Alaye siwaju sii ― Yoruba

Porokeratosis jẹ ipo awọ to ṣọwọn ti o jẹ ifihan nipasẹ awọn iṣoro keratinization, ti o yọrisi dide, awọn abulẹ ti o ni iwọn tabi awọn bumps ti o ni inira lori awọ ara. Ẹya asọye rẹ labẹ maikirosikopu ni wiwa cornoid lamella, eto kan pato ti awọn sẹẹli ni ipele oke ti awọ ara. Porokeratosis wa ni orisirisi awọn fọọmu (disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, linear porokeratosis) . O ṣe pataki lati ṣe akiyesi pe porokeratosis le ṣe idagbasoke sinu akàn ara. Ọna ti o dara julọ lati ṣe iwadii porokeratosis jẹ nipasẹ biopsy ti aala ti o dide, botilẹjẹpe lọwọlọwọ ko si ilana itọju boṣewa.
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) jẹ arun ti keratinization ti o bajẹ. O jẹ ọkan ninu awọn oriṣi mẹfa ti porokeratosis, ati pe o maa n kan awọn agbegbe nla ni akawe si awọn miiran (linear, Mibelli's, punctate, palmoplantar disseminated, superficial porokeratosis). Iru eruptive ti porokeratosis nigbagbogbo ni asopọ si akàn, immunosuppression (immunosuppression), tabi proinflammatory state (proinflammatory state). Awọn okunfa ewu jẹ pẹlu genetics (genetics), immunosuppression (immunosuppression), ati ultraviolet light (ultraviolet light). DSAP bẹrẹ bi pink to brown papules and macules (pink to brown papules and macules) pẹlu awọn egbegbe ti o ga (raised border) ni awọn agbegbe ti oorun ti han, nigbamiran asymptomatic or slightly pruritic (asymptomatic or slightly pruritic). Awọn itọju yatọ ati pe o le pẹlu topical diclofenac (topical diclofenac), photodynamic therapy (photodynamic therapy), 5‑fluorouracil (5‑fluorouracil) tabi retinoids (retinoids). Awọn egbo wọnyi ni a ka pe o ṣaju, pẹlu aye 7.5‑10 % ti yi pada si squamous cell carcinoma tabi basal cell carcinoma (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.

Ọkunrin 52 kan, ti ko ni itan iṣoogun tẹlẹ, wa pẹlu àpẹrẹ oruka atrophic lori ipari ika ẹsẹ kẹrin rẹ, eyiti o ti wa fun ọdun 2 laisi awọn aami aisan eyikeyi. O bẹ̀rẹ̀ bi papule keratotic kekere tí ó ń pọ̀ sí i ní àkúnya. Pelu igbiyanju awọn itọju orisirisi bi cryotherapy, corticosteroids, antifungals, ati antibiotics, àpẹrẹ naa ko dara julọ. Ìṣàyẹ̀wò dermoscopic fìhàn àgbàra tí ó ní àwọ̀-ara gbigbẹ, àgbègbè atrophic erythematous ní àárín pẹ̀lú aala tó ṣàlàyé kedere tí ó jẹ́ hyperkeratotic. Biopsy awọ ara lórí àgbègbè àpẹrẹ náà fìhàn cornoid lamella (cornoid lamella) pẹ̀lú ọ̀wọn sẹẹli parakeratotic tí ń gùn láti inú àkúnya epidermis tí kò ní granular layer. Ìbáṣepọ̀ clinicopathologic jẹ́ pẹ̀lú 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.