Fibromyalgia - New Concepts of Pathogenesis and Treatment

H, Lucas; Brauch, C.M.; Settas, L.; Theoharides, Theoharis C.

doi:10.1177/205873920601900102

Cited by 86 publications

(48 citation statements)

References 35 publications

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“…Evidence has been presented that MCAS may be an underlying cause of various frequent clinical presentations; for example, in subsets of patients with fibromyalgia [18], [19] and irritable bowel syndrome [20]. Accordingly, the prevalence of MCAS, and therewith that of MCAD, was expected to be at least within the single-figure percentage range [3].…”

Section: Discussionmentioning

confidence: 99%

Familial Occurrence of Systemic Mast Cell Activation Disease

et al. 2013

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Systemic mast cell activation disease (MCAD) comprises disorders characterized by an enhanced release of mast cell mediators accompanied by accumulation of dysfunctional mast cells. Demonstration of familial clustering would be an important step towards defining the genetic contribution to the risk of systemic MCAD. The present study aimed to quantify familial aggregation for MCAD and to investigate the variability of clinical and molecular findings (e.g. somatic mutations in KIT) among affected family members in three selected pedigrees. Our data suggest that systemic MCAD pedigrees include more systemic MCAD cases than would be expected by chance, i.e., compared with the prevalence of MCAD in the general population. The prevalence of MCAD suspected by symptom self-report in first-degree relatives of patients with MCAD amounted to approximately 46%, compared to prevalence in the general German population of about 17% (p<0.0001). In three families with a high familial loading of MCAD, the subtype of MCAD and the severity of mediator-related symptoms varied between family members. In addition, genetic alterations detected in KIT were variable, and included mutations at position 816 of the amino acid sequence. In conclusion, our data provide evidence for common familial occurrence of MCAD. Our findings observed in the three pedigrees together with recent reports in the literature suggest that, in familial cases (i.e., in the majority of MCAD), mutated disease-related operator and/or regulator genes could be responsible for the development of somatic mutations in KIT and other proteins important for the regulation of mast cell activity. Accordingly, the immunohistochemically different subtypes of MCAD (i.e. mast cell activation syndrome and systemic mastocytosis) should be more accurately regarded as varying presentations of a common generic root process of mast cell dysfunction, than as distinct diseases.

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Section: Discussionmentioning

confidence: 99%

Familial Occurrence of Systemic Mast Cell Activation Disease

et al. 2013

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“…Recently, some reports have noted alterations in proinflammatory cytokine levels in the serum and biopsies of FM patients [3,4], which might be associated with disease symptoms [5-7]. …”

Section: Introductionmentioning

confidence: 99%

Proinflammatory cytokine levels in fibromyalgia patients are independent of body mass index

Hernández

Becerril

Pérez³

et al. 2010

BMC Res Notes

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BackgroundFibromyalgia (FM) is characterized by chronic, widespread muscular pain and tenderness and is generally associated with other somatic and psychological symptoms. Further, circulatory levels of proinflammatory cytokines (IL-1β, TNF-α, and IL-6) may be altered in FM patients, possibly in association with their symptoms. Recently, rises in BMI have been suggested to contribute to increased circulating levels of proinflammatory cytokines in FM patients. Our aim was to measure the circulatory levels of proinflammatory cytokines to determine the influence of BMI on these levels in FM patients and healthy volunteers (HVs). In Spanish FM patients (n = 64) and HVs (n = 25), we measured BMI and serum concentrations of proinflammatory cytokines by capture ELISA.FindingsThere were significant differences in BMI levels between FM patients (26.40 ± 4.46) and HVs (23.64 ± 3.45) and significant increase in IL-6 in FM patients (16.28 ± 8.13 vs 0.92 ± 0.32 pg/ml) (P < 0.001). IL-1β and TNF-α decreased in FM patients compared with HVs. By ANCOVA, there was no significant association between BMI and TNF-α (F = 0.098, p = 0.75) or IL-6 (F = 0.221, p = 0.63) levels in FM patients.ConclusionsOur analysis in FM patients of BMI as a covariate of proinflammatory cytokines levels showed that serum TNF-α and IL-6 levels are independent of BMI. Further studies are necessary to dissect these findings and their implication in future therapeutic approaches for FM patients.

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“…In a similar vane fibromyalgia, with its symmetrical distribution of tender points and abnormal substance P concentrations, possibly suggests a muscular form of the above joint patterns and aetiology (Lucas et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Inflammopharamacology

2008

Inflammopharmacol

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Fibromyalgia - New Concepts of Pathogenesis and Treatment

Cited by 86 publications

References 35 publications

Familial Occurrence of Systemic Mast Cell Activation Disease

Familial Occurrence of Systemic Mast Cell Activation Disease

Proinflammatory cytokine levels in fibromyalgia patients are independent of body mass index

Inflammopharamacology

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