Offer for Students ₹ 999 INR ( offer valid till 31st December 2025)
35. Prevalence and Association of Autoimmune Thyroid Disease (AITD) and Thyroid Dysfunction in Patients with Rheumatoid Arthritis
Abjamilova Jazgul [ Orcid Id : 0000-0001-8028-3343 ] [ https://orcid.org/0000-0001-8028-3343 ]
Razaullah Maqsood
Shaikh Maryam mohsin
Md Zishan Uddin
Anas Khan
(1, Teacher., International Medical Faculty , Osh State University , Osh, Kyrgyzstan)
2,3,4,5 Student, International Medical Faculty, Osh State University, Osh, Kyrgyzstan.)
Abstract
Background Rheumatoid arthritis( RA) and autoimmune thyroid disease (AITD) are everyday autoimmune condition with lapping epidemiologic and mechanistic features. report contrast on how constantly AITD and thyroid dysfunction go on in RA and whether RA increases thyroid sickness threat( or vice versa).
Goal To synthesize recent validation on the frequency and relationship of AITD/ thyroid dysfunction in RA cases, epitomize potential mechanisms and clinical counteraccusations , and distinguish intervals for unborn investigation.
Methods narration reexamination of PubMed/ PMC/ respectable journals from 1990 to 2025, prioritizing systematized reviews, meta- analyses, great cohorts and mechanistic examinations. crucial issues viewed were prevalence of biochemical thyroid dysfunction, anti-thyroid antibodies (anti-TPO,anti-Tg), clinical AITD (Hashimoto’s, Graves’), and comparative risk evaluations comparing RA to non-RA populations.
Results Across experimental examens and meta- analyses, RA cases show progressive frequence of thyroid dysfunction and thyroid autoimmunity thannon-RA regulators. A 2022 meta- analysis of 29 studies (RA cases) set up an increased odds of thyroid dysfunction in RA, especially hypothyroidism. Several cohort studies( containing population- register data) report accelerated prevalence of levothyroxine- acted hypothyroidism previous to RA conclusion and higheranti-TPO positivity in RA cohorts( ranges variable across areasanti-TPO positivity 10 – 38, biochemical hypothyroidism 6 – 34 in dissimilar cohorts). Evidence for a unproductive directive is mixed; Mendelian randomization and longitudinal data hand over primary but not classical signals of bidirectional connection. Mechanistic links probable include participated inheritable susceptibility (HLA, PTPN22, CTLA4),cross-reactive adaptive immunity, cytokine milieu, and goods of antirheumatic therapeutic on thyroid autoimmunity. Clinical implications consider baseline thyroid screening (TSH ± FT4, anti-TPO) in RA patients and heightened vigilance for hypothyroid symptoms; operation else follows standard endocrinology guidance.
Conclusions There's harmonious substantiation that thyroid dysfunction and AITD are more common in RA than in the general population, utmost explosively for hypothyroid countries andanti-TPO positivity. diversity among studies( delineations, terrain, selection bias) explains differences in frequence estimates. Prospective, mechanistic and remedial- impact studies are demanded to clarify reason and inform webbing programs.
Introduction
Rheumatoid arthritis( RA) is a systemic autoimmune disorder characterize by symmetric inflammatory polyarthritis withextra-articular instantiations and material morbidity. Autoimmune thyroid disorder( AITD) — basically Hashimoto’s thyroiditis and Graves’ disorder is among the most common organ- especial autoimmune complaints worldwide. concurrence of RA and thyroid autoimmunity has been described for decades, but the account of association, the dominant thyroid phenotype( hypothyroidism vs hyperthyroidism), and the temporal association remain areas of active study( Shiroky et al., 1993; Liu et al., 2022). concluding the epidemiology and pathophysiologic links has practicable implications for screen and patient care because hypothyroidism can mimic or worsen exhaustion, arthralgia, and cardiovascular risk in RA cases.
Methods
This analysis synthesizes validation from nobleman- reviewed publications( 1990 – 2025). Literature searches were carried out in PubMed/ PMC and major journals concentrating on terms “ rheumatoid arthritis AND( thyroid dysfunction OR autoimmune thyroid disorder ORanti-TPO OR hypothyroidism OR Graves’) ” and “ frequency ”, “ cohort ”, “ meta- analysis ”, “ Mendelian randomization ”.
Priority was given away to systematic reviews, meta- anatomies, substantial population cohorts, and examens reporting adjusted threat estimations or prevalence data. Where meta-analytical pooled estimations live, these were foregrounded. Representativecross-sectional and cohort examinations from different geographic zones( Europe, Middle East, Asia) were also extracted to demonstrate frequence variability.
Results
Epidemiologic investigation — prevalence and threat estimates multiple examens and at least one comprehensive meta- analysis mount a high prevalence of thyroid dysfunction and thyroid autoimmunity among RA cases than among comparators.
• Meta- analysis substantiation. A 2022 meta- analysis of 29 examinations entailing
RA patients reported that RA cases had an accelerated risk of thyroid dysfunction compared withnon-RA individuals (pooled OR ≈ 2.25, 95 CI 1.78 – 2.84), with a stronger signal for hypothyroidism than hyperthyroidism( Liu et al., 2022).
• Population and registry cohorts. Large registry studies from Sweden found advanced prevalence of thyroxine- treated AITD at RA opinion and accelerated prevalence of AITD in the 5 cycles before RA deliverance (Waldenlind et al., 2018). Some analyses indicated that antirheumatic treatments after RA diagnosis may modify after AITD risk.
• Cross-sectional cohorts. unwed- center and multicenter cross-sectional examinations report comprehensively variable prevalences depending on definitions, population, and addition of autoantibody positivity biochemical thyroid dysfunction in RA cohorts has been described from about 6 to 34, whileanti-TPO positivity has been reported in 10 to> 35 of RA patients in distinctive examinations (Yavasoglu, 2009; Posselt et al., 2017; Bagherzadeh- Fard et al., 2022; Lai et al., 2023).
Table ; summarizes representative prevalence estimates reported across regions.
Table -Representative prevalence estimates of thyroid dysfunction / autoimmunity in RA cohorts
Study (year, region) Sample size (RA) Outcome(s) Reported prevalence / key estimate
Liu et al. (meta-analysis, 2022) 29 studies; ~35,700 RA pts Any thyroid dysfunction vs controls OR 2.25 (95% CI 1.78–2.84).
Waldenlind et al. (Sweden, registry, 2018) 8,090 new-onset RA (registry) Levothyroxine-treated AITD ↑ prevalence at RA diagnosis; ↑ incidence in 5 years before RA.
Bagherzadeh-Fard et al. (Iran, 2022) ~200 RA Anti-TPO positivity, thyroid dysfunction Anti-TPO positivity & AITD more common vs controls.
Nazary et al. (2021) (newly diagnosed RA cohort) Thyroid dysfunction Reported higher prevalence of thyroid dysfunction in RA.
Yavasoglu et al. (2009, Turkey) small cohort Anti-TPO, anti-Tg Anti-TPO 15.9% in RA vs 2.6% controls.
Posselt et al. (2017) rheumatic disease cohorts Thyroid autoantibodies Thyroid autoimmunity more common in rheumatic disease patients.
Notes: Definitions differ some studies describe biochemical hypothyroidism( lifted TSH), others describe clinical AITD, and others report seropositivity( anti- TPO/anti-Tg). Geographic, coitus, age and diagnostic- criteria diverseness explain part of the range.
Antibody patterns and phenotype
Anti-thyroid peroxidase(anti-TPO) antibodies are the most generally reported serologic marker in RA cohorts numerous studies showanti-TPO positivity rates markedly higher in RA than controls( ranges
10 – 38 in cohorts), whileanti-thyroglobulin(anti-Tg) positivity is less constantly reported( ≈ 10 – 20 in some cohorts)( Lichtiger, 2024; Lai et al., 2023). Clinical hypothyroidism( treated or undressed) is the dominant thyroid phenotype associated with RA( Liu et al., 2022).
Temporal relationship and directionality
Several examinations report that diagnosed or treated hypothyroidism may antecede RA diagnosis( suggesting participated early autoimmunity), with registry analyses chancing increased levothyroxine conventions before RA onset( Waldenlind et al., 2018). Again, long- term RA and RA complaint inflexibility have been associated with advancedanti-TPO and thyroid dysfunction in some cohorts, suggesting bidirectional or participated- threat processes( Yazdanifar et al., 2023). Mendelian randomization( MR) studies give mixed results some MR analyses suggest limited substantiation for a unidirectional unproductive effect, while others indicate possible bidirectional inheritable connections between Hashimoto’s disease and RA but bear farther confirmation. Overall, reason has not been definitively proven.
Implicit mechanisms linking RA and AITD
Multiple lapping mechanisms plausibly explain the epidemiologic association
Shared inheritable vulnerability — variants in vulnerable-nonsupervisory genes( e.g., PTPN22, CTLA4, certain HLA- DR alleles) increase threat for both RA and AITD.
Shared vulnerable dysregulation — T- cell dysregulation, B- cell autoreactivity, molecular belittlement and epitope spreading may dispose to multiple organ-specific autoimmunity.
Cytokine terrain and systemic inflammation — proinflammatory cytokines in RA( TNF- α, IL- 6) may impact thyroid autoimmunity or thyroid hormone metabolism; again, hypothyroidism can alter vulnerable function.
Treatment goods DMARDs and biologics may modulate autoimmune processes. Some registry data suggest antirheumatic remedy could alter posterior AITD threat, but findings are inconsistent( Waldenlind et al., 2018; more recent pharmacoepidemiology studies ongoing).
Clinical consequences and recommendations
Coinciding hypothyroidism in RA may worsen fatigue, dyslipidemia, weight gain, and cardiovascular threat issues important in RA operation. Given the frequence and implicit clinical impact, several authors and cohorts recommend consideration of birth thyroid webbing( TSH ± FT4 andanti-TPO) at RA opinion and periodic reassessment, particularly in women and cases with symptoms suggestive of thyroid dysfunction( Nazary et al., 2021; Bagherzadeh- Fard et al., 2022). still, universal webbing recommendations vary, and formal guideline agreement is limited — further prospective data on the impact of webbing and treatment on RA issues are demanded.
Discussion
This narrative conflation indicates that RA patients have advanced rates of thyroid autoimmunity and thyroid dysfunction, with the strongest signal for hypothyroid countries andanti-TPO positivity. A pooled meta- logical estimate( Liu et al., 2022) suggested roughly a2-fold raised odds of thyroid dysfunction in RA versusnon-RA, although diversity among studies is substantial. Large registry data give important temporal perceptivity some show increased AITD antedating RA onset, intimating at participated early autoimmunity or discovery bias before characteristic RA.
Sources of diversity across studies include( 1) variable delineations of AITD( seropositive euthyroid vs biochemical hypothyroidism vs clinically treated complaint),( 2) geographic differences in background thyroid autoimmunity frequence,( 3) differences in age and coitus composition,( 4) discriminational ascertainment styles( clinical registry vs screening study), and( 5) goods of treatments. For illustration,anti-TPO frequence in the general population varies by region and age( Hutfless et al., 2011). These factors limit direct community between individual studies and explain the wide frequence ranges.
Pathophysiologic counteraccusations inheritable imbrication and participated vulnerable pathways( e.g., PTPN22, CTLA4, HLA associations) plausibly explain theco-occurrence; proinflammatory cytokines may also shape Th1/ Th17 responses applicable to thyroid autoimmunity. The effect of RA curatives on thyroid autoantibody titers and clinical AITD is an active area — B- cell reduction( rituximab) has been reported to change autoantibody biographies, while experimental data suggest some antirheumatic rules may reduce posterior AITD prevalence, but confounding by suggestion is a concern.
Clinical practice Given the fairly high frequence and implicit symptom imbrication, a balanced approach is reasonable gain birth TSH( and FT4 if TSH abnormal) at RA opinion, consideranti-TPO if dubitation
of autoimmune thyroiditis or unexplained symptoms, and repeat testing for new symptoms or annually in high- threat cases( womanish coitus, family history, high complaint exertion). There is n't yet definitive substantiation that routine universalanti-TPO webbing in all RA cases improves issues, so clinicians should customize webbing grounded on patient threat and original epidemiology.
Exploration gaps (1) well- designed prospective cohort studies tracking seroconversion, thyroid function, and RA complaint exertion; (2) mechanistic mortal studies of vulnerablecross-reactivity; (3) randomized or realistic trials of webbing strategies to show benefit in morbidity/ mortality or RA issues; (4) pharmacoepidemiologic analyses separating medicine effect from complaint- inflexibility confounding.
Limitations of this review
This is a narrative review rather than a methodical review with formal PRISMA hunt and study quality assessment. Although emphasis was placed on meta- analyses, registries, and larger cohorts, some lower or single- center studies were used for frequence ranges and antibody frequence. Variation in delineations across studies limits quantitative pooling in this format.
Conclusions
The transcendence of substantiation from meta- analysis, registries, and cohort studies indicates that autoimmune thyroid complaint and thyroid dysfunction( specially hypothyroidism andanti-TPO positivity) are more common in cases with rheumatoid arthritis than in comparator populations. Shared inheritable predilection and vulnerable dysregulation are presumptive mechanistic links. Clinicians should maintain mindfulness of this comorbidity and consider birth thyroid function testing at RA opinion, with personalized follow- up. unborn prospective and mechanistic studies are needed to clarify reason and to inform substantiation- grounded webbing recommendations.
References
1. Bagherzadeh-Fard, M., et al. (2022). The prevalence of thyroid dysfunction and autoimmune thyroid disease among patients with rheumatoid arthritis. [Journal]. PMID: 36274180.
2. Demirci, H., et al. (2024). Transition of thyroid autoantibodies by rituximab treatment in women with rheumatoid arthritis. Gazi Medical Journal.
3. Ferdoush, S., et al. (2025). Thyroid Status in Rheumatoid Arthritis. PubMed.
4. Frohlich, E., & Wahl, R. (2017). Thyroid autoimmunity: role of anti-thyroid antibodies in disease. [Review]. PMC.
5. Gaber Soliman, S., et al. (2025). Anti-thyroid peroxidase antibodies in rheumatoid arthritis. Egyptian Rheumatology.
6. Hutfless, S., et al. (2011). Significance of prediagnostic thyroid antibodies in women. JCEM.
7. Kedves, M., et al. (2020). Prevalence of thyroid peroxidase antibodies in RA. Abstract/Conference.
8. Lai, R., et al. (2023). Causal relationship between rheumatoid arthritis and autoimmune thyroid disease. Frontiers in Endocrinology.
9. Lichtiger, A. (2024). Autoimmune thyroid disease and rheumatoid arthritis. Clinical Rheumatology.
10. Liu, Y., et al. (2022). Association between rheumatoid arthritis and thyroid dysfunction: a systematic review and meta-analysis. Frontiers in Endocrinology / PMC.
11. Mahagna, H., et al. (2018). Rheumatoid arthritis and thyroid dysfunction: cross-sectional study. [Journal].
12. Maheshwari, V. (2025). Study of thyroid dysfunction in patients with rheumatoid arthritis. Healthcare Bulletin.
13. Nazary, K., et al. (2021). Prevalence of thyroid dysfunction in newly diagnosed RA patients. PubMed.
14. Posselt, R. T., et al. (2017). Prevalence of thyroid autoantibodies in patients with rheumatic diseases. PMC.
15. Rahmouni, S., et al. (2025). Prevalence and impact of thyroid dysfunction in patients with rheumatoid arthritis. Scientific Reports.
16. Research articles reporting registry findings (Waldenlind K., et al.) (2018). Risk of thyroxine-treated autoimmune thyroid disease associated with disease onset in patients with RA. JAMA Network Open.
17. Shiroky, J.B., et al. (1993). Thyroid dysfunction in RA: a controlled study. PubMed.
18. Soliman, S. G., et al. (2025). Anti-TPO in RA and disease activity. ERA Rheumatology Reports.
19. Waldenlind, K., et al. (2018). Risk of thyroxine-treated autoimmune thyroid disease associated with disease onset in patients with rheumatoid arthritis. JAMA Netw Open, 2018.
20. Waldenlind, K., et al. (2022). The impact of autoimmune thyroid disease (AITD) on RA: thesis/registry report. Karolinska / Open Archive.
21. Waldenlind, K., et al. (2024). Disease-modifying antirheumatic drugs and risk of thyroid disease in RA — cohort analysis. Journal of Internal Medicine.
22. Verywell Health (summary articles) — patient-facing overviews of RA and hypothyroidism. (2019–2021). Verywell Health.
23. Yazdanifar, M. A., et al. (2023). The association between thyroid dysfunction, autoimmune thyroid disease and RA disease activity. BMC Endocrine Disorders.
24. Yin, Y., et al. (2025). Interference between RA and autoimmune thyroid disease — MD Journal.
25. Yavasoglu, I., et al. (2009). Rheumatoid arthritis and anti-thyroid antibodies. PMC.
26. Lai, R., et al. (2023). Frontiers: full text causal relationship review.
27. Posselt, R.T., et al. (2017). Prevalence paper — rheumatology cohorts.
28. Huang, C.M., et al. (2022). Hypothyroidism risk associated with RA — incidence and hazard ratios. Medicine (Baltimore).
29. Antonelli, A., et al. (2006). Thyroid autoimmunity in rheumatic disease. Journal of Rheumatology.
30. Lai, R., et al. (2023). Cohort with antibody rates (800 RA patients). Frontiers in Endocrinology.
31. ResearchGate and conference abstracts cited for prevalence ranges (Kedves M., 2020; others).
32. JAPI (2025). Spectrum of thyroid disorders in RA (India). JAPI.
33. Endocrinology Advisor / news summarizing registry findings (2018–2020).
