Postinflammatory hyperpigmentation - Hyperpigmentation Ea Postinflammatory
Hyperpigmentation Ea Postinflammatory (Postinflammatory hyperpigmentation) ke boemo ba letlalo bo khetholloang ke ho eketseha ha 'mala letlalong ka mor'a ho ruruha ha letlalo. hyperpigmentation ea postinflammatory (postinflammatory hyperpigmentation) e ka bakoa ke ho pepesehela letsatsi nako e telele, ho ruruha, kapa likotsi tse ling tsa letlalo, ho kenyelletsa le tse amanang le makhopho. Batho ba nang le letlalo le lefifi hangata ba atisa ho ba le hyperpigmentation le ho pepesehela letsatsi ho feteletseng.
☆ 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.
References
Postinflammatory hyperpigmentation (PIH) ke bothata ba letlalo khafetsa bo etsahalang ka mor'a ho ruruha ha letlalo kapa kotsi. E atisa ho tšoarella nako e telele 'me e mpe ho batho ba nang le letlalo le lefifi (Fitzpatrick skin types III–VI) . Le hoja hangata e ka ba betere ka boeona, sena se ka nka nako e telele, kahoo hangata phekolo e hlokahala nako e telele. Ho kopanya liphekolo tse fapaneng ho sebetsa hantle.
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 ke sequelae e tloaelehileng ea ho ruruha ha letlalo. E atisa ho ama batho ba letlalo le letšo ka thata le khafetsa. Boithuto bo bontša hore litaba tse kang postinflammatory hyperpigmentation ke tse ling tsa mabaka a mantlha a etsang hore batho ba nang le letlalo le lefifi ba batle tlhokomelo ea letlalo. Kalafo ea pele e bohlokoa bakeng sa ho rarolla postinflammatory hyperpigmentation mme hangata e qala ka ho laola boemo ba pele ba ho ruruha. Mokhoa oa pele oa kalafo o kenyelletsa ho sebelisa li-topical agents tse khantšang letlalo hammoho le setlolo se sireletsang letlalo letsatsing bakeng sa tšireletso. Mahlahana ana, joalo ka hydroquinone, azelaic acid, kojic acid, arbutin, licorice extracts , a ka fokotsa mebala e feteletseng. Ho feta moo, retinoids, mequinol, ascorbic acid, niacinamide, N-acetyl glucosamine, soy li boetse li sebelisoa e le li-antipigmenting agents, 'me litlhare tse ncha lia hlaha. Le hoja litlhare tsa lihlooho hangata li sebetsa hantle bakeng sa hyperpigmentation ea boemo bo holimo, mekhoa ea (laser, chemical peel) e ka 'na ea hlokahala bakeng sa linyeoe tse manganga. Ho bohlokoa ho ba hlokolosi ka liphekolo tsena ho qoba ho teneha le ho mpefala ha 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.
