The aim of our study was to analyse the serum interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) levels in patients with AS and their relationship with disease activity. An ELISA test was used to analyse serum cytokine (IL-6, TNF-alpha, IL-1 beta and IFN-gamma) levels in 69 patients with AS. Results were compared with those from 43 patients with RA and 36 patients with non-inflammatory back pain. The relationship between serum concentrations of the different cytokines and parameters of disease activity and severity in AS patients was also evaluated. IL-6 and TNF-alpha serum levels, but not IL-1 beta and IFN-gamma, were significantly higher in AS than in NIBP. However, patients with RA showed higher serum levels of IL-6, TNF-alpha and IFN-gamma than both AS and NIBP patients. In AS, IL-6 correlated with clinical parameters of disease activity with significant correlation being observed with laboratory parameters of inflammation such as ESR, CRP, platelet count and clinical parameters of severity such as vertebral mobility. TNF-alpha did not correlate with laboratory or clinical parameters of activity. Macrophagic cytokines (TNF-alpha and IL-6), are increased in AS patients and IL-6 closely correlated with the activity of the disease.

We show for the first time that the majority of fibromyalgia patients have abnormal C nociceptors. Many silent nociceptors exhibit hyperexcitability resembling that in small-fiber neuropathy, but high activity-dependent slowing of conduction velocity is more common in fibromyalgia patients, and may constitute a distinguishing feature. We infer that abnormal peripheral C nociceptor ongoing activity and increased mechanical sensitivity could contribute to the pain and tenderness suffered by patients with fibromyalgia.

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Objective. Fibromyalgia (FM) has been defined as a systemic disorder that is clinically characterized by pain, cognitive deficit, and the presence of associated psychopathology, all of which are suggestive of a primary brain dysfunction. This study was undertaken to identify the nature of this cerebral dysfunction by assessing the brain metabolite patterns in patients with FM through magnetic resonance spectroscopy (MRS) techniques.Methods. A cohort of 28 female patients with FM and a control group of 24 healthy women of the same age were studied. MRS techniques were used to study brain metabolites in the amygdala, thalami, and prefrontal cortex of these women.Results. In comparison with healthy controls, patients with FM showed higher levels of glutamate/ glutamine (Glx) compounds (mean ؎ SD 11.9 ؎ 1.6 arbitrary units [AU] versus 13.4 ؎ 1.7 AU in controls and patients, respectively; t ‫؍‬ 2.517, 35 df, corrected P ‫؍‬ 0.03) and a higher Glx:creatine ratio (mean ؎ SD 2.1 ؎ 0.4 versus 2.4 ؎ 1.4, respectively; t ‫؍‬ 2.373, 35 df, corrected P ‫؍‬ 0.04) in the right amygdala. In FM patients with increased levels of pain intensity, greater fatigue, and more symptoms of depression, inositol levels in the right amygdala and right thalamus were significantly higher.Conclusion. The distinctive metabolic features found in the right amygdala of patients with FM suggest the possible existence of a neural dysfunction in emotional processing. The results appear to extend previous findings regarding the dysfunction in pain processing observed in patients with FM. Fibromyalgia (FM) is a clinical syndrome definedby the presence of chronic widespread musculoskeletal pain and the presence of at least 11 of 18 body tender points that are representative of a possible enhanced sensitivity to painful stimulation (1), and these features are often accompanied by other symptoms such as fatigue, poor sleep quality, loss of memory, and mood disturbances. The lack of clear evidence of peripheral tissue damage to which such symptoms could be attributed (2) and the findings of peculiar abnormalities in both the neural pain modulation pattern (3,4) and the hypothalamic-pituitary-adrenal axis (5) in these patients have contributed to the current understanding of FM as a central sensitization syndrome of unknown origin. In our conceptual framework, FM symptoms are related to neural and psychological abnormalities in sensory and emotional processing that result from biologic (genetic) predispositions, early adverse experiences (emotional neglect, physical or sexual abuse, family dysfunction), psychological vulnerabilities (neuroticism, negative affect, social learning), and biographically related precipitating factors (physical or psychosocial stress) (6,7).In the last decade, the important progress made in neuroimaging techniques has enabled the study of several aspects of cerebral pain processing. Research on Supported by the Ministerio de Sanidad y Consumo, Spain (grant FIS PI 04/1077).

Objective. To analyze whether inflammatory disease activity plays a substantial role in the loss of bone mass observed in ankylosing spondylitis (AS) patients who have not yet developed ankylosis.Methods. A longitudinal cohort study of 34 patients with early AS (duration <10 years) without ankylosis was conducted. The mean followup was 19 months. Loss of bone mass in defined regions of the lumbar spine and femoral neck was analyzed by dual x-ray absorptiometry. Patients were grouped according to biologic parameters of disease activity (erythrocyte sedimentation rate or C-reactive protein level). Group 1 consisted of 14 patients with active disease; group 2 comprised 20 patients with inactive disease. Serum levels of interleukin-6 (IL-6) and of hormones (sex, thyroid, and calciotropic), vertebral mobility (Schober test), daily physical activity, and treatment administered were recorded every 6 months for all patients.Results. At the end of the followup period, patients with active AS showed a significant reduction in bone mass in the lumbar spine (mean 1.01 gm/cm 2 at study entry versus 0.961 gm/cm 2 at followup [P ‫؍‬ 0.005]) and femoral neck (0.849 gm/cm 2 versus 0.821 gm/cm 2 [P ‫؍‬ 0.015]), which represented losses of 5% and 3%, respectively. In contrast, no significant reduction in bone mass was observed in patients with inactive AS. As expected, serum IL-6 levels were significantly higher in patients with active AS than in those with inactive disease (mean ؎ SD 8.3 ؎ 9 pg/ml versus 2.8 ؎ 5 pg/ml [P ‫؍‬ 0.008]). No significant differences were observed between the 2 groups in any of the other variables analyzed.Conclusion. The observation that loss of bone mass in AS occurred only in patients with persistent active disease strongly suggests that inflammatory activity of the disease itself plays a major role in the pathophysiology of the early bone mineral disorders observed in these patients.