In 30 patients with diagnosed fibromyalgia, the CSF level of immunoreactive substance P (SP) was investigated. Compared to normal values (9.6 +/- 3.2 fmol/ml), all the patients had elevated CSF levels of SP (36.1 +/- 2.7 fmol/ml, range 16.5-79.1 fmol/ml). Anamnestic information from the patients revealed that 53.3% had Raynaud/Raynaud-like phenomenon localized in the fingers, the toes or both. Although SP levels did not differ significantly in patients with or without the Raynaud phenomenon, elevated activity may be present in the peripheral branches of SP neurons which could be responsible for the last (rubor) phase of the triphasic Raynaud's phenomenon. SP levels were significantly higher in patients who were smokers (40.1 +/- 2.7 fmol/ml, range 25.3-64.1 fmol/ml), compared to patients who were non-smokers (29.2 +/- 5.0 fmol/ml, range 16.5-79.1 fmol/ml). We propose elevated CSF levels of SP and the Raynaud phenomenon as characteristic features for fibromyalgia with potential as diagnostic markers of the disease and further that smoking might be an aggravating factor for its pathogenesis or development.

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Cyclosporine (10 mglkglday) and azathioprine (2.5-3 mg/kg/day) were compared for 26 weeks in an open, controlled, randomized study of 24 patients with rheumatoid arthritis. Each treatment group consisted of 12 patients. Those patients who took cyclosporine improved significantly in the SO-foot walk time, circumferences of proximal interphalangeal joints, Ritchie articular index, global assessment by investigator, and grip strength, when compared with baseline findings. In the azathioprine group, there was improvement only in grip strength.Immune reactions are involved in the pathogenesis of rheumatQid arthritis (RA) (1). Synovial T cells produce interleukin-2, which is essential for the proinflammatory immune reactions in rheumatoid tissues (2,3). Cyclosporine (CS) suppresses immune responses by inhibition of the production of interleukin-2 by T lymphocytes (4). CS can also prevent the devel-

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Forty-three of fifty-eight (74.1%) female patients with fibromyalgia completed an eight-week treatment period testing the combination of carisoprodol, paracetamol (acetaminophen) and caffeine versus placebo. Twenty-three patients received placebo and twenty active medication. In the placebo group 56.5% of the patients used additional analgesics or nonsteroidal anti-inflammatory drugs compared to only 20% in the active treatment group (p = 0.015). Forty-three percent of the patients in the placebo group and none of the patients in the active treatment group used tricyclic antidepressants, anxiolytics or sedatives (p = 0.0008). Active treatment gave statistically significant improvement after treatment for pain (p less than 0.01), for sleep quality (p less than 0.01) and for the general feeling of sickness (p less than 0.05). In the active treatment group increased pressure pain threshold after eight weeks was found at 70% of the sites measured, while the pressure pain threshold was increased at only 30% of the sites in the placebo group. In the placebo group improvement was found for the pain and sleep quality (p less than 0.05). This improvement may in part be due to the large amounts of extra medication in this group. Thus, the combination of carisoprodol and paracetamol (acetaminophen) and caffeine are effective in the treatment of fibromyalgia.