ArticleTropical medicine and health2025
Toxoplasmic encephalitis unmasked during treatment for miliary tuberculosis in a patient with human immunodeficiency virus infection: a case report and literature review.
Article in Tropical medicine and health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundToxoplasmic encephalitis (TE) and tuberculoma are the leading causes of ring-enhancing brain lesions in patients with human immunodeficiency virus (HIV) infection. Because imaging findings of the two conditions overlap and cerebrospinal fluid (CSF) tests lack sensitivity, timely diagnosis is critical. Herein, we report the rare case of a patient with HIV infection and miliary tuberculosis who developed intracranial mass lesions after antiretroviral therapy (ART) initiation with high-dose prednisolone administration. CASE PRESENTATION: A 53-year-old Nepalese man who had been living in Japan was diagnosed with HIV infection (CD4 count, 146 cells/µL) and miliary tuberculosis. Four-drug rifabutin-based therapy was initiated. However, trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis was discontinued because of a rash and replaced with monthly pentamidine. ART (dolutegravir/lamivudine) was initiated 3 weeks later. Prednisolone (60 mg/day) was administered for refractory tuberculous ascites, and the dose was tapered over 6 weeks. Eight weeks after ART, the patient developed a headache, and laboratory tests revealed a CD4 count of 384 cells/µL. Magnetic resonance imaging (MRI) revealed right frontal ring-enhancing lesions. CSF was acellular; polymerase chain reaction yielded negative results for several pathogens including Mycobacterium tuberculosis and positive results for Toxoplasma gondii. After a 5-day graded TMP-SMX desensitization, the patient received full-dose therapy for 6 weeks, followed by secondary prophylaxis. The patient's headache resolved, and repeat MRI after 2 weeks revealed marked regression of the lesions. No radiological relapse was observed 3 months after treatment completion.
conclusionsTE can emerge during immune recovery at CD4 counts > 100 cells/µL when corticosteroid administration coincides with early ART. In patients receiving tuberculosis treatment who develop new brain lesions soon after ART, T. gondii polymerase chain reaction and prompt antiparasitic therapy should be pursued. Rifabutin permits concomitant use of dolutegravir, and TMP-SMX desensitization allows effective treatment and prophylaxis.
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