Coulter J Brian S, Baretto Richard L, Mallucci Connor L, Romano Maria I, Abernethy Laurance J, Isherwood David M, Kumararatne Dinakantha S, Lammas David A
Royal Liverpool Children's NHS Trust, Liverpool, UK.
Lancet Infect Dis. 2007 Mar;7(3):225-32. doi: 10.1016/S1473-3099(07)70054-3.
A 12-year-old girl with protracted tuberculous meningitis received standard chemotherapy and dexamethasone and had a progressive cerebrospinal fluid neutrophilia, raised protein and depressed glucose levels. Her temperature was raised for 5 months until a second course of dexamethasone was given. At week 15, multiple tuberculomas and hydrocephalus were detected followed by acute hydrocephalus (week 58), which required a ventricular-peritoneal shunt. Tuberculomas resolved after a second course of dexamethasone but recurred 15 months later. Immunological investigations were normal including integrity of the type 1 cytokine pathway. From month 24, interferon-gamma was given subcutaneously (initially 50 microg/m(2)) and continued for 19 months. Within 2 weeks she responded clinically followed by a reduction in inflammatory signs on magnetic resonance imaging scan (but not in the tuberculomas). At month 44, when chemotherapy was stopped, the cerebrospinal fluid/serum albumin quotient was 57x10(-3) (normal <6.0x10(-3)), which supports continuing major impairment of the blood-brain barrier. Gene expression in peripheral blood mononuclear cells before and during treatment with interferon-gamma, assessed by gene array analysis, showed reduction in a number of cytokine and chemokine genes. The response to interferon-gamma might have been secondary to downregulation of certain cytokine and chemokine genes.
