Cerebral cryptococcoma in an immunocompetent patient: diagnostic challenge and neoplastic mimicry

Abstract

Case Presentation: A 54-year-old female patient, previously healthy and immunocompetent, presented with a nodular cutaneous lesion on the upper limb. Histopathological examination and culture of the lesion confirmed infection by Cryptococcus spp. sensitive to fluconazole, and oral therapy was initiated. Complete blood count and hepatic and renal function tests were normal; C-reactive protein was slightly elevated and HIV serology was negative. After several weeks, the patient developed sensory changes and progressive weakness in the left hemibody. On physical examination, she presented grade IV hemiparesis and ipsilateral hypoesthesia. Brain magnetic resonance imaging (MRI) revealed a cortical–subcortical expansive lesion in the right hemisphere, with nodular post-contrast enhancement and perilesional edema. Lumbar puncture showed clear cerebrospinal fluid, normal opening pressure, cellularity of 18 cells/mm³ (lymphomononuclear), protein of 75 mg/dL, and glucose of 52 mg/dL. Cryptococcal antigen in the cerebrospinal fluid was positive at a low titer, with negative culture. Given the progressive deficit and mass effect, surgical resection was performed. Histopathology confirmed a cerebral cryptococcoma. Postoperatively, antifungal therapy was maintained for 30 days, with clinical stabilization and partial improvement of the deficit. Discussion: Cerebral cryptococcoma is a focal presentation of cryptococcosis, characterized by expansive granulomas in the central nervous system (CNS). Unlike diffuse meningitis, cryptococcoma occurs predominantly in immunocompetent individuals. It manifests with focal deficits due to mass effect and may present cerebrospinal fluid parameters close to normal, making the diagnosis difficult. In this case, the patient had preserved immune status and a previous diagnosis of cutaneous infection by Cryptococcus spp., later evolving with left hemiparesis. The topographic correlation of the lesion on MRI, with nodular enhancement and edema, reinforces its mimicry with neoplasms or abscesses. Cerebrospinal fluid analysis showed a mild inflammatory pattern, with slight lymphomononuclear pleocytosis and low-titer positive cryptococcal antigen, without growth in culture—findings compatible with localized involvement. In healthy patients, an effective cellular immune response favors granulomatous organization and delimitation of the focus, explaining the formation of the mass and the low fungal burden in the cerebrospinal fluid. Although the gold standard treatment includes amphotericin B and flucytosine, neurological compression required a surgical approach. Final Comments: The diagnosis of cryptococcoma is complex and may arise from extracerebral manifestations. The progression from a cutaneous lesion to neurological deficit in a previously healthy patient highlights that the absence of immunosuppression does not exclude dissemination to the CNS. The normal cerebrospinal fluid findings and negative culture reinforce that imaging and histopathology are decisive.