a short list of recent research

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a short list of recent research

Postby Min » Sun Apr 13, 2008 9:36 pm

Research findings in FM include the following:

In 1997 it was shown that levels of somatomedin C are lower in FM patients (AL Bennett et al. J Psychiat Res 1997:31:1:91-96).

In 1998 researchers showed that levels of Substance P are elevated in FM patients (Evengaard B et al. Pain 1998:78:2:153-155).

In 2003 it was shown that endothelin-1 is raised in FM patients (Pache M et al. Rheumatology 2003:42:493-494).

Research in 2005 indicated that FM is the result of internal biochemical imbalances that cause the physical symptoms (Co-Cure MED: 2nd January 2005: Fibromyalgia: new insights into a Misunderstood Ailment).

Different research in 2005 found elevated N(epsilon)-carboxymethyllysine levels in muscular tissue and in serum of patients with FM, with more intensive staining in the interstitial connective tissue of fibromyalgic muscles (Ruster M et al. Scand J Rheumatol 2005:34(6):460-463).

Again in 2005, more serious abnormalities were demonstrated by histologic studies particularly on electron microscopy, revealing disorganisation of Z bands and abnormalities in the number and shape of mitochondria: biochemical studies and P31 magnetic resonance spectroscopy showed inconstant abnormalities of ATP and phosphocreatine levels. The authors noted that “Mitochondrial abnormalities, reduced capillary circulation and thickened capillary endothelium may result in decreased availability of oxygen and impaired oxidative phosphorylation as well as ATP synthesis” and commented that these abnormalities do not seem to be the consequences of de-conditioning (Le Goff P. Joint Bone Spine 2005, November 9th).

In 2006, an important review in the Annals of the New York Academy of Sciences (Sarzi-Puttini P et al, Ann N Y Accad Sci 2006:1069:109-117) demonstrated orthostatic intolerance in FM, suggesting underlying abnormalities in cardiovascular neural regulation: “Research suggests that various components of the central nervous system are involved, including the HPA axis, pain-processing pathways, and the autonomic nervous system”

Again in 2006, research showed a greater prevalence of FM in HTLV-1 (human T cell lymphotrophic virus) infected individuals, suggesting that FM may be associated with this viral infection (Cruz BA et al: J Rheumatol: 2006:33(11):2300-2303).

In 2007, researchers at Yale University School of Medicine showed muscle hypoperfusion induced by regional vasomotor dysregulation in FM, noting that this vasoconstriction in muscle would lead to low-level ischaemia and its metabolic sequelae (Katz DL et al. Med Hypotheses 2007: March 19th).

More research into FM in 2007 demonstrated bladder symptomatology (Brand K et al. Clin Rheumatol 2007: May 3rd).

Further research in 2007 showed that autoimmune thyroiditis is present in an elevated percentage of FM patients and that patients with thyroid autoimmunity showed a higher percentage of dry eyes, burning or pain with urination, allodynia, blurred vision and sore throat (Bazzichi L et al. Clin Rheumatol 2007: May 9th).

In 2007, Bazzichi et al also showed evidence of abnormal levels of cytokines in FM: “The higher levels of cytokines found in FM patients suggest the presence of an inflammatory response system (IRS) and highlight a parallel between the clinical symptoms and biochemical data” (Clin Exp Rheumatol 2007:25(2):225-230).

Another paper in 2007 revealed a conspicuous pattern of altered brain morphology, suggesting that FM is associated with structural changes in the central nervous system of patients (Schmidt-Wilcke T et al. Pain: 2007: June 21st).

In January 2008 researchers provided compelling evidence of a demyelinating polyneuropathy in FM, with electrodiagnostic (EDX) evidence of both polyneuropathy and demyelination. The authors concluded that 33% of FM patients have clinical and EDX findings of chronic inflammatory demyelinating polyneuropathy / CIDP. (Caro XJ et al. Rheumatology (Oxford) 2008:47(2):208-211).

In February 2008 researchers from McGill University, Montreal, Canada, presented evidence that “neurotransmitter studies show that FM patients have abnormalities in dopaminergic, opioidergic, and serotonergic systems” and that “studies of brain anatomy show structural differences between the brains of FM patients and healthy individuals” (Schweinhardt P et al. Neuroscientist 2008: February 12th).

Also in 2008, in a blinded study, skin biopsy samples showed electron microscopic evidence of unusual patterns of unmyelinated nerve fibres as well as associated Schwann cells, which the researchers considered may contribute to the lower pain threshold seen in FM patients (Kim SH et al. Clin Rheumatol 2008:27(3):407-411).

In a study published in March 2008, US researchers noted that previously, functional magnetic resonance imaging (fMRI) had shown that the insula displays augmented activity in FM, which means that neurons in FM patients are more active in this part of the brain. This linked to their own findings that pain decreased when levels of the brain molecule glutamate went down, glutamate being a neurotransmitter that conveys information between neurons in the nervous system (Clauw D et al. Arthritis and Rheumatism 2008:58:3).



from:
http://www.investinme.org/Article-130%2 ... 20Ways.htm

yet it's still a dustbin diagnosis!
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Min
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