The DP approach showed advantages over FB translation in terms of preference by the target population and by lay people, whereas there were no obvious psychometric differences. This suggests advantages of DP over FB translation from the patients' perspective, and does not support the commonly held view that FB translation is the "gold standard."

The American Fibromyalgia Impact Questionnaire (FIQ) was translated into Swedish. The FIQ is a brief 10-item self-administered instrument designed to evaluate the special problems bothering fibromyalgia patients. After the translation procedure, 73 Swedish women fibromyalgia patients answered the translated FIQ. The questionnaire was fast and simple to handle both for the patients and the investigators. There was a good level of correspondence between FIQ items and related items in the Health Assessment Questionnaire, the Nottingham Health Profile and the Psychological General Well-Being Index. There were no significant differences in a test-retest analysis. The study has provided evidence that the translated and slightly modified Swedish version of the American Fibromyalgia Impact Questionnaire has the validity and sensitivity to be able to function as a relevant and comprehensible tool to monitor FMS-patients.

CPH 82 is a non-steroid antirheumatic drug containing two benzylidenated podophyllotoxin glucosides with no affinity for the glucocorticoid receptor. Treatment with CPH 82 as single drug therapy significantly decreased serum and urinary cortisol and cortisol metabolites, serum adrenal androgens and urinary androgen metabolites, plasma ACTH and serum interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), and increased serum levels of sex hormone-binding globulin (SHBG). Significant positive correlations were found between serum TNF-alpha and plasma ACTH and between serum IL-6 and TNF-alpha on the one hand and serum and urinary cortisol and cortisol metabolites on the other. The initial action of CPH 82 on adrenal steroidogenesis may be a reduction in cytokine levels due to the drugs' antiinflammatory effect. This causes decreased ACTH stimulation, resulting in a reduced adrenocortical steroid secretion. Accumulation of the drug in the adrenal cortex may also affect adrenal steroidogenesis. The elevated SHBG levels may be caused by a weak estrogenic activity of the drug.

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