ABSTRACT
Ten female and 2 male patients with chronic hepatitis C infection had fibromyalgia as a prominent musculoskeletal problem. In 9 patients, the fibromyalgia developed a mean of 13.4 years after the hepatitis C infection. In 2 patients, the 2 diseases occurred within weeks to a few months of each other, and in 1 patient, preexisting fibromyalgia was apparently aggravated by the hepatitis C infection. All patients had a possible blood or body fluid exposure event or high risk activity: intravenous blood products in 3, occupational needle stick in 1, tattoos in 3, intravenous drug use in 3 and promiscuous sexual practices in 2. Transaminases were moderately elevated in 10 patients, and chronic active hepatitis was found in 4 patients who were biopsied. All patients had prominent fatigue. Additional features not commonly seen in fibromyalgia patients included fluctuating synovitis in 5 patients, biopsy-proven leukocytoclastic vasculitis in 5, sicca symptoms in 3, Raynaud's phenomenon in 3, and cryoglobulinemia in 2. One patient died in multi-organ failure after treatment for systemic vasculitis. Rheumatologists and internists should be aware that patients with hepatitis C infection can have fibromyalgia that occurs concomitantly with other extrahepatic manifestations of hepatitis C.
ABSTRACT
Sodium L-ascorbate (ascorbate) and sodium D-ascorbate produced a dose-related rise of guanosine 3':5'-cyclic monophosphate (cGMP) in platelets with a maximum increment averaging 25-fold at 5 mM ascorbate. The ascorbate-induced increment in cGMP reached a peak after 1 min and was maintained for 1 h in the presence of ascorbate. 5-hydroxytryptamine (5-HT) also produced a dose-related rise of cGMP in platelets with a peak effect of approximately 25-fold at 16 micrometer 5-HT. The elevation of cGMP in platelets by both ascorbate and 5-HT did not require extracellular calcium and was blocked by inhibitors of cyclo-oxygenase such as aspirin or indomethacin. A maximum ascorbate-induced rise in platelet cGMP at the time of addition of epinephrine, collage or thrombin did not augment the release of [14C]5-hydroxytryptamine ([14C]5-HT) measured over 30 min. Although ascorbate appeared to increase platelet cGMP by modulation of endoperoxide formation, its failure to aggregate platelets or to influence the release reaction indicates that the ascorbate-stimulated rise in cGMP does not have a simple relationship to thromboxane formation.
