Successful Treatment of Multiple Cerebral Histoplasmomas with Itraconazole
Author(s) -
David M. Bamberger
Publication year - 1999
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1086/517242
Subject(s) - itraconazole , medicine , dermatology , antifungal
midbrain and brain stem (figure 1). The lesions enhanced after revealed a decrease in the number and size of the lesions and in intravenous injection of gadolinium, and some had surrounding the surrounding edema. She continued to receive itraconazole for edema. An abdominal CT scan showed the left adrenal to be 3.4 1 year. Another MRI scan done 4 months after discontinuation of 1 3.9 cm with a hypodense center and hyperdense rim. A chest therapy revealed no change from the scan at the end of therapy. radiograph was normal. A fine-needle adrenal aspirate showed More than 2.5 years after discontinuing therapy, the patient renondiagnostic results. On CSF testing, the following values were mains asymptomatic. noted: glucose, 52 mg/dL; protein, 61 mg/dL; RBCs, 0/mm; The patient described had evidence of cerebral histoplasmomas, WBCs, 1/mm (100% mononuclear). Bone marrow and CSF culdespite the lack of a brain biopsy. H. capsulatum was found in tures were negative. The Histoplasma capsulatum polysaccharide the adrenal gland, antibodies to H. capsulatum were present in antigen level in serum was 0.5 U and in CSF was 0.7 U. The CSF, and the lesions and symptoms responded to antifungal therpatient was negative for IgG antibodies to Echinococcus species apy. Negative cultures of CSF and a negative result on CSF hisand HIV and IgM antibodies to Toxoplasma species in serum. Her toplasma polysaccharide antigen testing are observed in about half serum was positive for IgG antibodies to Toxoplasma species, but of cases of CNS histoplasmosis [1]. It is likely that her disease the ratio of Toxoplasma IgG antibodies to total IgG was twofold was related to the immunosuppressive effects of the corticostegreater in serum than in CSF. Her titer of complement fixation roids, despite discontinuation of corticosteroids 3 weeks before antibody to H. capsulatum in CSF was 1:2 for the mycelial antigen her neurological symptoms began. and 1:4 for the yeast antigen. An open adrenal biopsy revealed Two cases of cerebral histoplasmomas have been successfully extensive necrosis, granulomatous inflammation, and organisms treated with ketoconazole after relapse following therapy with inconsistent with histoplasmosis. Culture of adrenal tissue yielded travenous amphotericin B [2, 3]. There has also been a report of H. capsulatum. treatment failure with ketoconazole therapy for cerebral histoplasThe patient refused therapy with amphotericin B. She began momas [4]. Ketoconazole has been associated with treatment failreceiving itraconazole, 200 mg three times daily for 3 days, folures in immunocompromised patients with histoplasmosis and has lowed by 200 mg twice daily. Her neurological signs and symppoor penetration into CSF [1]. Two reported cases of CNS histotoms improved over the next 3 months, and repeat MRI scans plasmosis have been treated with fluconazole, which crosses the
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