TAK-242 Cutaneous eruptions have been increasingly reported

Cutaneous eruptions have been increasingly reported after the use of tumor necrosis factor (TNF) blockers, such as acneiform eruption, alopecia areata, urticaria, and palisaded neutrophilic and granulomatous dermatitis. Lichen striatus is an enigmatic self-limiting inflammatory dermatosis with lesions following the lines of Blaschko, particularly common in children. The etiology of the eruption is unknown, but environmental factors, viral infection, cutaneous injury, hypersensitivity, and genetic predisposition have been implicated. The differential diagnosis includes epidermal nevi, linear psoriasis, linear morphea, linear lichen planus, and linear cutaneous lupus erythematosus. Lichen striatus typically presents as a nonpruritic continuous or interrupted linear band of small (1–3 mm) pink or hypopigmented papules, with a smooth surface or mild scaling. Histopathologic findings depend on the stage of evolution, with variable epidermal changes and lichenoid inflammation. Perivascular and deep lymphocytic infiltrate surrounding the hair follicles and TAK-242 are characteristic. Lichen striatus can be associated with psoriasis or eczema. In a small case series of 18 patients with lichen striatus, Taieb et al described two patients with psoriasis and six patients with atopic diathesis. Another three cases of psoriasis coexisting with lichen striatus were also found in our literature search. In the first case, unilateral lichen striatus preceded unilateral eruptive psoriasis on the contralateral side, and a common trigger was suspected to be the cause. In the second case report, lichen striatus developed in a patient with chronic plaque psoriasis after ultraviolet phototherapy. However, the authors thought that phototherapy did not cause lichen striatus, because lichen striatus resolved despite continuous phototherapy. In the third case, lichen striatus occurred after adalimumab treatment in a patient with long-standing psoriasis. The extent of the eruption was more extensive than in our case, but both occurred 3 months after adalimumab treatment. The mechanism of this unique phenomenon is unknown. It could be Th1/Th2 imbalance, cytokine imbalance between TNF-alpha and interferon-alpha, or loss of immune tolerance induced by an acquired stimulus, after TNF blockers. Lichen striatus associated with etanercept therapy in rheumatoid arthritis was reported recently. In our case, however, lichen striatus did not happen during the course of etanercept treatment. Although both are TNF blockers, etanercept and adalimumab still differ in terms of the mode of action. We speculate that the difference in the degree of immunosuppression may be one reason. Adalimumab is considered more immunosuppressive because clinical improvement of psoriasis is higher after adalimumab compared to etanercept. In addition, infection rate (in particular, tuberculosis) is also higher for adalimumab compared to etanercept. In our previous report, maximal improvement of psoriasis occurred 3 months after adalimumab treatment, coincidental with the time of onset of lichen striatus in our case.
Disseminated superficial actinic porokeratosis (DSAP), the most common subtype of porokeratosis, is a chronic autosomal dominant cutaneous disorder characterized by multiple superficial keratotic lesions surrounded by a slightly raised keratotic border. Generally, the lesions begin to develop in teenagers in sun-exposed areas of skin and reach near-complete penetrance by the third or fourth decade of life. The histological feature of the disease is the cornoid lamella. Exome sequencing identified that mutation of the mevalonate kinase gene () on chromosome 12q24 is the cause of DSAP; this has been supported by subsequent studies in additional individuals with DSAP. To date, due to relatively rare incidence and genetic heterogeneity, information on the causative mutations of found in DSAP patients are very limited. We carried out a genetic investigation on a family of Chinese DSAP patients (A and B) in which we identified one novel mutation of the gene (D).