Correlation between Monocyte Gene Expression and Inflammation on Brain Imaging in Patients with Solitary Cerebral Cysticercus Granuloma.

Prior work has shown that 14 monocyte genes are upregulated in patients with different forms of parenchymal neurocysticercosis, including solitary cysticercus granuloma (SCG). The aim of this study was to investigate whether changes in inflammation associated with SCG seen on follow-up brain imaging are also reflected in changes in expression of these 14 genes. Peripheral blood CD14+ monocytes were isolated from 20 patients with SCG at initial diagnosis and at clinical and imaging follow-up of 6 months or more. Expressions of 14 target monocyte genes were determined by quantitative polymerase chain reaction at each visit. At a median follow-up of 14 months, the SCG had resolved in 11 patients, was persistent in four patients, and had calcified in five patients. Edema seen in the initial imaging in 17 patients had resolved in 15 patients and was markedly reduced in two patients. The expression levels of the monocyte genes LRRFIP2, TAXIBP1, and MZB1 were significantly lower at follow-up, regardless of the status of SCG on follow-up imaging. Our findings show that expression levels of monocyte genes involved with inflammatory processes decrease in patients with SCG concomitant with follow-up imaging that reveals a reduction in inflammation as revealed by complete or near-complete resolution of edema, as well as resolution or reduction in the enhancement of the granuloma.

Imaging correlates of serum enzyme-linked immunoelectrotransfer blot (EITB) positivity in patients with parenchymal neurocysticercosis: results from 521 patients.

BACKGROUND: The presence of perilesional edema among patients with parenchymal neurocysticercosis (pNCC) of various lesion subtypes has not been correlated with results of serum enzyme-linked immunotransfer blot (EITB) for cysticercal antibodies. METHODS: In total, 521 patients with pNCC were classified into solitary cysticercus granuloma (SCG), multiple lesions, at least one of which was an enhancing granuloma (GMNCC), solitary calcified cysticercal lesion (SCC) and multiple calcified cysticercal lesions (CMNCC). The proportion of EITB positivity among each lesion subtype and its association with perilesional edema were determined. RESULTS: There were significantly higher positive EITB results in patients with GMNCC (90/111, 81.1%) compared with other lesion types. Perilesional edema was associated with positive EITB in patients with CMNCC. On univariate analysis, perilesional edema and GMNCC were associated with EITB positivity. On multivariate analysis, only GMNCC (OR 7.5; 95% CI 3.5 to 16.2) was significantly associated with EITB positivity. CONCLUSIONS: In patients with pNCC, the presence of perilesional edema is associated with a higher probability of a positive EITB result in patients with CMNCC, suggesting a synchronicity in the mechanisms associated with formation of perilesional edema and the antibody response in this subtype. In patients with enhancing granulomas, edema is not an independent predictor of a positive EITB, suggesting that the enhancement itself is associated with a strong antibody response.

Monocyte Gene Expression Distinguishes Enhancing Brain Parenchymal Cysticercal Granulomas From Tuberculomas.

BACKGROUND: In patients with enhancing brain parenchymal lesions, parenchymal neurocysticercosis (pNCC) is often difficult to distinguish from tuberculoma, necessitating biopsy or empirical therapy. METHODS: In a prospective study, peripheral blood monocytes were isolated from patients with definitive pNCC (n = 39) and brain tuberculomas (n = 20). Patients with tuberculomas were diagnosed by the presence of concurrent systemic tuberculosis (n = 7), pathological or bacteriological confirmation (n = 5), and resolution of typical brain lesions following a therapeutic trial of antituberculous therapy (n = 8). Expressions of 14 NCC-associated monocyte genes were determined by quantitative polymerase chain reaction and analyzed for diagnostic usefulness between the 2 groups. RESULTS: Expression of 7 genes (TAX1BP1, RAP1A, PLCG2, TOR3A, GBP1P1, LRRFIP2, and FEZ2) was significantly higher in pNCC patients than in tuberculoma patients, with TAX1BP1 and RAP1A expressions more than 22- and 5-fold higher in pNCC patients. TAX1BP1 had the highest sensitivity of 66.7% at a specificity of 100% in discriminating pNCC from tuberculoma. A combination of TAX1BP1 and RAP1A increased the sensitivity to 84.6%, and including GBP1P1 with TAX1BP1 and RAP1A further increased sensitivity to 87.2% while maintaining specificity of 100%. CONCLUSIONS: Expression of a panel of genes in blood monocytes distinguishes pNCC from brain tuberculomas in patients with enhancing brain lesions.