The question of whether hypothyroidism can cause rheumatoid arthritis (RA) is common, as both conditions frequently appear together. Hypothyroidism, often caused by the autoimmune disorder Hashimoto’s thyroiditis, involves an underactive thyroid gland that fails to produce sufficient thyroid hormones, slowing the body’s metabolism. Rheumatoid arthritis is a chronic inflammatory disorder where the immune system primarily attacks the lining of the joints, leading to pain, swelling, and potential joint destruction. Both hypothyroidism and RA are chronic conditions rooted in immune system dysfunction, which explains their frequent co-occurrence.
Is There a Causal Link?
Hypothyroidism does not directly cause rheumatoid arthritis, nor does RA directly cause hypothyroidism; however, there is a strong epidemiological association between the two conditions. This relationship is described as a comorbidity, meaning they frequently coexist in the same individual. Studies consistently show that having one of these autoimmune diseases significantly increases the likelihood of developing the other.
Research indicates that individuals with an RA diagnosis are approximately 1.74 times more likely to develop hypothyroidism compared to those without RA. Conversely, people diagnosed with hypothyroidism show a higher risk of developing RA, with one study reporting a 1.68 times increased risk. This bidirectional relationship suggests a shared underlying susceptibility rather than a direct cause-and-effect pathway, rooted in shared risk factors and a generalized predisposition toward autoimmune activity.
Shared Autoimmune Roots
The frequent co-occurrence of hypothyroidism and RA is best explained by the concept of polyautoimmunity, where an individual’s immune system is primed to attack multiple different body tissues. Both Hashimoto’s thyroiditis and RA are autoimmune diseases, meaning the body mistakenly targets its own cells—the thyroid gland in the former and the joint lining in the latter. The immune system’s error is often linked to shared genetic vulnerabilities.
Specific genetic predispositions, particularly within the Human Leukocyte Antigen (HLA) gene complex, are implicated in both conditions. The HLA system plays a large role in immune regulation and how the body presents foreign invaders to T-cells, and defects in this sequence can increase the risk of multiple autoimmune disorders. Furthermore, researchers have identified shared risk genes, such as TYK2, IL2RA, and IRF5, that contribute to the pathogenesis of both hypothyroidism and RA.
These genetic overlaps lead to common pathways of immune dysfunction, including T-cell dysregulation and an increase in pro-inflammatory cytokines like interleukin-1 (IL-1) and interleukin-6 (IL-6). This state of systemic inflammation, common in one autoimmune disease, can act as a trigger for the development of a second autoimmune condition. The presence of autoantibodies, such as anti-thyroid peroxidase (TPO) antibodies, is also found at a higher rate in RA patients, even those without overt thyroid dysfunction, supporting a common immunological background.
Symptom Overlap and Differentiation
A significant challenge when both conditions are present is that many symptoms overlap, making initial diagnosis and monitoring difficult. Both RA and hypothyroidism can cause profound fatigue, generalized aches, and stiffness, which may be mistakenly attributed to a flare of one disease when the other is the true cause. Swelling in the extremities is also a common feature, but the source differs between the two disorders.
The joint pain in RA is inflammatory, symmetrical, and focused on the synovial joints, often manifesting as morning stiffness that lasts for hours and improves with movement. Conversely, the aches and pains associated with hypothyroidism (myalgia or arthralgia) are more generalized, muscle-based, and relate to soft tissue swelling rather than joint destruction. Hypothyroidism can cause puffiness in the face and swelling in the soft tissues of the hands and feet, which is distinct from the joint-specific swelling of RA.
Differentiating the cause of symptoms requires specific diagnostic testing for each condition. Hypothyroidism is diagnosed by measuring blood levels of Thyroid-Stimulating Hormone (TSH) and free T4. The diagnosis of RA relies on inflammatory markers like C-reactive protein (CRP) and Erythrocyte Sedimentation Rate (ESR), alongside specific autoantibodies such as Rheumatoid Factor (RF) and anti-Cyclic Citrullinated Peptide (anti-CCP) antibodies.
Treatment Considerations for Dual Diagnosis
The management of a patient with both RA and hypothyroidism requires careful, integrated care between an endocrinologist and a rheumatologist. Hypothyroidism is treated with levothyroxine, a synthetic thyroid hormone replacement. Optimizing thyroid hormone levels with levothyroxine can sometimes alleviate generalized fatigue, muscle aches, and joint stiffness that were mistakenly attributed to RA activity.
Conversely, the medications used to treat RA, such as Disease-Modifying Anti-Rheumatic Drugs (DMARDs) and biologics, target the underlying immune system dysfunction and inflammation. Effectively treating RA can potentially reduce the overall systemic inflammation that may be contributing to the thyroid issue. Thyroid medication must be well-controlled, as some studies suggest that RA patients with concurrent thyroid disorders may have a poorer initial response to RA treatment. Regular monitoring of both thyroid function and RA disease activity is necessary to ensure that treatment for one condition does not negatively impact the other.