RESUMEN
A 53-year-old woman with recurrent stomatitis, genital ulcers, and folliculitis was admitted to our hospital after experiencing visual disturbances for the past two weeks, and a non-throbbing headache for the past three days. She had also developed numbness in her left extremities. An ophthalmological examination revealed inflammatory changes in the eye. Cerebrospinal fluid analysis showed increased cell counts, protein, and interleukin-6 levels. Brain magnetic resonance imaging revealed multiple high signal intensities on T2-weighted (T2W)/fluid-attenuated inversion recovery (FLAIR) images of the pons and occipital and parietal lobes. The T2W/FLAIR high-signal-intensity lesion in the pons was hyperintense on diffusion-weighted imaging (DWI) and hypointense on apparent diffusion coefficient mapping (ADC), suggesting cytotoxic edema. Another high-signal-intensity lesion on T2W/FLAIR was isointense to hyperintense on DWI and hyperintense on ADC, indicating vasogenic edema. The vasogenic edema in the left occipital lobe contained a small core that was hyperintense on DWI and hypointense on ADC, suggesting cytotoxic edema. The patient was diagnosed with acute neuro-Behçet's disease (neuro-BD) and responded well to high-dose glucocorticoid and colchicine treatment. The present report emphasizes that patients with acute neuro-BD may present with cytotoxic edema in the pons and cerebral spheres. Further reports of similar cases would contribute to a better understanding of the role of cytotoxic edema in the pathophysiology of neuro-BD and help elucidate the mechanisms underlying a unique presentation characterized by a central cytotoxic edema core within vasogenic edema. (233 words).
RESUMEN
Renal involvement is underestimated as an extramuscular manifestation of dermatomyositis (DM). Here, we describe a 67-year-old woman with anti-glycyl-transfer ribonucleic acid synthetase (anti-EJ) antibody and anti-ribonucleoprotein antibody-positive DM complicated by systemic sclerosis, who developed nephrotic syndrome concurrently with the exacerbation of DM, as indicated by incremental serum creatine kinase levels, high-intensity lesions on muscle magnetic resonance imaging, and active interstitial pneumonitis on chest computed tomography. Renal biopsy revealed the presence of immune-deposition in the glomerulus by immunofluorescence. To our knowledge, this is the first report describing the coexistence of anti-EJ antibody-positive DM and nephrotic syndrome. More reports of similar cases are warranted to substantiate the association.
RESUMEN
Favipiravir, an antiviral agent, is undergoing clinical trials for treating novel coronavirus disease 2019 (COVID-19). Here, we report two cases of COVID-19 with favipiravir-induced fever. In both cases, pyrexia was observed following the administration of favipiravir despite improvements in symptoms of COVID-19. No other cause for fever was evident after careful physical examination and laboratory investigation. The fever subsided in both patients after the discontinuation of favipiravir. To the best of our knowledge, this is the first report of favipiravir-induced fever in COVID-19 patients.
Asunto(s)
Amidas/efectos adversos , Antivirales/efectos adversos , Tratamiento Farmacológico de COVID-19 , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/etiología , Fiebre/etiología , Pirazinas/efectos adversos , SARS-CoV-2/fisiología , Adulto , Amidas/administración & dosificación , Antivirales/administración & dosificación , Temperatura Corporal , COVID-19/fisiopatología , Femenino , Fiebre/fisiopatología , Humanos , Masculino , Pirazinas/administración & dosificación , SARS-CoV-2/efectos de los fármacos , SARS-CoV-2/genética , Resultado del TratamientoRESUMEN
Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease that develops in genetically susceptible individuals in response to environmental factors. SLE and primary immunodeficiency disease (PID) share some clinical manifestations in that certain PIDs present with autoimmune phenomena. Patients with SLE become susceptible to infection via three pathways. First, SLE and PID share some genetic factors, such as complement and mannose-binding lectin genes, which predispose patients to infection. Second, patients with SLE have an inherently high risk of infection because of their intrinsic immunological abnormalities induced by SLE. Third, patients with SLE receiving immunosuppressive treatment are at high risk of infection. Further studies delineating the abnormalities related to both autoimmunity and immunodeficiency would be warranted to identify a new potential drug target for SLE.