Early immunological defects in comatose patients after acute brain injury.

OBJECT: The aim of this prospective study was to evaluate the phagocytic, humoral, and cellular arms of the immune system in comatose patients shortly after severe brain injury and to compare the findings with those reported earlier in patients in a persistent vegetative state. The study was conducted in intensive care units and immunology laboratories of university-affiliated hospitals in central Israel. METHODS: The study group consisted of 14 men aged 16 to 65 years who were comatose as a result of acute brain injury due to mechanical trauma. All were studied within 72 hours of injury. Brain damage was severe in all cases (Glasgow Coma Scale score < 8). Healthy age- and sex-matched volunteers served as simultaneous controls. Infections arose in nine (75%) of the 12 patients in whom data were available; the cumulative mortality rate was 38% (five of 13 patients in whom outcome data were available). Every patient exhibited one or more defects in at least one arm of the immune system. Significant deficiencies were noted in neutrophil superoxide release, immunoglobulin (Ig)G, IgG1, IgM, C1q, C2, properdin, alternate C pathway, T cells, T helper cells, T suppressor cells, and natural killer cells. In an earlier series of patients examined by the authors months after the primary insult, these impairments were absent in most of the patients in the vegetative state. CONCLUSIONS: Significant deficiencies of the immune system, particularly the cellular arm, are precipitated by severe brain injury within 72 hours of the event. These impairments probably play a role in the high rate of complicating infections and multiple organ failure. Together with earlier findings, the results of this study indicate that if brain-injured patients survive these hazards, their immune system will eventually recover.

Impairment of non-specific immunity in patients under persistent vegetative state resulting from trauma.

OBJECTIVE: To investigate the immune response in patients under persistent vegetative state (PVS) resulting from trauma. METHODS: Peripheral blood monocytes were obtained from 12 PVS patients (Group PVS)and individuals in normal control group by density gradient centrifugation; the enzyme linked immunosorbent assay kit was then used to measure monocyte HLA-DR antigen expression on the surface of peripheral blood monocytes before and after monocyte activation with either IFN-gamma or LPS. RESULTS: Compared with normal control group, the peripheral blood monocyte HLA-DR antigen expression in the Group PVC fell significantly in PV S patients (P<0.001); the level of HLA-DR antigen express ion on the monocyte surface rose notably after stimulation with either IFN-gamma or LPS (P<0.01). As for PVS patients, it was still difficult to restore to normal (P<0.05). CONCLUSIONS: The level of HLA-DR antigen expression on the sur face of peripheral blood monocytes in PVS patients decreases obviously. Therefore, the function of non-specific immunity in PVS patients is suppressed.

Impairment of non-specific immunity in patients in persistent vegetative state.

In fourteen patients in persistent vegetative state (PVS) immune responsiveness was investigated. In particular, we studied the relationship between brain lesions following traumatic injury and immune system. In this respect, phagocytosis and killing of Candida albicans by polymorphonuclear cells (PMN) and monocytes were tested. In addition serum levels of Interferon-gamma (IFN-gamma) were evaluated. The patients come out from PVS by 3-4 month were used as control group. Data shown a profound impairement of phagocytosis and killing of monocytes and low serum levels of IFN gamma when compared with normal values. Taken together, these findings suggest that brain lesions, may affect non-specific immune response.