Postinflammatory hyperpigmentation
Postinflammatory hyperpigmentation iine mamiriro eganda anoratidzwa nekuwedzera pigment paganda zvichitevera kuzvimba kweganda. Postinflammatory hyperpigmentation inogona kukonzerwa nekus exposure kwenguva refu kuzuva, kuzvimba, kana kukuvadzwa kweganda, kusanganisira kunobva paacne. Vanhu vane ganda rakasviba vanowanzova nehyperpigmentation, zvikuru kana vachiratidzwa zuva kwenguva refu.
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ReferencesPostinflammatory hyperpigmentation (PIH) idambudziko reganda rinowanzoitika mushure mekuputika kweganda kana kukuvara. Inowanzogara kwenguva yakareba uye yakaipisisa muvanhu vane ganda rakasviba (Fitzpatrick skin types III–VI). Kunyange zvazvo inowanzovanduka, izvi zvinogona kutora nguva, saka kurapwa kunowanzodiwa kwenguva yakareba. Kubatanidza marapirwo akasiyana kunoshanda zvakanyanya.
Postinflammatory hyperpigmentation (PIH) is a common acquired cutaneous disorder occurring after skin inflammation or injury. It is chronic and is more common and severe in darker-skinned individuals (Fitzpatrick skin types III–VI). While the condition typically improves spontaneously, this process can take months to years, necessitating prolonged treatment. Combination therapy is the most effective.
Postinflammatory hyperpigmentation (PIH) is a common acquired cutaneous disorder occurring after skin inflammation or injury. It is chronic and is more common and severe in darker-skinned individuals (Fitzpatrick skin types III–VI). While the condition typically improves spontaneously, this process can take months to years, necessitating prolonged treatment. Combination therapy is the most effective.
Postinflammatory hyperpigmentation ndiyo yakajairika sequelae yekuzvimba kweganda. Zvinowanzobata vanhu vane ganda rakasviba zvakanyanya. Zvidzidzo zvinoratidza kuti nyaya dzakaita se postinflammatory hyperpigmentation ndedzimwe dzezvikonzero nei vanhu vane ganda rakasviba vachitsvaga dermatological care. Kurapa kwakakosha pakugadzirisa postinflammatory hyperpigmentation, uye kunowanzo kutanga nekugadzirisa mamiriro ekutanga ekuzvimba. Mutsara wekutanga wekurapa unowanzo sanganisira kushandisa topical agents anoderedza pigment, pamwe ne sunscreen yekudzivirira. Aya maajenti, akadai se hydroquinone, azelaic acid, kojic acid, arbutin, licorice extracts, anogona kudzikisa zvakanyanya pigmentation. Pamusoro pezvo, retinoids, mequinol, ascorbic acid, niacinamide, N‑acetyl glucosamine, uye soy anoshandiswawo se anobvisa pigment, pamwe nemishonga mitsva iri kubuda. Nepo marapirwo epamusoro achiwanzo shanda kune hyperpigmentation yakadzama, maitiro akadai se laser kana chemical peel anogona kushandiswa kune nyaya dzakasindimara. Zvakakosha kushandisa mishonga iyi nekungwarira kudzivirira kushatirwa uye kuipa kwe postinflammatory hyperpigmentation.
Postinflammatory hyperpigmentation is a common sequelae of inflammatory dermatoses that tends to affect darker skinned patients with greater frequency and severity. Epidemiological studies show that dyschromias, including postinflammatory hyperpigmentation, are among the most common reasons darker racial/ethnic groups seek the care of a dermatologist. The treatment of postinflammatory hyperpigmentation should be started early to help hasten its resolution and begins with management of the initial inflammatory condition. First-line therapy typically consists of topical depigmenting agents in addition to photoprotection including a sunscreen. Topical tyrosinase inhibitors, such as hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts, can effectively lighten areas of hypermelanosis. Other depigmenting agents include retinoids, mequinol, ascorbic acid, niacinamide, N-acetyl glucosamine, and soy with a number of emerging therapies on the horizon. Topical therapy is typically effective for epidermal postinflammatory hyperpigmentation; however, certain procedures, such as chemical peeling and laser therapy, may help treat recalcitrant hyperpigmentation. It is also important to use caution with all of the above treatments to prevent irritation and worsening of postinflammatory hyperpigmentation.
Postinflammatory hyperpigmentation is a common sequelae of inflammatory dermatoses that tends to affect darker skinned patients with greater frequency and severity. Epidemiological studies show that dyschromias, including postinflammatory hyperpigmentation, are among the most common reasons darker racial/ethnic groups seek the care of a dermatologist. The treatment of postinflammatory hyperpigmentation should be started early to help hasten its resolution and begins with management of the initial inflammatory condition. First-line therapy typically consists of topical depigmenting agents in addition to photoprotection including a sunscreen. Topical tyrosinase inhibitors, such as hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts, can effectively lighten areas of hypermelanosis. Other depigmenting agents include retinoids, mequinol, ascorbic acid, niacinamide, N-acetyl glucosamine, and soy with a number of emerging therapies on the horizon. Topical therapy is typically effective for epidermal postinflammatory hyperpigmentation; however, certain procedures, such as chemical peeling and laser therapy, may help treat recalcitrant hyperpigmentation. It is also important to use caution with all of the above treatments to prevent irritation and worsening of postinflammatory hyperpigmentation.
