Lintlha tse ling ― Sesotho

Urticarial vasculitis ke boemo bo sa tloaelehang bo tšoauoang ka linako tse telele kapa tse etsahalang khafetsa. Le hoja matšoao a letlalo a ka tšoana le hives e sa foleng, a ikhethile hobane li-hives li khomarela bonyane lihora tse 24 'me li ka baka matheba a lefifi ka mor'a ho fela. Le hoja hangata e le sesosa se sa tsejoeng, ka linako tse ling e ka bakoa ke meriana e itseng, tšoaetso, mafu a autoimmune, mafu a mali, kapa kankere. Lithuto tse ling li bile li e hokahanya le COVID-19 le H1N1 flu. E ka boela ea ama likarolo tse ling tsa 'mele tse kang mesifa, liphio, matšoafo, mpa le mahlo. Le hoja mofuta o itseng oa tlhahlobo ea lisele o ka tiisa hore o na le lefu lena, hase kamehla ho hlokahalang. Kalafo hangata e qala ka lithibela-mafu, dapsone, colchicine, kapa hydroxychloroquine bakeng sa linyeoe tse bobebe. Bakeng sa linyeoe tse matla le ho feta, lithethefatsi tse hatellang sesole sa 'mele joalo ka methotrexate kapa corticosteroids li ka hlokahala. Haufinyane tjena, liphekolo tsa biologic (rituximab, omalizumab, interleukin-1 inhibitors) li bontšitse ts'episo bakeng sa linyeoe tse thata.
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.

Monna ea lilemo li 35 o ile a tla ka histori ea matsatsi a 15 ea bofubelu bo khanyang, lekhopho le bohloko liropeng le maotong ka bobeli, hammoho le bohloko ba manonyeletso. O ne a e-na le tšoaetso ea moroto bakeng sa beke pele ho hlaha lekhopho. Letlalo la hae le ne le e-na le li-plaque tse 'maloa tse bonolo, tse bōpehileng joaloka lesale, tse ka bang blanchable, tse khubelu mahlakoreng a mabeli a lirope le maotong. O ile a fuoa prednisolone ea molomo (40mg / letsatsi) bakeng sa beke hammoho le antihistamine e sa otseleng (fexofenadine) . Ka mor'a beke, makhopho 'ohle a ile a nyamela ka ho feletseng. Ha hoa ka ha hlola ho e-ba le makhopho nakong ea likhoeli tse 6 tse latelang tsa tlhahlobo ea kamehla.
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.