Mamwe mashoko ― Shona

Urticarial vasculitis chiitiko chisingawanzo kuratidzwa neanogara kwenguva refu kana anodzokororwa episodhi yemikoko. Kunyange zvazvo zviratidzo zveganda zvaro zvichiita semikoko isingaperi, yakasiyana nekuti mikoko inonamatira kwemaawa angangoita makumi maviri nemana uye inogona kukonzera rima mushure mekupera. Kunyangwe kazhinji zvisingazivikanwe chikonzero, dzimwe nguva zvinogona kukonzereswa nemimwe mishonga, hutachiona, autoimmune zvirwere, kusagadzikana kweropa, kana kenza. Zvimwe zvidzidzo zvakatozvibatanidza neCOVID-19 uye H1N1 furuwenza. Inogonawo kukanganisa dzimwe nhengo dzemuviri semhasuru, itsvo, mapapu, dumbu, uye maziso. Kunyange zvazvo imwe mhando yekuongorora kwenyama inogona kusimbisa kuongororwa, haisi nguva dzose inofanirwa. Kurapa kunowanzotanga nemishonga inorwisa mabhakitiriya, dapsone, colchicine, kana hydroxychloroquine kune zviitiko zvidiki. Kune dzimwe nyaya dzakakomba, mishonga inodzvinyirira immune system se methotrexate kana corticosteroids inogona kudiwa. Munguva pfupi yapfuura, biologic therapies (rituximab, omalizumab, interleukin-1 inhibitors) yakaratidza vimbiso yenyaya dzakaoma.
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.

Mumwe murume ane makore 35 okuberekwa akauya ane nhoroondo yemazuva 15 yezvitsvuku zvakatsvuka, zvipembenene zvinorwadza pazvidya zvose nemakumbo, pamwe chete nemarwadzo emajoini. Aive nechirwere cheweti kwesvondo rese risati rabuda. Ganda rake rairatidza zvinyoro zvinyoro, zvakaita serin'i, zvisingaite blanchable, zvikwangwani zvitsvuku kumativi ese ezvidya nemakumbo. Akapiwa oral prednisolone (40mg / zuva) kwevhiki pamwe chete neasina-hope antihistamine (fexofenadine) . Mukati mevhiki, mapundu ose akapera zvachose. Pakanga pasisina mapundu mukati memwedzi mitanhatu yakatevera yekuongororwa nguva dzose.
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.