Evaluation of fibronectin and c-reactive protein levels in patients with sepsis: a case-control study

Sepsis is a significant health problem with an estimated 750,000 new cases in the USA annually. It is also the third leading cause of death in developed countries, equaling the number of fatalities from acute myocardial infarction. The high sepsis-related mortalities mean there is an urgent need to improve the diagnosis and management of sepsis patients. The aim of this study was the evaluation of fibronectin and C-reactive protein [CRP] plasma levels in patients with sepsis and other infectious diseases without sepsis. In a case-control study, 90 patients with sepsis and 90 patients with other infectious diseases without sepsis were studied. Serum levels of fibronectin and CRP were measured. The data were analyzed by SPSS version 15. The mean levels of fibronectin in the cases and controls were 288.97 +/- 89.10 mg/l and 341.24 +/- 110.53 mg/l respectively [P=0.001]. The mean levels of CRP in the cases and controls were 89.42 +/- 54.05 micro g/ml and 27.42 +/- 25.89 micro g/ml respectively [P<0.001]. Concerning the source of infection, the mean CRP levels were significantly higher in septic patients with urinary tract infection, pneumonia, and soft tissue infection [P<0.001]. Decreased levels of fibronectin and increased levels of CRP may be considered as reliable diagnostic markers for sepsis. Also, CRP could be a better predictive factor for sepsis than fibronectin

Nosocomial bacterial infections and their antimicrobial resistance paterns in university hospitals of Hamedan, Iran

Nosocomial infections constitute a global health problem, leading to a high rate of morbidity and mortality. The aim of this study was to determine the frequency and antimicrobial resistance patterns of nosocomial infections in educational hospitals of Hamadan, western, Iran. During a 1-year period from April 2006 to March 2007, all patients with culture-proven nosocomial infections from educational hospitals in Hamedan, western Iran were included. Nosocomial infections were defined as a culture-proven infection, which occurred more than 48h after admission in the hospital. Antimicrobial susceptibility testing of isolated bacteria was performed by disc diffusion method. A total of 170 cases of culture-proven nosocomial infections were diagnosed. Most cases were in intensive care units [ICUs] [57.4%]. The common sites of infection were lower respiratory tract [51.8%] and urinary tract [31.9%]. Klebsiella pneumoniae, Pseudomonas aeruginosa, and Escherichia coli, were the most prevalent pathogens [32.7%, 22.9%, and 14.8% respectively]. Most enterobacteriacea isolates were resistant to third generation cephalosporins. The resistant rates to ceftriaxone were 75.5% for K. pneumoniae, and 76% for E. coli. Among P. aeruginosa isolates, 26.5% were resistant to ceftazidim, and 36% to ciprofloxacin. Among S. aureus isolates, 80% were methicillin-resistant. The patients in the ICUs are at a higher risk of nosocomial infections. The high prevalence of antimicrobial resistance in the hospitals highlights the need of further infection control activities and surveillance programs

Antinociceptive effect of promethazine in mice

The present study was undertaken to investigate the nociception activity of promethazine, a tranquillizer devoid of hypnotic activity in mice. Antinociception was evaluated, using the acetic acid-induced writhing, tail flick, hot plate and formalin pain tests. Promethazine [4 and 6 mg/kg] and acetylsalicylic acid [100 mg/kg] produced a significant inhibition of the second phase response in the formalin pain model [P<0.05] and the drug couldn't show an antinociceptive effect in the first phase. Morphine [10 mg/kg] inhibited both first and second phase response [P<0.01]. Drug also showed a dose-dependent inhibition of acetic acid-induced abdominal writhes. The tail flick and hot plate latency weren't different from control [P>0.05] and administration of naloxone [0.1 mg/kg] couldn't block the antinociceptive effect of promethazine. The data obtained suggest that antinociceptive effects of the promethazine may be mediated via peripheral and not central mechanisms