Is it all cerebral toxoplasmosis?

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A 43-year-old Nigerian man presented in April, 2010, with a 1 week history of progressive left leg weakness, urinary incontinence, and weight loss. Neurological examination showed left-sided neglect and hemiparesis. Physical examination was otherwise unremarkable. Blood test results were normal. MRI of the brain showed multiple bilateral ring-enhancing lesions; the largest was centred on the right basal ganglia with pronounced mass eff ect (fi gure A). Treatment for cerebral toxoplasmosis was initiated with sulfadiazine (15 mg/kg, four times daily), pyrimethamine (200 mg loading dose followed by 75 mg daily), and folinic acid (10 mg daily). IgG active against toxoplasma was detected and HIV-1 infection was confi rmed with a baseline viral load of 870 976 copies/mL and CD4 T-cell count of 68 cells/μL (11%). Left arm tone and power normalised after 24 h of treatment, but there was residual left leg weakness and over the next 2 weeks our patient developed a new rightsided hypertonia and he became progressively mute. Repeat MRI showed moderate improvement of the changes in the right hemisphere with reduction of vasogenic oedema (fi gure B). There was, however, a gradual progression of a solid mass in the left corona radiata on MRI; on fl uorine-18-labelled fl uorodeoxyglucose PET-CT (done 3 weeks after presentation) it showed signifi cantly higher uptake than the other lesions, which had lower uptake than normal cortex (see webappendix). These fi ndings suggested dual pathology, with lymphoma being the most likely secondary diagnosis. Despite initiation of highly active antiretroviral therapy and high-dose dexamethasone, our patient became less responsive and had generalised seizures necessitating ventilation 4 weeks after the initial presentation. A biopsy of the solid mass in the left hemisphere confi rmed primary cerebral diff use large B-cell lymphoma. We started our patient on high-dose methotrexate then cytarabine but there was no improvement. 8 weeks after initial presentation, treatment was withdrawn and the patient died on July 3, 2010. Cerebral toxoplasmosis is one of the commonest presenting diagnoses in advanced HIV disease. Primary cerebral lymphoma is uncommon, but over 30% of cases are associated with HIV infection. Diff erentiation of the two pathologies is diffi cult owing to the similar clinical and radiological presentation, but MRI and PET are the imaging modalities of choice, and tissue diagnosis is the gold standard. Prognosis in HIV-infected patients with primary cerebral lymphoma is poor, with median survival of 2 months, but antiretroviral therapy may improve life expectancy. The choice of chemotherapy tends to be a methotrexate-based regimen with a combination of other agents such as vincristine or cytarabine. This case serves as a reminder of the complexity of patients with late presentation of HIV infection in the UK, where the Health Protection Agency estimates that around 30% of individuals with HIV infection are undiagnosed and a similar percentage of those diagnosed present late. The HIV-infected population is predicted to reach 100 000 by 2012, therefore, the proportion of undiagnosed patients and late presenters must be reduced. Recent guidance from the Health Protection Agency recommends implementation of screening in health-care settings where the prevalence of HIV infection is higher than 2 per 1000, which may help to achieve this goal.