Ētahi atu korero ― Maori

Ko te Urticarial vasculitis he āhua o te urticaria e roa ana te roanga, e mau tonu ana ngā hives. Ahakoa he rite ngā tohu o te kiri ki te hives tawhito, he mea ahurei nā te mea ka mau tonu ngā hives mō te 24 haora, ka puta he wāhi pouri i muri i te memenge. Ahakoa he maha ngā take kāore e mōhiotia, ka taea e ētahi rongoā, ngā māuiui, ngā māuiui autoimmune, ngā māuiui toto, ngā māuiui pūkūpuku rānei te whakaaweawe. Kua hono ētahi rangahau ki te rewharewha COVID‑19 me te H1N1. Ka pā anō ki ētahi atu wāhanga o te tinana pērā i ngā uaua, ngā whatukuhu, ngā ngongo, te puku, me ngā kanohi. Ahakoa ka taea e tētahi momo whakamātautau toto te whakatau i te mate, kāore e tika ana. Ko te tikanga, ka tīmata te maimoatanga me te paturopi, dapsone, colchicine, hydroxychloroquine rānei mō ngā keehi ngawari. Mō ngā keehi kino ake, ka hiahiatia ngā rākau taero e pehi ana i te punaha immune pērā i te methotrexate, corticosteroids rānei. I ngā tau tata nei, kua oati ngā rongoā hou (rituximab, omalizumab, interleukin‑1 inhibitors) mō ngā keehi 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 pakeke, 35 tau te pakeke, i tae mai me te 15 rā te hitori o te whero kanapa, te mamae i runga i ngā huha me ngā waewae, me te mamae tahi. He mate mimi ia mō te wiki i mua i te puta mai o te ponana. I kitea i tōna kiri he maha ngā tohu ngawari, te āhua whakakai, he wāhi parakore, he whero i ngā taha e rua o ōna huha me ōna waewae. I whakawhiwhia ia ki te prednisolone waha (40 mg/ra) mō te wiki me te antihistamine kore-moe (fexofenadine). I roto i te wiki, kua ngaro katoa ngā ponana. Kāore he ponana i roto i ngā 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.