Porokeratosis
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References
Porokeratosis bụ ọnọdụ akpụkpọ ahụ na-adịghị ahụkebe nke nsogbu keratinization na-egosipụta, na-ebute elu, mgbanaka yiri mgbaaka ma ọ bụ ọnya siri ike na akpụkpọ ahụ. Ihe na-akọwapụta ya n'okpuru microscope bụ ọnụnọ cornoid lamella, nhazi nke mkpụrụ ndụ n'ime elu akpụkpọ ahụ. Porokeratosis na-abịa n'ụdị dị iche iche (disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, linear porokeratosis) . Ọ dị mkpa iburu n'obi na porokeratosis nwere ike ịmalite ịghọ ọrịa kansa anụ ahụ. Ụzọ kachasị mma isi chọpụta porokeratosis bụ site na biopsy nke oke ebili elu, ọ bụ ezie na ugbu a enweghị usoro ọgwụgwọ ọkọlọtọ.
Porokeratosis is an uncommon dermatologic disorder. It is a disorder of keratinization that presents with keratotic papules or annular plaques with an elevated border. It has a distinct histologic hallmark of cornoid lamella, which is a column of tightly fitted parakeratotic cells in the upper epidermis. There are multiple clinical variants of porokeratosis, including disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, and linear porokeratosis. Porokeratosis is a precancerous lesion that can undergo malignant transformation. Evaluation of porokeratosis is best with a biopsy of the elevated border. There are no standard guidelines for treatment.
Porokeratosis is an uncommon dermatologic disorder. It is a disorder of keratinization that presents with keratotic papules or annular plaques with an elevated border. It has a distinct histologic hallmark of cornoid lamella, which is a column of tightly fitted parakeratotic cells in the upper epidermis. There are multiple clinical variants of porokeratosis, including disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, and linear porokeratosis. Porokeratosis is a precancerous lesion that can undergo malignant transformation. Evaluation of porokeratosis is best with a biopsy of the elevated border. There are no standard guidelines for treatment.
Disseminated superficial actinic porokeratosis (DSAP) bụ ọrịa nke keratinization mebiri emebi. Ọ bụ otu n'ime ụdị porokeratosis isii, ọ na-emetụtakwa akụkụ buru ibu ma e jiri ya tụnyere ndị ọzọ (linear, Mibelli's, punctate, palmoplantar disseminated, superficial porokeratosis) . Ụdị porokeratosis nke na-agbawa agbawa na-ejikọtakarị na ọrịa kansa, ihe mgbochi adịghị ike, ma ọ bụ mbufụt. Ihe ndị dị ize ndụ gụnyere mkpụrụ ndụ ihe nketa, mgbochi mgbochi, na ikpughe anyanwụ. DSAP na-amalite dị ka pink ma ọ bụ nchara nchara nchara nwere akụkụ dị elu na mpaghara anwụ na-ekpuchi, mgbe ụfọdụ na-ebute ntakịrị itching. Ọgwụgwọ dịgasị iche ma nwee ike ịgụnye ude dị n'elu, ọgwụgwọ ọkụ, ma ọ bụ ọgwụ dịka 5-fluorouracil ma ọ bụ retinoids. A na-ahụta ọnya ndị a dị ka ihe buru ibu, na-enwe ohere 7. 5 - 10 % nke ịtụgharị ghọọ cell squamous ma ọ bụ basal cell carcinoma.
Disseminated superficial actinic porokeratosis (DSAP) is a disease of disordered keratinization. Disseminated superficial actinic porokeratosis is one of six variants of porokeratosis. It has more extensive involvement than most other variants. These other variants include linear porokeratosis, porokeratosis of Mibelli, punctate porokeratosis, porokeratosis palmaris et plantaris disseminata, and disseminated superficial porokeratosis. The eruptive form of porokeratosis is associated with malignancy, immunosuppression, and a proinflammatory state. Risk factors for porokeratosis include genetics, immunosuppression, and ultraviolet light. The lesions in disseminated superficial actinic porokeratosis start as pink to brown papules and macules with a raised border in sun-exposed areas that can be asymptomatic or slightly pruritic. There are many options for the treatment of disseminated superficial actinic porokeratosis, including topical diclofenac, photodynamic therapy (PDT), 5-fluorouracil (5-FU), imiquimod, vitamin D analogs, retinoids, and lasers. These lesions are considered precancerous. There is a 7.5 to 10% risk of malignant transformation to squamous cell carcinoma or basal cell carcinoma.
Disseminated superficial actinic porokeratosis (DSAP) is a disease of disordered keratinization. Disseminated superficial actinic porokeratosis is one of six variants of porokeratosis. It has more extensive involvement than most other variants. These other variants include linear porokeratosis, porokeratosis of Mibelli, punctate porokeratosis, porokeratosis palmaris et plantaris disseminata, and disseminated superficial porokeratosis. The eruptive form of porokeratosis is associated with malignancy, immunosuppression, and a proinflammatory state. Risk factors for porokeratosis include genetics, immunosuppression, and ultraviolet light. The lesions in disseminated superficial actinic porokeratosis start as pink to brown papules and macules with a raised border in sun-exposed areas that can be asymptomatic or slightly pruritic. There are many options for the treatment of disseminated superficial actinic porokeratosis, including topical diclofenac, photodynamic therapy (PDT), 5-fluorouracil (5-FU), imiquimod, vitamin D analogs, retinoids, and lasers. These lesions are considered precancerous. There is a 7.5 to 10% risk of malignant transformation to squamous cell carcinoma or basal cell carcinoma.
Otu nwoke dị afọ 52, bụbu ahụike, batara na mgbanaka dị larịị, nke yiri mgbanaka na nsọtụ mkpịsị ụkwụ ya nke anọ, bụ nke nọrọla ebe ahụ afọ 2 n'enweghị ihe mgbaàmà ọ bụla. Ọ malitere dị ka obere mkpọtu siri ike ma tolite n'èzí ka oge na-aga. N'agbanyeghị ịnwale ọgwụgwọ dị iche iche dị ka cryotherapy, ude, antifungals, na ọgwụ nje, patch ahụ adịchaghị mma. Nyochaa ya nke ọma site na dermocopsy gosipụtara ebe akọrọ, ọbara ọbara na-acha uhie uhie nwere oke siri ike. Obere akpụkpọ ahụ e wepụtara na nsọtụ nke patch ahụ gosipụtara uto mkpụrụ ndụ na-adịghị mma na oyi akwa nke akpụkpọ ahụ, na-akwado nyocha nke porokeratosis of Mibelli.
A 52-year-old man with no past medical history presented with an asymptomatic annular atrophic patch on the distal portion of the fourth toe of 2 years’ duration. The lesion began as a small keratotic papule that gradually enlarged centrifugally. He had received multiple treatments including cryotherapy, topical corticosteroids, antifungals, and antibiotics without improvement. Dermoscopic examination revealed a scaly atrophic erythematous central area with a sharply demarcated peripheral hyperkeratotic structure. A skin biopsy of the edge of the lesion revealed a cornoid lamella with a column of parakeratotic cells extending from an invagination of the epidermis with absence of granular layer. The clinicopathologic correlation was consistent with porokeratosis of Mibelli.
A 52-year-old man with no past medical history presented with an asymptomatic annular atrophic patch on the distal portion of the fourth toe of 2 years’ duration. The lesion began as a small keratotic papule that gradually enlarged centrifugally. He had received multiple treatments including cryotherapy, topical corticosteroids, antifungals, and antibiotics without improvement. Dermoscopic examination revealed a scaly atrophic erythematous central area with a sharply demarcated peripheral hyperkeratotic structure. A skin biopsy of the edge of the lesion revealed a cornoid lamella with a column of parakeratotic cells extending from an invagination of the epidermis with absence of granular layer. The clinicopathologic correlation was consistent with porokeratosis of Mibelli.
Ọtụtụ mgbe, a na-eme biopsy n'ihi na ọ nwere ike ịdị ka actinic keratosis ma ọ bụ squamous cell carcinoma.