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[AIDS encephalopathy in childhood or the late sequela of central nervous system leukemia?]
W Brunhuber1, J Emhofer, R Ploier
1Kinderabteilung Landeskrankenhaus Steyr.
Insights
This case report details an 11-year-old boy with acquired immunodeficiency syndrome (AIDS) encephalopathy and CNS-leukemia. Diagnostic challenges arose from overlapping neurological symptoms, highlighting the need for definitive HIV testing.
Area of Science:
- Pediatric Neurology
- Infectious Diseases
- Neuroimmunology
Background:
- A case report focusing on an 11-year-old boy presenting with new-onset cellular immunodeficiency and positive HIV serology.
- The patient had a history of central nervous system (CNS) leukemia relapse 33 months prior to the development of these symptoms.
Observation:
- Progressive neurological deterioration including motor, cognitive, and behavioral disturbances was observed after 18 weeks.
- Cerebral atrophy was noted on CT scan, with symptoms potentially attributable to both HIV and CNS leukemia-induced encephalopathy.
Findings:
- Subacute sclerosing panencephalitis (SSPE) was ruled out.
- Diagnostic imaging (CT, EEG, Evoked Potentials) did not provide definitive differential diagnostic findings between HIV and CNS leukemia.
- Cerebrospinal fluid (CSF) findings suggested a persistent viral infection consistent with the pathogenesis of AIDS encephalopathy.
Implications:
- Definitive etiological diagnosis in such complex cases necessitates histological examination of brain tissue and demonstration of HIV or HIV antigen.
- Treatment with AZT, a potential therapy for cerebral AIDS manifestations, was not feasible due to the patient's pancytopenia.
Abstract:
This case report is about an eleven year old boy with new developed symptoms of a cellular immundeficiency and a positive HIV-serology 33 months after a CNS-leukemia relapse. After 18 weeks a progredient neurological symptomatology is beginning with motor, cognitive and behavioral disturbances and a brain atrophy in the CT-scan. These cerebral manifestations are explainable as an encephalopathy both through HIV and after CNS-leukemia. A SSPE has been excluded. CT, EEG, Evoked Potentials do not show differential diagnostic pathognomonic findings regarding both diseases. The CSF findings hint at a persistent virus infection compatibel with the postulated slow virus pathogenesis of the AIDS-Encephalopathy. We conclude, that in this case an etiological diagnoses is only possible through histological brain examination and through demonstration of HIV or HIV-antigen in brain tissue respectively. AZT, which is reported to be effective against the cerebral AIDS-manifestations could not be applicated because of the existing pancytopenia.