A 43-year-old homosexual patient with HIV-1 was diagnosed with ISP in February 2009.
The patient had a history of P. jiroveci pneumonia, oropharyngeal-esophageal candidiasis and CMV infection of undefined location, which were treated timely.
ART was initiated with zidovudine (AZT), lamivudine (3TC), atazanavir/ritonavir (ATV/r) in May 2009 with a viral RNA load RNA/mL of 136mL.
This was not controlled but the medication was withdrawn monthly.
Seven months after starting HAART, she developed a confusional syndrome and was hospitalized in November 2009.
Physical examination at admission revealed stable hemodynamics, absence of fever and the presence of algorrhythmia.
It was described with temporo-spatial disorientation, short- and long-term memory impairment and occasionally sporadic.
There was no motor or sensory deficit.
Blood count and blood biochemistry showed no clinically significant changes.
The following tests: HBsAg, anti-HCV, IgG and IgM antibodies to T. gondii, anti-T. cruzi antibodies, and CMV antigenemia were reported as negative.
Blood VDRL was non-reactive.
Brain CT showed no abnormalities.
In an initial CSF there were 7 episodes of vomiting, glucose 44 mg/mL, protein 0.35 mg/dL and adenosine deaminase 2.5 mg/dL.
No microorganisms were observed in direct Gram stain of CSF, culture, sputum smear and India ink staining were negative.
CSF VDRL was also non-reactive.
The evaluation by the ophthalmologist was normal.
Brain MRI showed extensive supratentorial white matter lesions and cerebral pedicle lesions.
A new lumbar puncture was performed to perform CSF PCR (adult) for JC virus with a positive result that confirmed the diagnosis of PML.
During the in-hospital evolution, neurological deterioration was observed, with progressive dysphasia, impossibility to diagnose and severe swallowing disorder the patient underwent gastrostomy.
It was then decided to modify their ART by changing the ATV/r by lopinavir/ritonavir (LPV/r) and AZT and 3TC were maintained.
In addition, mitopine was initiated 15 mg/day via nasogastric tube three weeks after admission.
She remained hospitalized for 48 days and, at the time of discharge in January 2010, was emaciated, watched but not connected to her environment, did not answer simple orders, did not emit language, and was unable to eat exclusively by gastrotomy.
He took care of his mother and sister.
Two months after discharge she was more reactive to the medium and had simple orders; her CD4 lymphocyte count was 210 cé/mL and her viral load was undetectable.
Five months after discharge, the patient was able to initiate oral feeding without problem, although he continued using gastrostomy, and was in verborrheic language with an age ranging from 3 to 4 years.
At 7 months post discharge her language was clearer and at 10 months she no longer used her gastrostomy, she was fed entirely by mouth and without restriction to the type of food.
At the last follow-up after one year of discharge from the hospital, the patient was independently diagnosed with dementia, was seated and fed alone, and her language was normal, although she showed some words as authentic.
At that time, he had a CD4 T-cell count of 312 (7%) cells/mL and his viral load remained undetectable as in all previous controls (4 in total).
Brain MRI control was performed eight months after discharge, demonstrating a marked regression of white matter involvement, with brain components.
