Ētahi atu korero ― Maori

Ko te Urticarial vasculitis he ahua onge e tohuhia ana e nga wahanga roa, e mau tonu ana rānei o te hives. Ahakoa he rite nga tohu o te kiri ki te hiwi tawhito, he mea ahurei nā te mea ka piri tonu ngā hive mō te 24 haora neke atu ka puta he wāhi pouri i muri i te memenge. Ahakoa he maha ngā take kāore e mōhiotia, ka taea e ētahi o ngā rongoā, ngā māuiui, ngā māuiui autoimmune, mate myelodysplastic (myelodysplastic disorders), me ngā māuiui pukupuku rānei. Ko ētahi rangahau kua hono atu ki te rewharewha COVID-19 me influenza A/H1N1. Ka pā anō ki ētahi atu wāhanga o te tinana pērā i te musculoskeletal, renal, pulmonary, gastrointestinal, me te ocular. Ahakoa ka taea e ētahi momo whakamātautau toto te whakau i te māuiui, kāore e tika ana. Ko te tikanga ka tiimata te māuiatanga mā te paturōpī, dapsone, colchicine, hydroxychloroquine rānei mō ngā kēhi ngawari. Mō ngā kēhi kino ake, ka hiahiatia ngā immunosuppressives e pā ana ki te punaha māuiui pērā i te methotrexate, corticosteroids rānei. Inā tata nei, kua oati ngā rongoā koiora (rituximab, omalizumab, interleukin-1 inhibitors) mō ngā kēhi uaua.
Urticarial vasculitis is a rare clinicopathologic entity that is characterized by chronic or recurrent episodes of urticarial lesions. Skin findings of this disease can be difficult to distinguish visually from those of chronic idiopathic urticaria but are unique in that individual lesions persist for ≥24 hours and can leave behind dusky hyperpigmentation. This disease is most often idiopathic but has been linked to certain drugs, infections, autoimmune connective disease, myelodysplastic disorders, and malignancies. More recently, some authors have reported associations between urticarial vasculitis and COVID-19, as well as influenza A/H1N1 infection. Urticarial vasculitis can extend systemically as well, most often affecting the musculoskeletal, renal, pulmonary, gastrointestinal, and ocular systems. Features of leukocytoclastic vasculitis seen on histopathologic examination are diagnostic of this disease, but not always seen. In practice, antibiotics, dapsone, colchicine, and hydroxychloroquine are popular first-line therapies, especially for mild cutaneous disease. In more severe cases, immunosuppressives, including methotrexate, mycophenolate mofetil, azathioprine, and cyclosporine, as well as corticosteroids, may be necessary for control. More recently, select biologic therapies, including rituximab, omalizumab, and interleukin-1 inhibitors have shown promise for the treatment of recalcitrant or refractory cases.

He tangata 35‑tau te pakeke i tae mai me te 15‑ra te hitori o te whero kanapa (bright red, painful rashes) i runga i nga huha me nga waewae, me te mamae tahi (joint pain). He mate mimi (urinary tract infection) ia mo te wiki i mua i te puta mai o te ponana (rash). I kitea e tona kiri he maha nga tohu ngawari (tender), te ahua whakakai (ring‑shaped), he wahi parakore (partially blanchable), he whero i nga taha e rua o ona huha me ona waewae. I whakawhiwhia ia ki te prednisolone waha (oral prednisolone) (40 mg/ra) mo te wiki me te antihistamine kore‑moe (fexofenadine). I roto i te wiki, kua ngaro katoa nga ponana. Karekau he ponana i roto i nga marama e ono e whai ake nei o te tirotiro auau.
A 35-year-old man came in with a 15-day history of bright red, painful rashes on both thighs and legs, along with joint pain. He had a urinary tract infection for a week before the rash appeared. His skin showed several tender, ring-shaped, partially blanchable, red plaques on both sides of his thighs and legs. He was given oral prednisolone (40mg/day) for a week along with a non-drowsy antihistamine (fexofenadine). Within a week, all the rashes disappeared completely. There were no more rashes during the next 6 months of regular check-ups.