Lupus erythematosus
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Mune 2022 Stiftung Warentest mhedzisiro kubva kuGermany, kugutsikana kwevatengi neModelDerm kwakangodzikira zvishoma pane nekubhadharwa kwe telemedicine kubvunzana.
Mune 2022 Stiftung Warentest mhedzisiro kubva kuGermany, kugutsikana kwevatengi neModelDerm kwakangodzikira zvishoma pane nekubhadharwa kwe telemedicine kubvunzana.
Inoratidzika sey erythema ine purplish zvishoma.
Butterfly rash inowanzoitika pachiso.
relevance score : -100.0%
ReferencesKuziva nekuona cutaneous lupus erythematosus (CLE) kunounza matambudziko ekuongorora, kusiyanisa kubva ku systemic lupus erythematosus nekubatanidzwa kweganda. Zvidzidzo zvenguva pfupi yapfuura zvinojekesa nezve zvigadzirwa zvegenetiki, zvakatipoteredza, uye immunological zvinhu zviri pasi peCLE. Kushandiswa kwezvinodhaka kwakaratidza kuva chimwe chezvinhu zvinonyanya kukonzera CLE. Kurapa kunosanganisira topical uye systemic therapies, kusanganisira biologics ane tariro (belimumab, rituximab, ustekinumab, anifrolumab, BIIB059) ayo akaratidza kushanda mumiedzo yekiriniki.
Diagnostic challenges exist in better defining cutaneous lupus erythematosus (CLE) as an independent disease distinct from systemic lupus erythematosus with cutaneous features and further classifying CLE based on clinical, histological, and laboratory features. Recent mechanistic studies revealed more genetic variations, environmental triggers, and immunologic dysfunctions that are associated with CLE. Drug induction specifically has emerged as one of the most important triggers for CLE. Treatment options include topical agents and systemic therapies, including newer biologics such as belimumab, rituximab, ustekinumab, anifrolumab, and BIIB059 that have shown good clinical efficacy in trials.
Diagnostic challenges exist in better defining cutaneous lupus erythematosus (CLE) as an independent disease distinct from systemic lupus erythematosus with cutaneous features and further classifying CLE based on clinical, histological, and laboratory features. Recent mechanistic studies revealed more genetic variations, environmental triggers, and immunologic dysfunctions that are associated with CLE. Drug induction specifically has emerged as one of the most important triggers for CLE. Treatment options include topical agents and systemic therapies, including newer biologics such as belimumab, rituximab, ustekinumab, anifrolumab, and BIIB059 that have shown good clinical efficacy in trials.
Cutaneous lupus erythematosus (CLE) inobata nyaya dzakasiyana dzeganda, dzimwe dzacho dzinogona kukonzera matambudziko ehutano. Inopatsanurwa mumhando dzakasiyana, dzakadai se acute CLE (ACLE), sub‑acute CLE (SCLE) uye chronic CLE (CCLE). CCLE inosanganisira discoid lupus erythematosus (DLE), LE profundus (LEP), chilblain cutaneous lupus, uye lupus tumidus.
Cutaneous lupus erythematosus (CLE) encompasses a wide range of dermatologic manifestations, which may or may not be associated with the development of systemic disease. Cutaneous lupus is divided into several sub-types, including acute CLE (ACLE), sub-acute CLE (SCLE) and chronic CLE (CCLE). CCLE includes discoid lupus erythematosus (DLE), LE profundus (LEP), chilblain cutaneous lupus and lupus tumidus.
Cutaneous lupus erythematosus (CLE) encompasses a wide range of dermatologic manifestations, which may or may not be associated with the development of systemic disease. Cutaneous lupus is divided into several sub-types, including acute CLE (ACLE), sub-acute CLE (SCLE) and chronic CLE (CCLE). CCLE includes discoid lupus erythematosus (DLE), LE profundus (LEP), chilblain cutaneous lupus and lupus tumidus.
Lupus erythematosus iboka rezvirwere zve autoimmune zvinogona kukanganisa nhengo dzakasiyana dzemuviri. Dzimwe mhando, senge systemic lupus erythematosus (SLE), inokanganisa nhengo dzakawanda, nepo dzimwe, senge cutaneous lupus erythematosus (CLE), inonyanya kukanganisa ganda. Isu tinotsanangura mhando dzakasiyana dzeCLE zvichienderana nemusanganiswa wezviratidzo zvekiriniki, kuongororwa kwematishu, uye kuongororwa kweropa, asi pane kusiyana kukuru pakati pevanhu. Zvinetso zveganda zvinowanzokura nekuda kwezvinhu zvakaita sekus exposure kuzuva, kuputa, kana kushandiswa kwemimwe mishonga.
Lupus erythematosus comprises a spectrum of autoimmune diseases that may affect various organs (systemic lupus erythematosus [SLE]) or the skin only (cutaneous lupus erythematosus [CLE]). Typical combinations of clinical, histological and serological findings define clinical subtypes of CLE, yet there is high interindividual variation. Skin lesions arise in the course of triggers such as ultraviolet (UV) light exposure, smoking or drugs
Lupus erythematosus comprises a spectrum of autoimmune diseases that may affect various organs (systemic lupus erythematosus [SLE]) or the skin only (cutaneous lupus erythematosus [CLE]). Typical combinations of clinical, histological and serological findings define clinical subtypes of CLE, yet there is high interindividual variation. Skin lesions arise in the course of triggers such as ultraviolet (UV) light exposure, smoking or drugs
Chikonzero che lupus erythematosus hachina kujeka. Pakati pemhuri dzine nhoroondo yakafanana, kana mumwe akabatwa, pane mukana we24 % kuti mumwewo atapukirwe. Mahomoni echikadzi epabonde, chiedza chezuva, kuputa fodya, kushomeka kwevitamini D, uye humwe hutachiona hunotendwa kuti hunowedzera njodzi.
Mishonga inogona kusanganisira NSAIDs, corticosteroids, immunosuppressants, hydroxychloroquine, uye methotrexate. Kunyange zvazvo corticosteroids achishanda, kushandiswa kwenguva refu kunoguma nemigumisiro yakaipa.