Biomarkers in fibromyalgia

Ablin, Jacob N.; Buskila, Dan; Clauw, Daniel J.

doi:10.1007/s11916-009-0056-3

Cited by 24 publications

(20 citation statements)

References 41 publications

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“…Again, further studies would need to be conducted to evaluate the benefits of combining these treatments in the general fibromyalgia population. Individual patient responses to monotherapies, as well as to combination therapies of medications with different mechanisms of action, highlight the ongoing need to study potential biomarkers of fibromyalgia to improve diagnosis and develop more targeted treatment strategies [Dadabhoy et al 2008;Ablin et al 2009]. …”

Section: Discussionmentioning

confidence: 99%

Milnacipran combined with pregabalin in fibromyalgia: a randomized, open-label study evaluating the safety and efficacy of adding milnacipran in patients with incomplete response to pregabalin

Mease

Farmer

Palmer³

et al. 2013

Therapeutic Advances in Musculoskeletal

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Objective: To evaluate the safety, tolerability, and efficacy of adding milnacipran to pregabalin in patients with fibromyalgia who have experienced an incomplete response to pregabalin. Methods: In this randomized, multicenter, open-label study, patients received pregabalin 300 or 450 mg/day during a 4-to 12-week run-in period. Patients with weekly recall visual analog scale (VAS) pain score of at least 40 and up to 90, Patient Global Impression of Severity score of at least 4, and Patient Global Impression of Change (PGIC) score of at least 3 were classified as incomplete responders and randomized to continue pregabalin alone (n = 180) or receive milnacipran 100 mg/day added to pregabalin (n = 184). The primary efficacy parameter was responder status based on PGIC score of up to 2. The secondary efficacy parameter was change from randomization in weekly recall VAS pain score. Safety parameters included adverse events (AEs), vital signs, and clinical laboratory tests. Results: The percentage of PGIC responders was significantly higher with milnacipran added to pregabalin (46.4%) than with pregabalin alone (20.8%; p < 0.001). Mean improvement from randomization in weekly recall VAS pain scores was greater in patients receiving milnacipran added to pregabalin (−20.77) than in patients receiving pregabalin alone (−6.43; p < 0.001). During the run-in period, the most common treatment-emergent AEs with pregabalin were dizziness (22.8%), somnolence (17.3%), and fatigue (9.1%). During the randomized period, the most common treatment-emergent AEs with milnacipran added to pregabalin were nausea (12.5%), fatigue (10.3%), and constipation (9.8%). Conclusions: In this exploratory, open-label study, adding milnacipran to pregabalin improved global status, pain, and other symptoms in patients with fibromyalgia with an incomplete response to pregabalin treatment.

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Section: Discussionmentioning

confidence: 99%

Milnacipran combined with pregabalin in fibromyalgia: a randomized, open-label study evaluating the safety and efficacy of adding milnacipran in patients with incomplete response to pregabalin

Mease

Farmer

Palmer³

et al. 2013

Therapeutic Advances in Musculoskeletal

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“…51,114,150,176,192 Emerging evidence suggests that dysfunctional pain states, such as rheumatoid arthritis, osteoarthritis, visceral pain hypersensitivity syndromes, fibromyalgia, inflammatory bowel syndrome, neuropathic pain, and headaches, including migraine headache, may be caused in part by a deficient endogenous pain inhibitory system that allows the development of central sensitization. 1,33,96,108,169,192 …”

Section: Central Sensitization and The Role Of Calcitonin Gene–relmentioning

confidence: 99%

The role of calcitonin gene–related peptide in peripheral and central pain mechanisms including migraine

Iyengar

Ossipov²,

Johnson

2017

Pain

458

364

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Calcitonin gene–related peptide (CGRP) is a 37-amino acid peptide found primarily in the C and Aδ sensory fibers arising from the dorsal root and trigeminal ganglia, as well as the central nervous system. Calcitonin gene–related peptide was found to play important roles in cardiovascular, digestive, and sensory functions. Although the vasodilatory properties of CGRP are well documented, its somatosensory function regarding modulation of neuronal sensitization and of enhanced pain has received considerable attention recently. Growing evidence indicates that CGRP plays a key role in the development of peripheral sensitization and the associated enhanced pain. Calcitonin gene–related peptide is implicated in the development of neurogenic inflammation and it is upregulated in conditions of inflammatory and neuropathic pain. It is most likely that CGRP facilitates nociceptive transmission and contributes to the development and maintenance of a sensitized, hyperresponsive state not only of the primary afferent sensory neurons but also of the second-order pain transmission neurons within the central nervous system, thus contributing to central sensitization as well. The maintenance of a sensitized neuronal condition is believed to be an important factor underlying migraine. Recent successful clinical studies have shown that blocking the function of CGRP can alleviate migraine. However, the mechanisms through which CGRP may contribute to migraine are still not fully understood. We reviewed the role of CGRP in primary afferents, the dorsal root ganglion, and in the trigeminal system as well as its role in peripheral and central sensitization and its potential contribution to pain processing and to migraine.

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“…The raised glutamate may be responsible for stimulation of N-methyl-D-aspartic acid (NMDA) glutamate receptors in the dorsal horn of the spinal cord responsible for the wind-up phenomenon [17]. In addition, the diffuse noxious inhibitory control (DNIC), which involves descending opioidergic and serotonergic-noradrenergic efferent pathways from the brain to the spinal cord that downregulate the pain signal, is aberrant in FM patients [18].…”

Section: Neurotransmitters and Central Sensitizationmentioning

confidence: 99%

Potential drug therapies for the treatment of fibromyalgia

Lawson

2016

Expert Opinion on Investigational Drugs

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Modest improvement of health status in patients with FM has been observed with drugs targeting a diverse range of molecular mechanisms. No single drug, however, offered substantial efficacy against all the symptoms characteristic of FM. Identification of new and improved therapies for FM needs to address the heterogeneity of the condition, which suggests existence of patient subgroups, the relationship of central and peripheral aspects of the pathophysiology and a requirement of combination therapy with drugs targeting multiple molecular mechanisms.

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Biomarkers in fibromyalgia

Cited by 24 publications

References 41 publications

Milnacipran combined with pregabalin in fibromyalgia: a randomized, open-label study evaluating the safety and efficacy of adding milnacipran in patients with incomplete response to pregabalin

Milnacipran combined with pregabalin in fibromyalgia: a randomized, open-label study evaluating the safety and efficacy of adding milnacipran in patients with incomplete response to pregabalin

The role of calcitonin gene–related peptide in peripheral and central pain mechanisms including migraine

Potential drug therapies for the treatment of fibromyalgia

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