Helicobacter pylori seropositivity in fibromyalgia syndrome.

Although there are some studies suggesting relation between different types of infection and fibromyalgia syndrome (FM), there is presently no proof that FM is caused by an infection. Helicobacter pylori (HP) infection may cause extragastric manifestations. Inflammation is an important mediator of increased sympathetic nervous system activity and may lead to pain in fibromyalgia patients. In this study, we aimed to investigate the HP seropositivity in fibromyalgia patients compared with controls for possible role of HP infection in FM. Sixty-seven patients with fibromyalgia were evaluated. Two of them were excluded from the study because of high level of acute phase reactants. Sixty-five female patients with fibromyalgia and 41 randomly selected age-matched female healthy controls were enrolled to study. Serum HP IgA and IgG antibodies were measured by enzyme-linked immunosorbent assay technique. Fibromyalgia Impact Questionnaire was assessed in patients and controls. Seropositivity of HP IgG antibody in the fibromyalgia patients was significantly higher than in the control group. No statistically significant differences were found regarding the clinical features between fibromyalgia patients with HP IgG antibody and patients without IgG antibody. Our study suggests that former HP infection may have a role in the etiopathogenesis of fibromyalgia syndrome or may act as a triggering factor. However, high seroprevalence of HP in general population and prevalent asymptomatic infection make it difficult to interpret these results for the definite role of HP in FM. Highlighting the pathophysiologic mechanisms of FM will result in more effective treatment regimens.

Manometric assessment of esophageal motility in patients with primary Sjögren's syndrome.

OBJECTIVE: The aim of this study was to assess the esophageal motility by manometry in patients with primary Sjögren's syndrome. METHODS: Esophageal manometry was carried out in 40 patients with primary Sjögren's syndrome (SS), 15 with rheumatoid arthritis (RA), 15 with RA and secondary SS, and 21 healthy volunteers. RESULTS: We found that the mean lower esophageal sphincter (LES) pressures measured by station pull-through and rapid pull-through techniques were significantly higher in primary SS patients than with healthy controls and RA patients with or without SS (P<0.05). Our study did not show any major differences when comparing the three patient groups (P>0.05). However, peristaltic contraction velocity was lower and peristaltic contraction duration significantly higher at the middle and lower thirds of the esophagus in primary SS patients than in healthy controls (P<0.05). CONCLUSION: The results of our study support the view that various esophageal motility disorders can be found in patients with primary SS which could be related to an increase in LES pressure. We also found no correlation of the esophageal abnormalities with other factors studied, suggesting that the cause of dysphagia is multifactorial in nature.

Platelet-activating factor and P-selectin activities in thrombotic and nonthrombotic Behçet's patients.

OBJECTIVE: The aim of this study was to compare plasma Platelet-activating factor (PAF) and P-selectin (CD62P) activities in Behçet's disease patients with and without thrombosis. METHODS: In this cross-sectional and descriptive study, 30 consecutive Behçet's patients were included, 15 of them with venous thrombosis. All patients were also divided into two subgroups according to the presence or absence of clinical activity. Plasma PAF levels, basal and Ca++ ionophore (A23187)-induced leukocyte (cellular) PAF activities, and platelet-rich plasma DeltaCD62P activity (the mean fluorescent density difference between CD62P phycoerythrin-positive and -negative stains) were evaluated. RESULTS: In the thrombotic group, plasma PAF (P=0.001), basal leukocyte PAF (P=0.017), induced leukocyte PAF (P=0.024), and DeltaCD62P (P=0.023) levels were significantly higher than in the nonthrombotic group. In the whole group of Behçet's patients, there was a positive correlation between plasma PAF and DeltaCD62P levels (r=0.533, P=0.002). When we compared clinically active and inactive patients with respect to the above parameters, there was no significant difference, irrespective of thrombosis. Plasma PAF (P=0.001), basal leukocyte PAF (P=0.004), and DeltaCD62P (P=0.038) levels were significantly higher in the presence of both clinical activity and thrombosis than of clinical activity alone. CONCLUSION: Platelet-activating factor and CD62P may contribute to endothelial injury and thrombosis development in Behçet's disease. These two parameters seem related to the presence of thrombosis rather than clinical activity.

Successful treatment of rheumatoid arthritis is associated with a reduction in serum sE-selectin and thrombomodulin level.

The aim of this study was to investigate the changes in serum levels of endothelial cell injury markers, soluble (s) E-selectin and thrombomodulin (TM), in patients with rheumatoid arthritis (RA) before and after antirheumatic drug treatment and to assess the relationship between these changes and clinical responses to the drug treatment. Eleven patients with RA having active arthritis and 12 healthy volunteers were enrolled in the study. They were monitored by clinical and laboratory parameters while receiving a combination of methotrexate, hydroxychloroquine and sulphasalazine. Pre- and post-treatment clinical and laboratory parameters, including sE-selectin and sTM levels, were measured. The ages of the patients were comparable with those of the control groups. Significant improvements were detected in erythrocyte sedimentation rate, C-reactive protein, hemoglobin, morning stiffness, patients' global assessment, physicians' global assessment, number of tender joints and number of swollen joints improved at the end of the therapy (for each parameter p < 0.05). Significant improvements were detected in clinical and laboratory parameters. In the patient group there were significant decreases in the levels of sTM and sE-selectin after treatment (p < 0.05). The patient group had significantly higher sTM and sE-selectin levels than the control group at the beginning of the study (p < 0.01), but the difference returned to normal after the treatment (p > 0.05). The sE-selectin and sTM levels significantly correlated with each other, and also with clinical and laboratory findings. Combination treatment successfully treated RA patients. sE-selectin and sTM levels probably reflect disease activity and can be helpful in monitoring disease status and response to therapy.