A 33-year-old woman with a 10-year history of HIV infection, with a history of pulmonary tuberculosis at the time of diagnosis.
She received antiretroviral therapy (HAV) with good adherence for eight years, with favorable immunological and virological response, which she abandoned, as she said, due to clinical improvement.
Two years after the abandonment, tuberculosis was diagnosed again, with lymph node involvement and multidrug resistance.
She had been treated with an individualised regimen (amikacin, pyrazinamide, cycloserine, ethionamide and levofloxacin) for seven months, with resumption four weeks after previous HAART, efavirenz.
However, she had finally abandoned both regimens due to medication intolerance.
In addition, the patient had been empirically treated for Toxoplasma encephalitis with cotrimoxazole cotrimoxazole (5 mg/kg/day trimethoprim-images favorable by clinical MRI every 12 h).
At discharge, the patient had restarted tuberculosis treatment, and continued on cotrimazol with manox doses (160/800 mg every 24 h); without regular adherence.
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Three months later she was readmitted to the Emergency Department with a neurological condition of approximately one week duration, characterized by progressive paraparesis in the lower limbs, urinary retention and sensory impairment at T8 level.
Magnetic resonance imaging of the spine and spinal cord revealed the presence of an intramedullary ring contrast-enhancing image (0.9 cm x 2.6 cm) with perilesional edema at T8 level.
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The cerebrospinal fluid (CSF) study showed 20 cells predominantly lymphomononuclear (90%), hyperproteinorrhachia (247 mg/dL), glycorrhachia and ADA test (adenosine deaminase) within normal limits.
Microbiological tests in CSF for bacteria (Gramin staining and culture) were negative (Chinese staining and Cryptococcus antigen) and bacteria (bacillus testing and GeneXpert MTB/RIF).
Toxoplasma PCR was not performed in CSF, and CMV and EBV viral loads in serum and CSF were undetectable.
The CD4+ T-cell count was 11 cells/mm3, with an HIV viral load of 548.800 copies RNA/ml; the IgG serum titers for Toxoplasma were positive in 4.37 (<0.8 = negativeCM particles).
Empirical therapy was restarted because a biopsy of the intramedullary lesion could not be performed with i.v. cotrimoxazole.
(5 mg/kg trimethoprim twice daily) for four weeks associated with IV dexamethasone.
Treatment was initiated every 12 h for seven days.
Subsequently, it continued for two weeks with cotrimoxazole at the same dose orally, and progressive weekly reduction of corticosteroids with prednisone, until completing six weeks.
She had imaging control four weeks after treatment, showing improvement of intramedullary lesion, with evident decrease in size and less contrast enhancement.
Clinically after one week of empirical treatment, there was an improvement in discriminatory sensitivity and muscle strength; however, it persisted with urinary sphincter (urinary tract) involvement.
After initial improvement, it was decided to continue treatment for toxoplasmosis (for six weeks), and physical rehabilitation therapy.
Before discharge, ART was restarted with the same regimen previously received.
Finally, the patient received regular anti-crystallous therapy with a dosage of manatee with co-trimazol 160/800 mg, continued to receive methotrexate every 12 h.
