YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==CREUTZFELDT-JAKOB DISEASE== 4 AUTHOR Wientjens DP AUTHOR Davanipour Z AUTHOR Hofman A AUTHOR Kondo K AUTHOR Matthews WB AUTHOR Will RG AUTHOR van Duijn CM TITLE Risk factors for Creutzfeldt-Jakob disease: a reanalysis of case-control studies. SOURCE Neurology; VOL 46, ISS 5, 1996, P1287-91 (REF: 28) ABSTRACT To review the evidence for risk factors of Creutzfeldt-Jakob disease (CJD), we pooled and reanalyzed the raw data of three case-control studies. The pooled data set comprised 178 patients and 333 control subjects. The strength of association between CJD and putative risk factors was assessed by computing the odds ratio as estimate of the relative risk. The risk of CJD was statistically significantly increased for subjects with a family history of CJD (odds ratio = 19.1; 95% CI 1.1 to 348.0). Further, there was a significant association between the risk of CJD and a history of psychotic disease (odds ratio = 9.9; 95% CI 1.1 to 86.1). Although not significantly increased, there was an elevated risk of CJD for subjects with a family history of dementia, a history of poliomyelitis, subjects employed as health professionals, and subjects ever exposed to cows and sheep. No association could be shown with organ meat consumption, including brain. The negative results of this reanalysis reassures the absence of a common risk factor in all CJD patients. However, the ongoing epidemiologic surveillance of CJD in several European countries may provide more evidence to exclude any environmental exposure early in childhood. 7 AUTHOR Deslys JP TITLE [Biological aspects of Creutzfeldt-Jakob disease related to the extractive growth hormone] SOURCE Pathol Biol (Paris); VOL 43, ISS 2, 1995, P97-103 (REF: 31) ABSTRACT Today 34 young patients have been infected by the Creutzfeldt-Jakob Disease (CJD) agent in France after treatment with pituitary derived growth hormone. 974 individuals received potentially contaminated batches of hormone. The authors then investigated the genetic structure of the prion protein (PrP) gene at the codon 129 in 32 of the 34 CJD patients. Their results show that all are homozygous, 50% of the individuals of the control group being heterozygous. These data strongly suggest that it may exist a genetic susceptibility to the early development of CJD in infected individuals. 8 AUTHOR Paul J TITLE [Prion, from crazy cows to iatrogenic Creutzfeldt-Jakob disease. Which risk in laboratory or in hospital?] SOURCE Pathol Biol (Paris); VOL 43, ISS 2, 1995, P114-20 (REF: 40) ABSTRACT The long latency time, without any characteristic clinical sign, of transmissible degenerative encephalopathies, the transmissibility of the called "prion" infectious agent, associated with its exceptional resistance to normal inactivation methods, are resulting in accidental transmissions, both human (Creutzfeldt-Jakob disease), and animal (bovine spongiform encephalopathy). Among data about physical and chemical inactivation methods tested, we retain, to avoid professional or iatrogenic transmissions in the laboratory or in hospital, steam autoclaving and sodium hypochlorite or hydroxide treatment. But inactivation shall not be performed using the current processes as regarding parameters such as temperature, concentration and duration of exposure.