Abstract: Investigation of cutaneous microvascular activity and flare response in patients with fibromyalgia syndrome
February 20, 2002
Rheumatology 2001; 40: 1097-1101
A. W. Al-Allaf, F. Khan1, J. Moreland, J. J. F. Belch1 and T. Pullar
Rheumatic Disease Unit and (1) Section of Vascular Medicine, University Department of Medicine, Ninewells Hospital & Medical School, Dundee DD1 9SY, UK
Objectives. To assess microvascular activity in the skin of patients with fibromyalgia syndrome (FMS) as compared with normal controls.
Methods. Fifteen patients, who fulfilled the American College of Rheumatology criteria for FMS, and 15 age- and sex-matched healthy controls, were studied.
The microvascular activity of the skin overlying the trapezius muscle was quantified using iontophoresis of acetylcholine as an endothelial-dependent vasodilator and sodium nitroprusside as an endothelial-independent vasodilator. We also studied the flare response by iontophoresing acetylcholine continuously for 10 min to stimulate a ring of nociceptor c-fibre endings in the skin.
Results. There was no significant difference in cutaneous vascular responses to short-duration iontophoresis of acetylcholine and sodium nitroprusside at the three different doses used. The area under the curve (AUC) (mean±s.e.m.) for acetylcholine baseline, 20, 40, and 80 s were 6±0.7, 23±6, 45±7 and 66±10 AU for patients and 11±4, 24±3, 49±7 and 62±12 AU for controls, respectively (P=0.2, 0.9, 0.7, 0.8, respectively). The corresponding figures for sodium nitroprusside were 5±1, 18±7, 51±14 and 68±14 AU for patients and 8±3, 13±2, 39±5 and 61±9 AU for controls, respectively (P=0.2, 0.5, 0.4, 0.7, respectively). There was also no significant difference in the flare response in patients with FMS as compared with control subjects (119±15 and 131±13 AU, respectively; P=0.57).
Conclusion. There are no significant differences in cutaneous microvascular reactivity between patients with FMS and control subjects.
KEY WORDS: Flare response, Microvascular function, Fibromyalgia syndrome.
Correspondence to: A. W. Al-Allaf.
© 2001 British Society for Rheumatology