Table 1 Clinical features of patients with progressive multifocal leukoencephalopathy related to thymoma
Reference | Age | Sex | Causes of immunodeficiency | Time | Treatment ofthymoma | JC virus in the CSF | CD19+ B cell (cells/μL) | CD4/CD8 | CD4+ T cell (cells/μL) | CD8+ T cell (cells/μL) | Ig level (mg/dL) | PML Treatment | Prognosis | Survival period |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
[14] | 65 | F | Good’s syndrome | 0 | SR | >1million copies/mL | No detectable | 0.66 (1.13–3.93) | NR | NR | IgG: 570 (670–1450) IgA: 22 (88–450) IgM: 22 (27–210) | Mirtazapine Mefloquine | Death | Probably 5–6 M |
[13] | 39 | M | Chemotherapy for thymoma | 10 Y | SR + CT | 9,200 gEq/μL | 1 (100–800) | 0.2 (0.9–2.8) | 19 (450–1500) | 113 (250–1000) | NR | Cidofovir | Death | NR |
[12] | 79 | F | Good’s syndrome | 8 Y | SR | 9,258 pairs/mL | Absent | 1.5 | 648 | 425 | IgG: 619 (700–1600) IgA: <25 (70–400) IgM: <18 (40–250) | Cidofovir | Death | 5 M |
[11] | 58 | M | Good’s syndrome | 5 M | SR | 810 copies/mL | NR | 0.6 (0.8–2.4) | NR | NR | IgM: 31 (40–300) | Cidofovir Risperidone IVIg | Alive | At least 11 M |
[10] | 44 | F | Immunosuppressive therapy for MG | 2 M | SR | Positive | NR | NR | NR | NR | NR | Reduction of immunotherapy | Alive | At least 19 M |
[9] | 58 | M | Chemotherapy Good’s syndrome? | 9 Y | RT + CT | NR | NR | NR | NR | NR | NR | Cytrabine | Death | 13 W |
[8] | 41 | F | Immunosuppressive therapy for MG | 29 Y | RT + SR | NR | NR | NR | NR | NR | NR | Reduction of immunotherapy | Death | 6 W |
[7] | 39 | F | Immunosuppressive therapy for MG Good’s syndrome? | 3 Y | RT | NR | NR | NR | NR | NR | NR | None | Death | 5 M |
Present case | 47 | F | Good’s syndrome Chemotherapy | 23 Y | RT + SR + CT | 6,283,000 copies/mL | 3 | 0.6 | 11 | 19 | IgG: 282 (870–1700) IgA: 58 (110–410) IgM: 15 (35–220) | Mirtazapine Mefloquine IVIg | Death | 3 M |