No abstract

Keratoacanthoma (KA) is a common epidermal tumor that originates from the hair follicle of the skin. It is generally considered as a benign neoplasm, but in rare cases, it can also transform into squamous cell carcinoma. Although surgical excision with a safety margin is considered to be the gold standard treatment for most subtypes of KA, several other treatment options are also available. Intralesional therapy is one of these options, which could be cosmetically and functionally a better alternative to surgical removal, while it provides similar outcomes. It is more effective than topical treatments, yet fewer side effects may be seen than in systemic treatments. Based on the literature, the most commonly used intralesional agent is methotrexate, followed by 5‐fluorouracil and interferon alpha. Regardless of the advantages, which make intralesional therapy a desirable treatment alternative, guidelines for the intralesional treatment of KA are not yet established. A histopathological confirmation before the start of treatment is still recommended to prevent any possible misdiagnosis of KA for SCC. In our present study, we set out to review the current state of the art of the intralesional treatment of KA.

Lichen planus (LP) is a relatively common inflammatory dermatosis (with a prevalence of approximately 0.5%), characterized by violaceous, polygonal, flat pruritic papules. It can involve both skin and mucous membranes and usually occurs in middle-aged persons. Mild cases usually heal spontaneously, but patients with widespread lesions are sometimes hard to treat. Different treatment modalities are available. Topical anti-inflammatory treatment with steroid ointments or calcineurin inhibitors have limited efficacy. Phototherapy, systemic treatment with retinoids, and depot steroids have been administered with limited success, and systemic ciclosporin is usually effective.Tumour necrosis factor alpha (TNF-a) has a key role in the pathogenesis of LP (1). Thalidomide, a potent anti-inflammatory drug, acting inter alia through TNF-a-mediated cellular responses, has been found effective in the treatment of LP (2). Only a few data on the efficacy of TNF-a inhibitors in LP are available in the literature (3, 4). CASE REPORTA 39-year-old woman developed 2-3-mm large itchy purplish lichenoid papules and plaques with Wickham's sign on the whole body surface, in especially large numbers on the buttocks, lower legs and forearms. White reticular striation and plaques were found bilaterally on the buccal mucosa. The diagnosis of lichen planus was confirmed by histology. The patient had no previous history of any other diseases. A general examination did not detect any underlying systemic disorders or background infections. The patient did not take any drugs. Hepatitis B and C sérologies were negative. Topical steroid creams, systemic glucocorticoids (0.5 mg/kg, 4-week-long therapy) and 20 sessions of psoralen plus ultraviolet A (PUVA) treatment were administered without any therapeutic effect. Acitretin therapy maintained for 3 months at a dose of 0.5 mg/kg/day did not result in clinical improvement. A side-effect of hair loss was detected. Meanwhile, her skin symptoms progressed significantly. Ten months after disease onset the TNF-a inhibitor adalimumab was requested for individual offlabel use, and initiation of therapy was permitted by the National Institute of Pharmacology.Adalimumab was administered subcutaneously for 3 months at the recommended dose (80 mg induction dose followed by 40 mg every second week from day 7) usually accepted for the treatment of psoriasis (Fig. 1). Fig. 1. (a, b) Disseminated papules of lichen planus, (c, d) regressed after adalimumab treatment.

No abstract

SummaryMastocytosis is a rare disease with reported high interleukin-6 (IL6) levels influencing disease severity. The present study investigated polymorphisms within the genes that encode IL6 and its receptor (IL6R) in relation to mastocytosis development in a case-control design. Analysis of the IL6R Asp358Ala polymorphism showed that carriers of the AA genotype had a 2Á5-fold lower risk for mastocytosis than those with the AC or CC genotypes. No association with mastocytosis was found for the IL6À174G/C polymorphism, however, it may influence the effect of IL6R polymorphism. To the best of our knowledge this is the first study analysing IL6/IL6R polymorphisms in mastocytosis.