Objective. To investigate the respective contribution of various biologic and psychosocial factors, especially initial health-related quality of life (HRQOL), in the natural history of acute low back pain (LBP) and to evaluate the impact of this condition on HRQOL. Methods. For 3 months, we assessed 113 patients consulting for nonspecific acute LBP of <72 hours duration at inclusion and treated with acetaminophen. Endpoints included pain, disability assessed by the Roland Disability Questionnaire, and HRQOL assessed by the Short Form 36 health survey (SF-36). Results. Seventy-three percent of patients recovered within 2 weeks and 5% of patients developed chronic LBP. Prior low back surgery, higher initial disability questionnaire score, lower SF-36 score, and temporary compensation status were independently associated with delayed recovery. The impact of the acute LBP episode on HRQOL was brief and moderate, except for patients with comorbidity, psychiatric disorders, those of foreign origin, unemployed, or with job dissatisfaction. The impact of compensation status, sick leave, and bed rest was more profound and lasting. Conclusions. This study highlights the large contribution of work-related factors, but also initial HRQOL, to the prognosis of LBP. It also suggests that LBP impairs HRQOL mainly through compensation and inappropriate medical care, and that, in turn, impaired HRQOL favors the condition becoming chronic. These findings have implications for future research into the management of LBP. KEY WORDS. Low back pain; Health-related quality of life; Psychosocial factors.
Anaemia during malaria is not completely understood. Fourteen cases of antierythrocyte autoimmunisation with anti-I specificity were investigated in a Paris hospital during a period of 2 years. The patients lived in Gabon and had not been taking antimalarial chemoprophylaxis. All had chronic malaria (strongly positive antimalarial immunofluorescent antibody tests). All the recognised caused for anti-erythrocyte autoimmunity were excluded. One possible explanation for these observations is some sort of interaction between I antigen and Plasmodium, the result of which facilitated penetration of the erythrocyte by the malarial parasite.
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