RESUMO
Resumen El síndrome de Guillain-Barré (SGB), es una polirradiculoneuropatía inflamatoria aguda, de origen autoinmune que suele ir precedido de una infección respiratoria o gastrointestinal. Se caracteriza por ser una parálisis fláccida, simétrica, ascendente, arrefléxica de evolución rápida. Presentamos un caso de un paciente de sexo masculino de 33 años, con antecedente de resfrío común dos semanas antes de su ingreso además deposiciones líquidas que revirtieron espontáneamente; asimismo posee un cuadro clínico de seis días en el cual presenta cuadriparesia que se agrava afectando los músculos de la respiración y terminando en ventilación mecánica. El examen de líquido cefalorraquídeo (LCR), reveló disociación albúmino-citológica y el examen de PCR dio positivo para Enterovirus. Se diagnosticó SGB por Enterovirus, por lo que recibió tratamiento con inmunoglobulina endovenosa con una evolución y resultados favorables. La finalidad de este trabajo fue presentar un caso clínico de SGB por un nuevo agente causal.
Abstract Guillain Barre syndrome (GBS) is an acute inflammatory polyradiculoneuropathy of autoimmune etiology that is usually preceded by a respiratory or gastrointestinal infection. It is characterized by a flaccid, symmetric, ascendent, arreflexic paralysis of rapid evolution. We describe a case of a 33 years old male patient, with a history of flu two weeks before admission, in addition to liquid stools that reverted spontaneously; his clinical picture consisted of a six days history of cuadriparesis aggravated by respiratory weakness, ending in mechanical ventilation. Examination of cerebrospinal fluid (CSF) revealed albumino-cytological disociation and PCR test resulted positive for Enterovirus. The patient received treatment with intravenous immunoglobulin with a favorable outcome. The purpose of this paper is to report a clinical case of GBS due to a new causal agent.
RESUMO
Ferrostatin-1 (Fer-1) is a lipophilic antioxidant that effectively blocks ferroptosis, a distinct non-apoptotic form of cell death caused by lipid peroxidation. During many infections, both pathogens and host cells are subjected to oxidative stress, but the occurrence of ferroptosis had not been investigated. We examined ferroptosis in macrophages infected with the pathogenic yeast Histoplasma capsulatum. Unexpectedly, Fer-1 not only reduced the death of macrophages infected in vitro, but inhibited the growth of H.â capsulatum and related species Paracoccidioides lutzii and Blastomyces dermatitidis at concentrations under 10â µm. Other antioxidant ferroptosis inhibitors, including liproxstatin-1, did not prevent fungal growth or reduce macrophage death. Structural analysis revealed a potential similarity of Fer-1 to inhibitors of fungal sterol synthesis, and ergosterol content of H.â capsulatum decreased more than twofold after incubation with Fer-1. Strikingly, additional Fer-1 analogues with slight differences from Fer-1 had limited impact on fungal growth. In conclusion, the ferroptosis inhibitor Fer-1 has unexpected antifungal potency distinct from its antiferroptotic activity.
