Treatment of hemophilia with factor VIII concentrates.
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A 31-year-old male presented with erythematous eruptions on the right side of the body since childhood. Physical examination revealed linear erythematous scaly papuloplaques at the right chest, abdomen, waist, suprapubic area, buttock, and back along Blaschko lines with a marked midline demarcation (Figure 1A,B). Similar skin lesions were distributed from the right thigh to the right ankle and from the right arm to the right thumb (Figure 1C,D) in a linear pattern along Blaschko lines. The patient's scalp, nails, and oral mucosa were all normal. Skin biopsy was performed. Histopathological examination revealed regular acanthosis, hypogranulosis, suprapapillary epidermal thinning, Munro microabscess, and parakeratotic stratum corneum. There were markedly dilated and tortuous capillaries within the dermal papillae and perivascular lymphocytic infiltration in the dermis (Figure 1E). Based on the clinical and the histopathological findings, blaschkoid psoriasis (BPso) was diagnosed. The eruptions were poorly controlled by topical corticosteroids and vitamin D analogues but then got improved gradually by combining narrowband ultraviolet B phototherapy, cyclosporine, and methotrexate. Treatment was started with narrowband UVB phototherapy three times per week and 7.5 mg methotrexate was added weekly initially. And then the dosage of methotrexate was titrated up to 15 mg weekly. After administration of methotrexate for 3 months, some plaques became less itchy, but still some new lesions appeared. Then methotrexate was discontinued and 125 mg cyclosporine was added daily. Most of the lesions became flatten under narrowband UVB phototherapy and cyclosporine. The patient remained stable condition under the daily dosage of cyclosporine 25 mg. BPso, an exceedingly rare variant of psoriasis, was first reported in 1951. It is characterized by linear distribution of psoriasis along Blaschko lines. The pathogenesis of BPso is unclear, but may be explained by genetic mosaics.1 The loss of heterozygosity in somatic cells during early embryogenesis and clone proliferation of stem cells may contribute to the characteristic pattern. Environmental factors, infection, and trauma are required as predisposing factors. Genetic mosaics followed by these factors explain why BPso usually does not appear at birth, but instead develops later. The patients of BPso are usually asymptomatic or only have mild pruritus. The majority of cases were noticed during infancy with positive family history. Some of the cases were affected extensively as ours. Interestingly, left side involvement was more common than right side. Classic psoriatic lesions can usually be found either before or after linear lesions, resulting in the superimposed form of BPso.2 The diagnosis of BPso is usually challenging for clinicians and should be differentiated from other dermatoses with similar blaschkoid distribution pattern including inflammatory linear verrucous epidermal nevus, blaschkoid lichen planus, lichen striatus, and linear lupus erythematosus. Skin biopsy plays an important role in making a correct diagnosis. Psoriasis is not only skin-deep inflammation, it can be associated with many systemic comorbidities such as major adverse cardiovascular events, metabolic syndrome, and so forth.3, 4 Early diagnosis and treatment may prevent serious comorbidities.5 Topical corticosteroids and vitamin D analogues are the mainstream treatment for localized BPso. Phototherapy, systemic antipsoriatic agents, and biologics should be considered in extensive and recalcitrant cases. In conclusion, we present an unusual variant of psoriasis with linear, blaschkoid asymmetric distribution pattern, lacking typical involved sites. This case reminds clinicians to take psoriasis into consideration under the differential diagnosis of blaschkoid dermatoses. Skin biopsy plays an important role in establishing the correct diagnosis. Psoriasis should be identified early from other similar blaschkoid dermatoses. Early and aggressive treatment may prevent serious comorbidities. The authors declare no potential conflict of interest.
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A hypertensive elderly male on amlodipine presented with a palpable purpuric rash on both legs followed by shoulder, buttocks, and back with foot ulcer, which was found to be leukocytoclastic vasculitis on skin biopsy. The patient recovered completely on discontinuation of amlodipine and short-term steroid.
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We have analyzed the clinical, analytical, radiologic, therapeutic an evolutive of cases of systemic mastocytosis (SM) skin lesions. The diagnostic of MS is difficult in the absence of skin lesions.
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