested that a diagnosis of nail LP may be made when it exists together with typical cutaneous/mucous membrane disease. Under the clinical impression of nail and oral lichen planus, twice daily treatment with topical triamcinolone ointment for the oral lesions and twice daily topical treatment with 0.1% diflucortolone valerate ointment along with intralesional triamcinolone injection every 2 weeks for the nail lesions were initiated. After 2 weeks of therapy, the buccal lesions resolved (A). However, onychodystrophy of the fingernails persisted after 2 months of topical and intralesional corticosteroid treatment. Therefore, treatment with topical and intralesional corticosteroids were both held and topical 0.1% tacrolimus ointment was then tried on the proximal and lateral nail folds twice a day. The nail lesions began to improve after 2 weeks of treatment and showed marked improvement 4 months after topical tacrolimus treatment (). Thus far, the patient has exhibited no signs of relapsing. Although mild nail LP is usually asymptomatic, deformation of the nails often causes depression among patients. Nail loss or permanent nail dystrophy may even occur in some cases. Treatment of nail LP is difficult, and an optimal therapy is confusing. Different treatment modalities have been used in nail LP. Although stabilizing selection are usually ineffective, topical corticosteroids are commonly considered as a first-line treatment for nail LP. For involvement of up to three nails, intralesional steroid injections can be considered, but such injections are very painful and relapses are common. If more than three nails are involved, systemic corticosteroids are considered as a first-line treatment; however, prolonged or repeated use of systemic corticosteroids may cause considerable side effects. To the best of our knowledge, there has only been a single previously published case report in English regarding the successful use of tacrolimus ointment to treat nail LP. Activated T cells are likely to play an important role in the pathogenesis of LP, and tacrolimus is an immunosuppressive agent which has been shown to be 10–100 times more potent than cyclosporine in the inhibition of T-cell activation. Topical tacrolimus has been reported as a safe, effective therapy for cutaneous, oral, and vulvar LP, even in patients whose lesions have shown recalcitrance to other treatments. In a previous report regarding topical tacrolimus treatment of nail LP, no recurrence after discontinuing treatment was noted in two patients at 16 months and 36 months of follow-up, respectively. Herein, we share an interesting case of nail LP with a good response to treatment with topical 0.1% tacrolimus ointment. Topical tacrolimus ointment can be an effective therapy for nail LP and further investigation is required to establish the effectiveness and the long-term prognosis after the cessation of topical tacrolimus treatment.