Background Fibromyalgia syndrome (FS) is characterised by chronic “widespread” musculoskeletal pain, presence of multiple tender points, fatigue, depression/anxiety, and sleep disturbance. Recently, evidence has accumulated to link the FS pathogenesis to serotonin (5-hydroxytryptamine, 5-HT) deficiency. Since melatonin, a pineal hormone responsible for the regulation of sleep and circadian rhythms, is closely related to 5-HT, it seems interesting to study the role of melatonin in FS.
Objectives The aim of the study was to examine the total 24-hr 5-HT and melatonin secretion in patients with FS and chronic low back pain (LBP) in relation to pain intensity, symptoms of anxiety/depression, and the severity of sleep disturbance.
Methods The 24-hr urinary excretion of the 6-sulphatoxymelatonin (aMT6s, main catabolite of melatonin) and the 5-hydroxyindoleacetic acid (5-HIAA, main catabolite of 5-HT) were measured using ELISA in women with FS (n = 18) and women with LBP (n = 15). The groups were matched with regard to age, diet, and the intensity of pain. Clinical measures of pain intensity, no of tender points, pain threshold (dolorimetry), psychological profile (SCL-90-R), and the severity of sleep disturbance (Schlaffragebogen-A and -B, SF-A and SF-B) were evaluated.
Results The excretion of aMT6s and 5-HIAA was lower in FS when compared to LBP (8.79 ± 1.90 micrograms/24 hrs vs 12.53 ± 3.01 micrograms/24 hrs and 4.72 ± 0.36 mg/24 hrs vs 8.79 ± 1.47 mg/24 hrs, respectively), but the difference was significant with regard to 5-HIAA only (p < 0.03). No correlation was found between the aMT6s and 5-HIAA within the study grups. In both groups, there was no relationship between the clinical measures of pain and tenderness and the excretion of the two catabolites. In FS, aMT6s excretion correlated weakly with the sleep quality (SQ, SF-B) (r = 0.4966, p < 0.05) and the symptom duration (r = -0.5101, p < 0.05). When compared with the LBP group, the FS patients scored significantly higher on the G1 and G4 (somatization and depressivity) scales of SCL-90-R, (p < 0.05 for both comparisons) and the FRS subscale (feeling of recovery after sleep) of SF-A and SF-B (p < 0.05 and p < 0.001, respectively).
Conclusion Since the 24-hr urinary excretion of aMT6s closely follows the total 24-hr melatonin secretion, our results do not support the hypothesis of the disturbed metabolism of melatonin in FS. The small differences seen may result from the differences in the severity of mood and sleep disturbance. Further research is necessary to look at possible abnormalities in the circadian rhythm of melatonin secretion in FS.
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