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Lead Article: Inflammatory Fibromyalgia

Metyas S* and Arkfeld DG

Department of Rheumatology, University of Southern California-Keck School of Medicine, California, USA

*Corresponding Author:
Samy Metyas
Department of Rheumatology, University of Southern California-Keck School of Medicine
500 W San Bernardino Rd , STE A, Covina, Ca 91722, USA
Tel: 626-966-1909
Fax: 626-966-2629
E-mail: [email protected]

Received date: May 08, 2017; Accepted date: June 19, 2017; Published date: June 26, 2017

Citation: Metyas S, Arkfeld DG (2017) Lead Article: Inflammatory Fibromyalgia. Fibrom Open Access 2:123.

Copyright: © 2017 Metyas S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Opinion Article

Attempts to understand fibromyalgia pathogenesis have eluded rheumatologists for decades. Treatment of Fibromyalgia (FM) has been lackluster in part due to this lack of understanding of mechanism. Updating the criteria in 2010 has taken into account other symptoms besides pain that was the focus of the original American College of Rheumatology (ACR) consensus which required only pain in 11 out of 18 tender points in all 4 quadrants. Recent studies of FM pain have led to new treatments with 3 FDA approved medications including duloxetine, pregabalin, and milnacaprin.

Current focus on FM research has additionally focused on fatigue, psychological state and quality of life as well as future treatment modalities. In this article we summarized a number of studies that explored inflammation and autoimmunity in FM [1].

In clinical practice, fibromyalgia patients can be divided into four subcategories: primary fibromyalgia, Secondary fibromyalgia to underlying autoimmune or other diseases, Inflammatory fibromyalgia, in which patients has fibromyalgia with high inflammatory markers without synovitis or joint swelling, neurologic fibromyalgia with small fiber neuropathy and Neuro-endocrine fibromyalgia Postural Orthostatic tachycardia syndrome (POTS).

In our article, we try to explain inflammatory fibromyalgia by reviewing English clinical literatures. We found that inflammatory fibromyalgia divided into three areas: inflammatory markers, cytokines and neuro-humoral transmitters and how they impact the old and new ACR criteria. It is hoped that through this review new treatments that target these 3 categories can be developed to help patients suffering with FM.

The first area explored in the literature looked at Sedimentation rate (ESR) and C - reactive protein (CRP) as inflammatory markers and Antinuclear Antibodies (ANA) and Rheumatoid Factor (RF) as autoimmune markers. Dr. Metyas et al. reported in 2015 on a 21 to 37% positivity of these 4 markers [2].

In addition, another study showed that through exercise and weight loss CRP could be reduced [3]. Other activities such as balneotherapy had no benefit. Thus exercise and dietary modification can be helpful in FM patients especially if inflammation was present.

The second category examined cytokines as messengers in signaling inflammatory FM. IL-6 and IL-8 were considered to be important in FM. One study concluded that chronic FM patients had an increase in soluble factors that stimulate substance P that has been shown to be elevated in FM [4].

Dysregulated cytokines also were assessed looking at pro and anti-inflammatory cytokines that have shown preliminary results [5]. A trend towards TH2 cytokines in the pain of FM was observed and they are looking into T helper TH1-TH2 imbalances in FM [6]. High levels of IL-10 with burst amplitude may reflect an anti-inflammatory predominance that could explain some of the insomnia and morning stiffness report in FM [7]. Interleukin IL-17 has been shown to be elevated which correlates with levels of IL-2, IL-4 and IL-10 reflecting an anti-inflammatory mechanism [8]. Dermal inflammation was seen in 30% of FM patients on skin biopsy with at a PGP 9.5 marker [9]. IL-10 and MCP-1 have been proposed as markers for monitoring a treatment response [10]. The above may relate to the potential improvement of some patients with nonsteroidal anti-inflammatory agents and steroids.

The third and final article looked at the dysfunction of neurohormonal transmitters including substance P, 5- Hydroxyindoleacetic acid (5-HIAA), and Leptin levels. Leptin levels were elevated in a subset of FM patients with inflammation [11]. 5- HIAA which reflects serotonin activity and substance P elevation where felt to be due to sleep quality and pain in FM [12] an immunomodulatory function was speculated due to these factors.

We concluded that these 3 categories of FM need further study to look at their role in an inflammatory etiology of a subset of FM patients. This may lead to new biomarker as well as leading to further treatments by understanding the pathogenesis of FM. Double blind and more evidence based review is necessary to develop future more effective therapies. To date, treatment has been very challenging for the provider as well as the patient. The exploration of new areas such as the immune system may recognize new autoimmune and autoinflammatory treatment options potentially helping even the most difficult to treat FM individual. Creating subsets to the FM criteria may lead to better care in FM by recognizing different pathways that need to be targeted in a more specific fashion.


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