Neuropatía vasculítica simulando síndrome de Guillain-Barré: manifestación inicial de una Poliangeítis Microscópica
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Vive Rev. Salud
Abstract
La poliangeítis microscópica puede manifestarse con una heterogeneidad clínica tan amplia que su identificación temprana exige una lectura integradora y crítica de los primeros síntomas. Presentamos el caso de un hombre de 68 años cuya enfermedad inició de manera inusual: debilidad ascendente, dolor neuropático e hipoestesia progresiva, un cuadro que imitaba un síndrome de Guillain-Barré y orientó inicialmente el abordaje hacia una neuropatía desmielinizante. No obstante, junto a ese aparente origen neurológico emergieron indicadores sutiles pero decisivos: fiebre intermitente, malestar general, hematuria, proteinuria, hipoalbuminemia e intensa respuesta inflamatoria que revelaban un proceso sistémico no atribuible a una enfermedad neurológica aislada. La tomografía de tórax evidenció micronódulos subpleurales y bronquiectasias, mientras que la serología mostró anticuerpos anticitoplasma de neutrófilo en baja titulación con anti-MPO discretamente elevado, un perfil serológico modesto, pero clínicamente relevante en presencia de daño renal. La biopsia renal resolvió el dilema diagnóstico al demostrar una glomerulonefritis necrotizante pauciinmune, confirmando poliangeítis microscópica como la causa unificadora del cuadro multisistémico. El tratamiento temprano con metilprednisolona y ciclofosfamida permitió la recuperación progresiva de la fuerza muscular, la reducción del dolor neuropático y la estabilización de la función renal, subrayando que el tiempo es un determinante crítico en estas vasculitis. Este caso demuestra cómo la poliangeítis microscópica puede presentarse enmascarada como un trastorno neurológico primario y destaca la necesidad de integrar datos clínicos, serológicos, radiológicos e histopatológicos para reconstruir coherentemente el diagnóstico y evitar retrasos potencialmente irreversibles.
Microscopic polyangiitis can manifest with such broad clinical heterogeneity that its early identification requires an integrative and critical interpretation of the initial symptoms. We present the case of a 68-year-old man whose illness began in an unusual manner: ascending weakness, neuropathic pain, and progressive hypoesthesia, a presentation that mimicked Guillain-Barré syndrome and initially led investigators to consider a demyelinating neuropathy. However, alongside this apparent neurological origin, subtle but decisive indicators emerged: intermittent fever, malaise, hematuria, proteinuria, hypoalbuminemia, and an intense inflammatory response, revealing a systemic process not attributable to an isolated neurological disease. Chest CT showed subpleural micronodules and bronchiectasis, while serology revealed low-titer antineutrophil cytoplasmic antibodies with a slightly elevated anti-MPO level-a modest serological profile, but clinically relevant in the presence of renal damage. The renal biopsy resolved the diagnostic dilemma by demonstrating pauci-immune necrotizing glomerulonephritis, confirming microscopic polyangiitis as the unifying cause of the multisystemic presentation. Early treatment with methylprednisolone and cyclophosphamide allowed for the progressive recovery of muscle strength, reduction of neuropathic pain, and stabilization of renal function, underscoring that time is a critical determinant in these vasculitides. This case demonstrates how microscopic polyangiitis can present masked as a primary neurological disorder and highlights the need to integrate clinical, serological, radiological, and histopathological data to coherently reconstruct the diagnosis and avoid potentially irreversible delays.
Microscopic polyangiitis can manifest with such broad clinical heterogeneity that its early identification requires an integrative and critical interpretation of the initial symptoms. We present the case of a 68-year-old man whose illness began in an unusual manner: ascending weakness, neuropathic pain, and progressive hypoesthesia, a presentation that mimicked Guillain-Barré syndrome and initially led investigators to consider a demyelinating neuropathy. However, alongside this apparent neurological origin, subtle but decisive indicators emerged: intermittent fever, malaise, hematuria, proteinuria, hypoalbuminemia, and an intense inflammatory response, revealing a systemic process not attributable to an isolated neurological disease. Chest CT showed subpleural micronodules and bronchiectasis, while serology revealed low-titer antineutrophil cytoplasmic antibodies with a slightly elevated anti-MPO level-a modest serological profile, but clinically relevant in the presence of renal damage. The renal biopsy resolved the diagnostic dilemma by demonstrating pauci-immune necrotizing glomerulonephritis, confirming microscopic polyangiitis as the unifying cause of the multisystemic presentation. Early treatment with methylprednisolone and cyclophosphamide allowed for the progressive recovery of muscle strength, reduction of neuropathic pain, and stabilization of renal function, underscoring that time is a critical determinant in these vasculitides. This case demonstrates how microscopic polyangiitis can present masked as a primary neurological disorder and highlights the need to integrate clinical, serological, radiological, and histopathological data to coherently reconstruct the diagnosis and avoid potentially irreversible delays.
Description
Vol. 8, No. 24
Keywords
Poliangitis Microscópica, Síndrome de Guillain-Barré, Vasculitis Asociada a Anticuerpos Citoplasmáticos Antineutrófilos, Microscopic Polyangiitis, Guillain-Barré Syndrome, Antineutrophil Cytoplasmic Antibody-Associated Vasculitis, Poliangeíte Microscópica, Síndrome de Guillain-Barré, Vasculite Associada a Anticorpos Anticitoplasma de Neutrófilos