Low-dose aspirin therapy is not a reason for repeating head computed tomographic scans in traumatic brain injury: a prospective study

Background

Most studies have categorized all antiplatelet drugs into one category. The aim of our study was to evaluate the utility of repeat head computed tomography (RHCT) and outcomes in patients on low-dose aspirin (acetylsalicylic acid; ASA) therapy.

Methods

Patients with traumatic brain injury with intracranial hemorrhage on initial head computed tomography (CT) were prospectively enrolled. Patients on prehospital low-dose (81 mg) aspirin therapy were matched with patients exclusive of antiplatelet and anticoagulation therapy using propensity score matching in a 1:1 ratio for age, Glasgow Coma Scale, head Abbreviated Injury Scale score, Injury Severity Score, and neurological examination. Outcome measures were progression on RHCT and subsequent neurosurgical intervention.

Results

A total of 144 patients who had intracranial hemorrhage on initial CT scan (ASA group: 72; No-ASA group: 72) were enrolled. The mean age was 72.8 ± 11.7 years, 59.7% were male, and median head Abbreviated Injury Scale was 3 (2–3). There was no difference in progression on RHCT (25% in ASA versus 16.6% in no-ASA), change in management as a result of RHCT (1.4% versus 1.4%), RHCT as a result of neurological decline (0 versus 1.4%), discharge Glasgow Coma Scale (15 [14–15] versus 15 [14–15]), and mortality (0 versus 1.4%) between the two groups.

Conclusions

Low-dose aspirin therapy is not associated with progression of initial insult on RHCT or clinical deterioration. Prehospital low-dose aspirin therapy as a sole criterion should not warrant a routine repeat head CT in traumatic brain injury.     

Protection effects of Taurine supplementation against cisplatin-induced nephrotoxicity in rats

BACKGROUND: Taurine, which is the major intracellular free beta-amino acid, is known to be an antioxidant and a membrane-stabilizing agent. This study was designed to investigate the protective role of taurine supplementation against cisplatin-induced nephrotoxicity. METHODS: Male Wistar rats were divided into six groups and treated as follows: (1) saline-treated control drinking tap water, (2) saline-treated plus taurine-supplemented (1.5% taurine in the drinking water), (3) saline-treated plus taurine-depleted (3% beta-alanine in the drinking water), (4) cisplatin-treated, CDDP 6 mg/kg intraperitoneally, (5) taurine-supplemented plus CDDP-treated and (6) taurine-depleted plus CDDP-treated. Rats were sacrificed 7 days after CDDP treatment, and serum as well as kidneys were isolated and analyzed. RESULTS: CDDP-treated rats showed increased kidney weight as a percentage of total body weight, serum creatinine and BUN levels and decreased serum albumin and calcium levels. Also, CDDP treatment resulted in a depletion of kidney GSH content, a reduction in the kidney glutathione peroxidase (GSH-Px) activity and increased kidney MDA production level. Taurine supplementation attenuated CDDP-induced nephrotoxicity which was manifested by jeopardizing the elevation in serum creatinine and BUN levels and the reduction in serum albumin and calcium levels. Moreover, taurine supplementation restored kidney GSH content and GSH-Px activity and reduced platinum accumulation and MDA production levels in the kidney tissue following CDDP treatment. Histopathological examination of the kidney of CDDP-treated rats revealed tubular atrophy, tubular necrosis and desquamation of renal tubular cells. However, taurine supplementation protected against CDDP-induced histopathological changes. CONCLUSIONS: The data suggest that taurine supplementation effectively attenuates the accumulation of platinum within kidney tissue and counteracts the deleterious effect of CDDP on the renal tubular function.