Abstract
It is well known that the acute phase response to tissue injury is manifested by increased synthesis of acute phase reactant proteins (APRPs) at the liver, which is mediated by cytokines. APRPs in subarachnoid hemorrhage (SAH) have not been thoroughly studied. We investigated the chronological changes of serum APRPs in 70 patients with SAH in order to determine how much APRPs correlate with the severity of initial clinical findings and hemorrhage on CT, and with the clinical outcome. None of the patients had steroid therapy, liver dysfunction, infections, malnutrition, or immune disease in the past and during the course of the study. Blood samples were taken on the 1st, 4th, 7th, 14th and 21st day after the catastrophe. APRPs examined were serum total protein (TP), albumin (Alb), alpha 1-acid glycoprotein (α1-AG), alpha 1-antitrypsin (α1-AT), alpha 2-macroglobulin (α2-MG), immunosuppressive acidic protein (IAP), interleukin-1 alpha (IL-1α) and tumor necrosis factor-alpha (TNF-α). As results, TP, Alb and α2-MG were depressed, and α1-AG, α1-AT, IAP and CRP were elevated throughout the study. Patients could be considered to be immunosuppressed from the early phase of SAH, because immunosuppressive agents like α1-AG, α1-AT and IAP were raised soon after the catastrophe. Further, α1-AG, α1-AT, IAP and CRP tended to be higher in patients with Hunt & Kosnik (H & K) III, IV, V grades, Fisher III, IV groups or dead outcome than in those with H & K I, II grades, Fisher I, II groups or good recovery. In other words, patients with bad clinical and CT findings or dead outcome tended to have high APRP levels. The acute phase response remained at least for 3 weeks. There was no any relationship of APRP changes with age, site of aneurysm, and presence or abscence of vasospasm and operative intervention. Neither IL-1α nor TNF-α was detected in any patient, presumably because of a short half-life time or very low undetectable circulating amounts. These results suggest that a follow-up study of serum APRPs is useful laboratory marker reflecting the degree of acute phase response after SAH, and becomes new adjunct data to understand the nature of SAH.
