Disease relevance of Porokeratosis

• We report on the occurrence of coronal craniosynostosis, anal anomalies, and porokeratosis in two male sibs [1].
• Actinic porokeratosis, discoid lupus erythematosus, pityriasis versicolor, and acne scars were considered as possible diagnoses, but none of these appeared appropriate [2].
• Overexpression of p2lWaf1/Cip1 immunohistochemical staining in Bowen's disease, but not in disseminated superficial porokeratosis [3].
• Subclinical amounts of amyloid found in porokeratosis of Mibelli, in superficial basal-cell carcinoma, in senile skin, and in clinically normal skin of a patient with malignant melanoma showed the same characteristics [4].
• Expression of p53, pRb, p16 and proliferating cell nuclear antigen in squamous cell carcinomas arising on a giant porokeratosis [5].

High impact information on Porokeratosis

• Familial craniosynostosis, anal anomalies, and porokeratosis: CAP syndrome [1].
• BACKGROUND: Disseminated superficial actinic porokeratosis (DSAP) is the most common porokeratosis and is characterized by multiple keratotic lesions which tend to occur at sun-exposed sites [6].
• Porokeratosis and povidone-iodine: a new clinical diagnostic sign [7].
• Immunosuppression and transplantation have been reported to induce porokeratosis (PK), especially its variant, disseminated superficial PK (DSP) [8].
• Porokeratosis of Mibelli associated with dermal amyloid deposits [9].

Chemical compound and disease context of Porokeratosis

• Generalized linear porokeratosis treated with etretinate [10].
• Porokeratosis (Mibelli): treatment with topical 5-fluorouracil [11].
• Porokeratosis of Mibelli: benzylhydrochlorothiazide-induced new lesions accompanied by eosinophilic spongiosis [12].
• Carbon dioxide laser treatment of porokeratosis of Mibelli [13].
• Porokeratosis plantaris, palmaris, et disseminata. Report of a case and treatment with isotretinoin [14].

Biological context of Porokeratosis

• The first locus for DSAP was localized to chromosome 12q23.2-24.1, but no gene responsible for porokeratosis has been identified to date [15].
• To elucidate the morphogenesis of cornoid lamellae (CL) in porokeratosis, skin lesions of three cases of disseminated superficial actinic porokeratosis and a case of linear porokeratosis were examined [16].

Anatomical context of Porokeratosis

• We describe a case of disseminated superficial porokeratosis (DSP) with clear histologic evidence of amyloid deposition in the upper dermis [17].
• In this study, we examined 15 lesions of porokeratosis immunohistochemically for evidence of aberrant keratinization using several markers of keratinocyte (KC) maturation and differentiation, including involucrin, filaggrin, cytokeratins, and the growth activation marker psi-3 [18].
• Interestingly, continuous subcutaneous infusion of peplomycin for the lymph node metastasis significantly improved the warty lesions of porokeratosis [19].

Gene context of Porokeratosis

• Thirty-three cases of the various types of porokeratosis were immunohistochemically studied for p53, mdm2, and p21 proteins [20].
• In contrast to involucrin, loricrin expression was consistently down-regulated in agranulotic, parakeratotic keratinization as observed in psoriasis, dermatitis, pityriasis lichenoides, porokeratosis, or precancerous and malignant squamous lesions [21].
• A patient with porokeratosis Mibelli is reported who suffered from long-standing chronic active hepatitis and rapidly expanding vitiligo of more recent onset [22].
• General porokeratosis associated with primary hypoparathyroidism [23].
• The cornoid lamella is a broad, solid keratin plug rather than a centrifugally enlarging annular or serpentine ridge as can been seen in other types of porokeratosis [24].

References