Resumen

ROCABADO CALIZAYA, Guillermo Omar et al. BILATERAL SUBACUTE SUBDURAL HEMATOMA CAUSED BY THE ADMINISTRATION OF METHOTREXATE AT HIGH DOSE AND REVERSED BY MOLECULAR DISPLACEMENT OF NMDA RECEPTORS, IN A PATIENT WITH ALL-B COMMON HIGH-RISK PHI (-). Rev. Méd. La Paz [online]. 2025, vol.31, n.1, pp.83-88.  Epub 30-Jun-2025. ISSN 1726-8958.

The high toxicity ofMTX-HD after use in oncohematological diseases such as acute lymphoblastic leukemia (ALL) or Hodgkin lymphoma (HL), among others, and high intravenous (IV) doses greater than 5 g/m2 are essential, with the risk of producing neurological complications or seizures. This raises the need to quantify MTX, measure enzymatic capacity, and determine brain injury biomarkers, which are very useful for ruling out injuries caused by retained MTX. This paper presents the case of a 23-year-old female patient diagnosed with high-risk ALL and a white blood cell count of 2.9x103. She received MTX-based chemotherapy at 8 g/m2. She developed febrile neutropenia, which was not reversed by SC or modified IV filgrastim. MTX was quantified by UV/Vis, showing elevated levels. Low enzyme expression and activity were determined by CellTiterGlow, and the concentration of brain injury biomarkers was within pathological ranges using fluorometry techniques. MTX was held responsible as the direct cause of the subdural hematoma. MTX complexes were formed after a physicochemical halogenation reaction by bromobenzene and subsequent displacement of NMDA receptors by dextromethorphan, with the aim of reversing the clinical picture, antagonizing MTX, reversing neutropenia, and obtaining medical discharge.

Palabras clave : MTX (Metotrexato); HD (Altas Dosis); TAC (Tomografía Axial Computarizada); RMN (Resonancia Magnética Nuclear); EMR (Enfermedad Minima Residual); CK-BB (Isoenzima Creatinasa Cerebral); NSE (Enolasa Neuro Especifica); HCU-L1 (Proteína Soluble Cerebral); GFAP (Proteína Acida Fibrilar de Glia).

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