Detection of elevated <i>N</i><sup>ε</sup>‐carboxymethyllysine levels in muscular tissue and in serum of patients with fibromyalgia

Rüster, Michael; Franke, Sybille; Späth, M.; Pongratz, D.; Stein, G; Hein, Gert

doi:10.1080/03009740510026715

Cited by 24 publications

(25 citation statements)

References 15 publications

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“…In addition, no inflammatory changes have been described in muscle biopsy samples from FMS patients. However, it has been reported that immunoreactivity for the advanced glycation end product (AGE), N ε -carboxymethyllysine (CML), is elevated in biopsy samples from the biceps brachii muscle of FMS patients compared to controls [500]. The CML receptor RAGE and its downstream effector, activated NF-kB, along with CD68+ cells (monocytes/macrophages) were detectable in FMS samples, but only rarely could be observed in control samples.…”

Section: Muscle Abnormalitiesmentioning

confidence: 98%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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Fibromyalgia is a disorder that is part of a spectrum of syndromes that lack precise classification. It is often considered as part of the global overview of functional somatic syndromes that are otherwise medically unexplained or part of a somatization disorder. Patients with fibromyalgia share symptoms with other functional somatic problems, including issues of myalgias, arthralgias, fatigue and sleep disturbances. Indeed, there is often diagnostic and classification overlap for the case definitions of a variety of somatization disorders. Fibromyalgia, however, is a critically important syndrome for physicians and scientists to be aware of. Patients should be taken very seriously and provided optimal care. Although inflammatory, infectious, and autoimmune disorders have all been ascribed to be etiological events in the development of fibromyalgia, there is very little data to support such a thesis. Many of these disorders are associated with depression and anxiety and may even be part of what has been sometimes called affected spectrum disorders. There is no evidence that physical trauma, i.e., automobile accidents, is associated with the development or exacerbation of fibromyalgia. Treatment should be placed on education, patient support, physical therapy, nutrition, and exercise, including the use of drugs that are approved for the treatment of fibromyalgia. Treatment should not include opiates and patients should not become poly pharmacies in which the treatment itself can lead to significant morbidities. Patients with fibromyalgia are living and not dying of this disorder and positive outlooks and family support are key elements in the management of patients.

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Section: Muscle Abnormalitiesmentioning

confidence: 98%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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“…They include appearance of ragged red fibers and moth-eaten fibers, inflammatory infiltrates, DNA fragmentation in muscle fibers, muscle perfusion deficits (confirmed by the reduction in pH related to ischemia), reduction in phosphorylation potential and total oxidative capacity, and increase in inflammatory mediators and cytokines as well as advanced glycation end products [17].…”

Section: Peripheral and Central Sensitization In Fm And Migrainementioning

confidence: 99%

Sensitization, glutamate, and the link between migraine and fibromyalgia

Sarchielli

Filippo²,

Nardi³

et al. 2007

Current Science Inc

100

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Recent advances have shed insight on the pathophysiologic mechanisms of fibromyalgia and migraine, especially in the chronic form. A growing body of evidence supports the involvement of peripheral and central sensitization disturbances of pain-related processes underlying both disorders. They involve increased glutamate transmission through interaction with its ionotropic and metabotropic receptors. Few studies supporting the implication of this excitatory amino acid in chronic migraine and primary fibromyalgia demonstrated increased levels of glutamate in the cerebrospinal fluid of affected patients. These findings have implications for future therapies directed against glutamate receptors (in particular, N-methyl-D-aspartate receptors). Limited clinical experience in this regard, although promising, does not exclude additional mechanisms contributing to the maintenance of pain, which can be the target of therapeutic approaches in both disorders.

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“…The presence of local alterations of muscular collagen in FM, with an increased content of advanced glycation end products causing a higher resistance to proteolysis, has been demonstrated and discussed (31).…”

Section: Discussionmentioning

confidence: 97%