RESUMO
La vasculitis leucocitoclástica, también denominada angeitis cutánea leucocitoclástica, es la forma más común de vasculitis. Si bien la mayoría de los casos son idiopáticos, entre los agentes etiológicos que podemos nombrar se encuentran los agentes infecciosos, las enfermedades del tejido conectivos, las reacciones de hipersensibilidad a medicamentos y las neoplasias solidas o hematológicas. Si bien los procesos infecciosos son una causa conocida de vasculitis leucocitoclástica, la infección por virus de Virus de hepatitis B (VHB) es muy infrecuente. Presentamos una mujer de 47 años, sin antecedentes patológicos previos, que consultó por artralgias en rodillas y tobillos, mialgias en gemelos y rash purpúrico con leve prurito en ambos miembros inferiores, de un mes de evolución. La biopsia cutánea de las lesiones de miembros inferiores fue compatible con vasculitis leucocitoclástica. La serología de hepatitis B fue positiva por lo que inició tratamiento antiviral con Tenofovir y Prednisona con buena evolución de sus lesiones cutáneas
Leukocytoclastic vasculitis, also called leukocytoclastic cutaneous angiitis, is the most common form of vasculitis. Although most cases are idiopathic, etiologic agents include infectious agents, connective tissue diseases, drug hypersensitivity reactions, and solid or hematologic malignancies. Although infectious processes are a known cause of leukocytoclastic vasculitis, hepatitis B virus (HBV) infection is very rare. We present a 47-year-old woman, with no previous pathologic history, who consulted for arthralgias in the knees and ankles, myalgia's and purpuric rash with mild pruritus in both lower limbs, of one month evolution. Skin biopsy of lower extremity lesions was compatible with leukocytoclastic vasculitis. Hepatitis B serology was positive, so she started antiviral treatment with tenofovir and prednisone with good evolution of her skin lesions
Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Vasculite/terapia , Vasculite Leucocitoclástica Cutânea/terapia , Hepatite B/terapiaRESUMO
BACKGROUND: Sudden sensorineural hearing loss (SSNHL) is defined as a sudden loss of hearing, usually unilateral, of more than 30 dB in 3 contiguous frequencies of the tonal audiometry. SSNHL estimates an incidence ranging from 5 to 20 per 100.000 people per year. In approximately 75% of cases, a cause cannot be identified. However, it could be a clinical manifestation of Systemic lupus erythematosus (SLE) and Antiphospholipid Syndrome (APS). OBJECTIVE: This review will focus on the clinical presentation, diagnosis, and management of the SLE and APS associated SSNHL. METHODS: We searched in PubMed, Scopus, Lilacs, and Cochrane reviewing reports of Sudden sensorineural hearing loss in SLE and/or APS. Articles written in English and Spanish, and were available in full text, were included. RESULTS: In patients with SLE, bilateral involvement was frequent. Antiphospholipid antibodies were positive in the majority of the patients. Corticosteroids were the mainstay of the treatment. The auditory prognosis was poor with total hearing loss recovery reached in only 22% of patients. On the other hand, most of the patients with SSNHL and APS were males and presented associated symptoms such as vertigo, tinnitus and/or headache, 75% had bilateral disease. Lupus anticoagulant and aCL were found in equal proportions, all patients were anticoagulated, and aspirin was associated in 25% of the cases. Complete resolution or improvement of symptoms was observed in 25% of the patients. CONCLUSION: Sudden sensorineural hearing loss, can be a clinical feature of SLE and APS. Treating physicians should be aware of this devastating complication, especially when bilateral involvement occurs.
Assuntos
Síndrome Antifosfolipídica/complicações , Perda Auditiva Neurossensorial/etiologia , Perda Auditiva Súbita/etiologia , Lúpus Eritematoso Sistêmico/complicações , Corticosteroides/uso terapêutico , Perda Auditiva Neurossensorial/tratamento farmacológico , Perda Auditiva Súbita/tratamento farmacológico , Humanos , Resultado do TratamentoAssuntos
Artrite Reumatoide/complicações , Azatioprina/administração & dosagem , Ciclofosfamida/administração & dosagem , Glomerulonefrite , Rim/patologia , Metilprednisolona/administração & dosagem , Adulto , Antirreumáticos/administração & dosagem , Antirreumáticos/classificação , Artrite Reumatoide/tratamento farmacológico , Artrite Reumatoide/imunologia , Artrite Reumatoide/fisiopatologia , Biópsia/métodos , Feminino , Glomerulonefrite/diagnóstico , Glomerulonefrite/tratamento farmacológico , Glomerulonefrite/etiologia , Glomerulonefrite/fisiopatologia , Humanos , Conduta do Tratamento Medicamentoso , Resultado do TratamentoRESUMO
Galectins, a family of animal lectins, play central roles in immune system regulation, shaping both innate and adaptive responses in physiological and pathological processes. These include rheumatoid arthritis (RA), a chronic multifactorial autoimmune disease characterized by inflammatory responses that affects both articular and extra-articular tissues. Galectins have been reported to play central roles in RA and its experimental animal models. In this perspective article we present new data highlighting the regulated expression of galectin-1 (Gal-1) and galectin-3 (Gal-3) in sera from RA patients under disease-modifying anti-rheumatic drugs (DMARDs) and/or corticoid treatment in the context of a more comprehensive discussion that summarizes the roles of galectins in joint inflammation. We found that Gal-1 levels markedly increase in sera from RA patients and positively correlate with erythrocyte sedimentation rate (ERS) and disease activity score 28 (DAS-28) parameters. On the other hand, Gal-3 is downregulated in RA patients, but positively correlates with health assessment questionnaire parameter (HAQ). Finally, by generating receiver-operator characteristic (ROC) curves, we found that Gal-1 and Gal-3 serum levels constitute good parameters to discriminate patients with RA from healthy individuals. Our findings uncover a differential regulation of Gal-1 and Gal-3 which might contribute to the anti-inflammatory effects elicited by DMARDs and corticoid treatment in RA patients.