Porokeratosis
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Liphethong tsa 2022 Stiftung Warentest tse tsoang Jeremane, khotsofalo ea bareki ka ModelDerm e ne e le tlase hanyane ho feta lipuisano tse lefelloang tsa telemedicine.
Liphethong tsa 2022 Stiftung Warentest tse tsoang Jeremane, khotsofalo ea bareki ka ModelDerm e ne e le tlase hanyane ho feta lipuisano tse lefelloang tsa telemedicine.
Lithako tse thata le tse hlahelletseng li na le sebopeho.
relevance score : -100.0%
ReferencesPorokeratosis ke boemo bo sa tloaelehang ba letlalo bo khetholloang ke mathata a keratinization, bo bakang maqeda a phahamileng, a sebopeho sa lesale kapa makukuno a makukuno letlalong. Sebopeho sa eona se hlalosang ka tlas'a microscope ke boteng ba cornoid lamella, tokisetso e khethehileng ea lisele tse karolong e ka holimo ea letlalo. Porokeratosis e tla ka mefuta e fapaneng (disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, linear porokeratosis). Ho bohlokoa ho hlokomela hore porokeratosis e ka fetoha leseli le se le lephakeng (precancerous lesion). Mokhoa o motle oa ho fumana porokeratosis ke ka biopsy ea moeli o phahamisitsoeng, leha hajoale ho se na protocol e tloaelehileng ea kalafo.
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) ke lefu la keratinization e sa sebetseng. Ke e ’ngoe ea mefuta e pharalletseng ea porokeratosis, ’me hangata e ama libaka tse kholoanyane ha li bapisoa le tse ling (linear, Mibelli’s, punctate, palmoplantar disseminated, superficial porokeratosis). Mofuta o phatlohang oa porokeratosis hangata o amahanngoa le kankere (malignancy), ho fokola ha ho itšireletsa mafung, kapa ho ruruha. Lintho tse kotsi li kenyelletsa lefa (genetics), ho fokola ha ho itšireletsa mafung, le leseli la ultraviolet (ultraviolet light). DSAP e qala e le makukuno a pinki kapa a sootho a nang le mahlakore a holimo libakeng tse pepesehileng letsatsi, a ka ba a se na matšoao kapa a nyenyefatswa hanyenyane. Liphekolo lia fapana ’me li ka kenyelletsa diclofenac topical, photodynamic therapy (PDT), 5-fluorouracil, imiquimod, vitamin D analogs, retinoids, kapa li‑laser. Maqeba ana a nkoa e le a pele ho kankere, ka monyetla oa 7.5‑10% oa ho fetoha ho squamous cell carcinoma kapa 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.
Monna ea lilemo li 52, eo pele a neng a phetse hantle, o ile a tla ka sekotoana se sephara, se bōpehileng joaloka lesale qetellong ea tseeho ea bone, o neng o le moo ka lilemo tse 2 ntle le ho baka matšoao. E qalile e le leqhubu le lenyenyane, le thata, ’me la hola ka ntle ha nako e ntse e ea. Ho sa tsotellehe ho leka mekhoa e fapaneng ea phekolo e kang cryotherapy, corticosteroids tsa topikale, antifungal le antibiotics, ha e ne e ka ntlafala. Ho hlahloba ka dermoscopic ho ile ha bontša cornoid lamella, e le kholomo ya disele tsa parakeratotic tse tšehang ho tsoa ho ho qhibidu ea epidermis ntle le sehlopha sa granular. Letlalo le lenyane le nkiloeng pheletsong ea leqhubu le bontša kholo e sa tloaelehang ea lisele karolong e kantle ea letlalo, e netefatsang tlhahlobo ea 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.
Hangata biopsy e etsoa hobane liso li ka tšoana le actinic keratosis kapa squamous cell carcinoma.