Livedoid vasculitis
Ko te Livedoid vasculitis he mate kiri kiri mau tonu, ā, ka kitea i te nuinga o ngā wahine rangatahi i waenga‑pakeke. He acronym i whakamahia hei whakaahua i ōna ahuatanga, ko “Painful purpuric ulcers with reticular pattern of the lower extremities” (PURPLE). E pā ana ki te maha o ngā māuiui, tae atu ki te whakaheke toto me ngā momo rereke.
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ReferencesKo te Livedoid vasculopathy he mate kiri onge e tohuhia ana e ngā whewhe māmae, ā, ka hoki tonu mai ki ngā waewae o raro.
Livedoid vasculopathy (LV) is a rare thrombotic vasculopathy of the dermis characterized by painful, relapsing ulcers over the lower extremities. Diagnosis is challenging due to the overlap in clinical appearance and nomenclature with other skin disorders. Treatment selection is complicated by poor understanding of the pathogenesis of LV and lack of robust clinical trials evaluating therapy efficacy. The terminology and pathophysiology of LV are reviewed here, along with its epidemiology, clinical and histologic features, and treatment options. A diagnostic pathway is suggested to guide providers in evaluating for comorbidities, referring to appropriate specialists, and choosing from the available classes of therapy.
Livedoid vasculopathy (LV) is a rare thrombotic vasculopathy of the dermis characterized by painful, relapsing ulcers over the lower extremities. Diagnosis is challenging due to the overlap in clinical appearance and nomenclature with other skin disorders. Treatment selection is complicated by poor understanding of the pathogenesis of LV and lack of robust clinical trials evaluating therapy efficacy. The terminology and pathophysiology of LV are reviewed here, along with its epidemiology, clinical and histologic features, and treatment options. A diagnostic pathway is suggested to guide providers in evaluating for comorbidities, referring to appropriate specialists, and choosing from the available classes of therapy.
Ko te livedoid vasculopathy he mate kiri onge e puta ai te whewhe i runga i ngā waewae o raro, ka mahue ngā whiu, ko te atrophie blanche e kīia ana. Ahakoa kāore i te tino mārama te take, e whakaponohia ana ko te pikinga o te toto (hypercoagulability) te take matua, ā, ko te mumura te mahi tuarua. Ko ngā mea e pā ana ki te whakaheke toto ko ēnei e whai ake nei: deficiencies in proteins C and S, genetic mutations like factor V Leiden, antithrombin III deficiency, prothrombin gene mutations, high levels of homocysteine. I roto i ngā biopsies, ka whakaatuhia e te ahuatanga ngā toto i roto i ngā ōkō, te matotoru o ngā pakitara o ngā ōkō, me te marumaru. Ko te maimoatanga he huarahi maha‑ā‑ringa e aro ana ki te aukati i ngā toto totika me ngā rongoā pērā i ngā rākau taero anti‑platelet, te whakaheke toto, me te rongoā fibrinolytic. Ka taea te whakamahi i ngā momo rongoā mō tēnei mate kiri: colchicine and hydroxychloroquine, vasodilators, immunosuppressants.
Livedoid vasculopathy is a rare skin condition that causes recurring ulcers on the lower legs, leaving behind pale scars known as atrophie blanche. While the exact cause is still unclear, it's believed that increased blood clotting (hypercoagulability) is the main factor, with inflammation playing a secondary role. Factors contributing to clotting include as follows - deficiencies in proteins C and S, genetic mutations like factor V Leiden, antithrombin III deficiency, prothrombin gene mutations, high levels of homocysteine. In biopsies, the condition shows blood clots inside vessels, thickening of vessel walls, and scarring. Treatment involves a multi-pronged approach focusing on preventing blood clots with medications like anti-platelet drugs, blood thinners, and fibrinolytic therapy. Various drugs can be used for this skin condition - colchicine and hydroxychloroquine, vasodilators, immunosuppressants.
Livedoid vasculopathy is a rare skin condition that causes recurring ulcers on the lower legs, leaving behind pale scars known as atrophie blanche. While the exact cause is still unclear, it's believed that increased blood clotting (hypercoagulability) is the main factor, with inflammation playing a secondary role. Factors contributing to clotting include as follows - deficiencies in proteins C and S, genetic mutations like factor V Leiden, antithrombin III deficiency, prothrombin gene mutations, high levels of homocysteine. In biopsies, the condition shows blood clots inside vessels, thickening of vessel walls, and scarring. Treatment involves a multi-pronged approach focusing on preventing blood clots with medications like anti-platelet drugs, blood thinners, and fibrinolytic therapy. Various drugs can be used for this skin condition - colchicine and hydroxychloroquine, vasodilators, immunosuppressants.
Ko te Livedoid vasculopathy he āhua onge e puta ai ngā whiu ki ngā waewae e rua. Ka pā ki te hanga o te toto i roto i ngā ōkō toto iti, ā, ka pā ki te nui haere o te tote, te iti o te pakaru o te toto, me te kino o te ararewa o ngā ōkō. He nui ake te pā ki ngā wāhine, inā koa i waenga i ngā tau 15 ki te 50. Ko te whakamutu i te kai paipa, te tiaki i ngā patunga, me te whakamahi rongoā pērā i te whakaheke toto me ngā rākau taero antiplatelet he hua.
Livedoid vasculopathy is a rare vasculopathy that is typically characterized by bilateral lower limb lesions. Increased thrombotic activity and decreased fibrinolytic activity along with endothelial damage are believed to be the cause of thrombus formation in the capillary vasculature. It is 3 times more common in females than in males, especially in patients between the ages of 15 to 50 years. There is no definite first-line treatment, but general measures like smoking cessation, wound care, and pharmacological measures like anticoagulants and antiplatelets have shown good results.
Livedoid vasculopathy is a rare vasculopathy that is typically characterized by bilateral lower limb lesions. Increased thrombotic activity and decreased fibrinolytic activity along with endothelial damage are believed to be the cause of thrombus formation in the capillary vasculature. It is 3 times more common in females than in males, especially in patients between the ages of 15 to 50 years. There is no definite first-line treatment, but general measures like smoking cessation, wound care, and pharmacological measures like anticoagulants and antiplatelets have shown good results.
