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Helicobacter pylori seropositivity in fibromyalgia syndrome
Authors:Nuray Akkaya  Semih Akkaya  Yusuf Polat  Meral Turk  Tufan Turk  Elif Turhal  Fusun Sahin
Affiliation:(1) Department of Physical Medicine and Rehabilitation, Pamukkale University Medical School, 20210 Kinikli, Denizli, Turkey;(2) Department of Orthopedics and Traumatology, Pamukkale University Medical School, 20210 Kinikli, Denizli, Turkey;(3) Clinical Microbiology, Denizli Government Hospital, Bayramyeri, Denizli, Turkey;(4) Clinical Parasitology, Denizli Government Hospital, Bayramyeri, Denizli, Turkey;(5) Clinic of Rheumatology, Denizli Government Hospital, Bayramyeri, Denizli, Turkey;(6) Department of Public Health, Pamukkale University Medical School, Kinikli, Denizli, Turkey
Abstract:
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.
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