Mortality after septic versus aseptic revision total hip arthroplasty: a matched-cohort study.

Mortality rates after revision total hip arthroplasty (THA) for periprosthetic sepsis were investigated in 93 patients and compared to 93 patients, matched for age, gender, year of surgery, who underwent revision for aseptic failures. The mortality rate was 33% (31/93) in the septic group and 22% (20/93) in the aseptic group at 5 and 6 year follow-up, respectively (P=0.10). Patients in the septic group died on average 6 years earlier (74 versus 80 yrs; P<0.05) than those in the aseptic group. Charlson Comorbidity Index (CCI) was an independent predictor of mortality among the both groups (P<0.05), while age (P<0.01) was a predictor of mortality only in the aseptic group. While revision THA for sepsis alone did not predict increased mortality, a 33% mortality rate at five years in patients with an average age of 66 years and earlier death by 6 years compared to aseptic revisions is alarming.

Redox modulation of the liver with chronic antioxidant enzyme mimetic treatment prevents age-related oxidative damage associated with environmental stress.

A reduction in stress tolerance is a hallmark of the aging process, and the lowered functional capacity observed in aged organisms is associated with an increased rate of oxidative stress and a greater susceptibility of aged tissues to oxidative injury. In this report, we show that chronic systemic administration of a superoxide dismutase (SOD)/catalase mimetic (EUK-189), delivered over a 1 month period via osmotic pump, prevents heat stress-induced liver injury by dramatically decreasing oxidative damage in aged animals. Widespread liver injury was present in old but not young vehicle-treated rats in response to a 2 day heating protocol. However, SOD/catalase mimetic treatment markedly decreased the hyperthermia-induced liver injury associated in old animals. The reversal of damage with EUK-189 was associated with an improvement in intracellular redox status and a striking reduction in hepatocellular lipid peroxidation. EUK-189 treatment also blocked the activation of activator protein-1 (AP-1), which is a redox-sensitive early response transcription factor involved in the regulation of cellular stress responses. These results demonstrate that oxidative stress plays a unique role in age-related hyperthermic injury and suggest that therapeutic strategies aimed at improving redox potential, such as chronic SOD/catalase mimetic treatment, can prevent the oxidative-mediated damage associated with environmental stress.