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Results for “Fibromyalgia”

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At least 19 recordsLinked to original sources
PubMed2025

The genetic architecture of fibromyalgia across 2.5 million individuals.

Fibromyalgia is a common and debilitating chronic pain syndrome of poorly understood etiology. Here, we conduct a multi-ancestry genome-wide association study meta-analysis across 2,563,755 individuals (54,629 cases and 2,509,126 controls) from 11 cohorts, identifying the first 26 risk loci for fibromyalgia. The strongest association was with a coding variant in HTT, the causal gene for Huntington's disease. Gene prioritization implicated the HTT regulator GPR52, as well as diverse genes with neural roles, including CAMKV, DCC, DRD2/NCAM1, MDGA2, and CELF4. Fibromyalgia heritability was exclusively enriched within brain tissues and neural cell types. Fibromyalgia showed strong, positive genetic correlation with a wide range of chronic pain, psychiatric, and somatic disorders, including genetic correlations above 0.7 with low back pain, post-traumatic stress disorder and irritable bowel syndrome. Despite large sex differences in fibromyalgia prevalence, the genetic architecture of fibromyalgia was nearly identical between males and females. This work provides the first robust genetic evidence defining fibromyalgia as a central nervous system disorder, thereby establishing a biological framework for its complex pathophysiology and extensive clinical comorbidities.

Journal Article↗
PubMed2025

Is there a genetic correlation between tinnitus and temporomandibular joint disorder?: A two-sample Mendelian randomization study.

Tinnitus and temporomandibular disorder (TMD) are frequent coexistence of clinical symptoms caused by some systemic diseases in all humans. The observational research results on the correlation between tinnitus and TMD are inconsistent with the reported findings. The purpose of the study was to explore the bidirectional causal relationship between tinnitus and TMD. This study adopts a two-sample Mendelian randomization (MR) methodology. Single-nucleotide polymorphisms from the genome-wide association study were used as instrumental variables to elucidate the bidirectional causal relationship between tinnitus and TMD. The quality of our study was evaluated in accordance with the STROBE-MR guidelines. The MR analysis results showed that tinnitus (yes, most or all of the time now) could be significantly reduced TMD muscular pain linked with fibromyalgia (OR = 0.239, 95% CI: 0.087-0.66, P = .0057), but there was no correlation between other frequencies of tinnitus and the increased risk of TMD in genetic predisposition (all P > .05). The reverse MR analysis revealed no causal relationship and correlation between TMD exposure and increased risk of tinnitus. Sensitivity analysis indicated no horizontal pleiotropy and insignificant heterogeneity. This MR study supports evidence of a correlation between high-frequency tinnitus and reduced risk of TMD muscle pain associated with fibromyalgia. Further research on disease mechanisms are needed to explore the correlation between tinnitus and TMD.

Humans↗
PubMed2026

Impact of creatine supplementation alone or combined with exercise on inflammatory and clinical outcomes in chronic musculoskeletal pain treated in the rheumatological field: a systematic review.

Creatine supplementation has demonstrated ergogenic and anabolic effects in healthy and clinical populations. However, its potential therapeutic role in individuals with chronic musculoskeletal pain treated in rheumatological contexts remains unclear. The aim was to evaluate the efficacy and safety of creatine supplementation on pain, physical function/disability, quality of life, muscle strength, skeletal muscle mass, and inflammatory markers in people with chronic musculoskeletal pain usually treated from the rheumatological field. A systematic review was conducted following PRISMA guidelines. Searches were performed in MEDLINE, Web of Science, CINAHL, Scopus, and EMBASE up to July 2026. Eligible studies were randomized or nonrandomized clinical trials that provided creatine supplementation alone or in combination with exercise as a treatment compared to a control or placebo group. Eight studies (n = 189) were included, encompassing fibromyalgia, osteoarthritis, rheumatoid arthritis, and juvenile idiopathic arthritis. Creatine dosages varied from chronic low-dose to loading protocols (20 g/d, 2-5 g/d). Combined creatine plus resistance training may improve strength, skeletal muscle mass, and quality of life beyond exercise alone in osteoarthritis. Trials on fibromyalgia suggest an increase in muscle strength, but inconsistent effects on pain. Rheumatoid arthritis studies suggest gains in skeletal muscle mass and, in pilot studies, reduced disease activity. No major adverse events were reported. In conclusion, creatine supplementation alone may be insufficient to obtain clinical benefits, while combined with resistance exercise it could offer potential benefits for muscle strength, skeletal muscle mass and certain aspects of quality of life in these clinical conditions. However, evidence on pain and inflammation remains limited; Furthermore, the response across different clinical conditions is heterogeneous, highlighting the need for larger, high-quality trials.

Humans↗
PubMed2025

Complex Genetics and Regulatory Drivers of Hypermobile Ehlers-Danlos Syndrome: Insights from Genome-Wide Association Study Meta-analysis.

BACKGROUND: Hypermobile Ehlers-Danlos syndrome (hEDS) is the most common subtype of EDS, a group of heritable connective tissue disorders. Clinically, hEDS is defined by generalized joint hypermobility and chronic musculoskeletal pain, but its impact extends beyond the musculoskeletal system. Affected individuals frequently experience autonomic, gastrointestinal, immune, and neuropsychiatric involvement, highlighting both the multisystemic nature of the condition and challenges of diagnosis. In contrast to other EDS subtypes with defined genetic causes, the molecular basis of hEDS has remained elusive. METHODS: We conducted a genome-wide association study (GWAS) of hEDS across three case controls studies, including 1,815 cases and 5,008 ancestry-matched controls. Fixed-effects meta-analysis of 6.2 million variants was complemented with LDAK gene-based association testing, transcriptome-wide association studies, and integrative annotation across multiple tissues and cell types including eQTLs, enhancer marks and open chromatin accessibility profiles, supported by luciferase assays on one candidate variant. LD-score genetic correlations were assessed between hEDS and 19 frequently reported comorbid conditions. RESULTS: Two loci reached genome-wide significance, including a regulatory region near the atypical chemokine receptor 3 gene (ACKR3) on chromosome 2. Functional annotation supports ACKR3 risk alleles colocalize with eQTLs in tibial nerve, alter enhancer activity, and generate a de novo AHR transcription factor regulatory site, implicating neuroimmune and pain signaling pathways. Gene-based and transcriptome-wide analyses identified common variants in a locus containing multiple candidates, including SLC39A13, a zinc transporter critical for connective tissue development previously implicated in a rare form of EDS, and PSMC3, a gene involved in central nervous system development. LD-score regression revealed significant genetic correlations between hEDS and joint hypermobility, myalgic encephalomyelitis/chronic fatigue syndrome, fibromyalgia, depression, anxiety, autism spectrum disorder, migraine, and gastrointestinal diseases. CONCLUSIONS: These results establish the first evidence of common variant contributions to hEDS, supporting a complex, multisystem model involving neuroimmune-stromal dysregulation. Our findings add novel indications to hEDS pathogenesis and provide solid foundations for future molecular definition and therapeutic discovery.

Genome-wide association study↗
PubMed1978

Extent and level of fascial involvement in 100 cases with nodular fasciitis.

Nodular fasciitis (NF) shows a cellular proliferation which leads to widening of the fascia. Frequently unilateral or more often bilateral disruption of the fascia, with an infiltrative pattern is present. Subcutaneous fascia and surrounding fat are involved. Superficially the cellular proliferation may extend into dermal connective tissue. Deeper muscular tissue may be involved, with transitional forms or purely intramuscular changes, compatible with proliferative myositis. Proliferative myositis is considered to be a deep-seated variant of NF with muscular involvement. Intramuscular myxoma may be thought of as an intramuscular and mucoid variant of NF. A bilateral infiltrative pattern was most frequently found at all levels; in cases with muscular involvement it was always present.

Adipose Tissue↗
PubMed1975

The subcutaneous fascial analogue of myositis proliferans: electron microscopic examination of two cases and comparison with myositis ossificans localisata.

Two cases of the so-called fascial analogue of myositis proliferans were investigated by histological and electron microscopic methods. It was found that the structure of the fascial variant corresponds almost completely to the true myositis proliferans localized within the musculature. The electron microscopic observations show a preponderantly histiocytic differentiation of the cells and strongly activated proliferating capillaries, and exclude a myogenic origin of the characteristic ganglion-like giant cells. Ultrastructurally a traumatic genesis appears possibly, the cells of the lesion could derive from multipotent cells of the microvasculature. The relations to myositis ossificans and fascitis nodularis are discussed.

Adult↗
PubMed1977

Injection of steroids in painful breasts.

Fibrositis of the breast results in unilateral localized pain and tenderness in one breast. In most cases it can be specifically and permanently relieved by injection of steroids.

Adult↗
PubMed1979

Fibrositic myofascial pain in intermittent claudication. Effect of anesthetic block of trigger points on exercise tolerance.

The blocking of trigger points in the calf by the local injection of an anesthetic agent was performed in 15 patients with intermittent claudication. Reactive and exercise hyperemia, work load and duration of exercise were recorded before and after infiltration of the trigger points. Reactive hyperemia does not change, but the exercise tolerance of the leg significantly improves after local blocking of the trigger areas and the exercise hyperemia increases because of the higher work load. The pain pattern of intermittent claudication can be activated by the summation of abnormal input from muscles, due to contraction in the presence of anoxia, with activity from trigger points. Local infiltration of trigger areas blocks theirir activity. The vicious cycle of pain is interrupted and the exercise tolerance of the leg is increased, without improving blood circulation.

Adult↗