Six months of anti-tumor necrosis factor therapy produced no substantial changes in thyroid function among patients with psoriatic arthritis, according to a prospective observational study published in Egyptian Rheumatology and Rehabilitation. The research, conducted with sixty adults who had never previously received biologic medication, measured thyroid hormones, thyroid autoantibodies, and thyroid gland ultrasound features before treatment began and again after half a year of anti-TNF therapy. At baseline, every participant showed normal thyroid function, and after six months of treatment the levels of thyroid stimulating hormone, free T3, and free T4 remained essentially stable, with only a minor, statistically non-significant reduction in thyroid stimulating hormone observed, from a mean of 2.28 plus or minus 1.14 to 2.12 plus or minus 1.01. The findings address a long-standing question about whether biologics that block tumor necrosis factor, a central inflammatory signaling molecule, might disturb the thyroid gland in patients with chronic inflammatory joint disease.
Psoriatic arthritis belongs to the seronegative spondyloarthropathy spectrum, involving peripheral and/or axial joints, and affects approximately twenty to thirty percent of patients with psoriasis. People with psoriasis are susceptible to multiple comorbid conditions, including metabolic syndrome and gastrointestinal diseases, along with an increased predisposition to autoimmune disorders such as inflammatory bowel disease, type 1 diabetes mellitus, and autoimmune thyroid disease. Because tumor necrosis factor participates in the immunopathology of autoimmune thyroid conditions as well as in psoriatic disease, researchers have wondered whether blocking this cytokine could alter thyroid hormone production, thyroid autoimmunity, or thyroid gland structure. Reports and case studies have described the occurrence of subacute thyroiditis in patients treated with biologics directed against TNF-alpha and IL-17A, and changes in anti-thyroid antibody measurements have been observed after administration of some of these drugs, making systematic evaluation in a defined patient group particularly relevant.
The study team enrolled adults aged eighteen years or older with a confirmed diagnosis of psoriatic arthritis according to the Classification Criteria for Psoriatic Arthritis, known as CASPAR. All participants were anti-TNF naïve at enrollment and were planned to initiate anti-TNF therapy as part of standard clinical management because they had persistent moderate to severe disease activity, measured by the Disease Activity in Psoriatic Arthritis score, despite conventional therapy, or because they had purely axial disease, inflammatory bowel disease, or uveitis. Patients were recruited from outpatient clinics of Rheumatology, Rehabilitation and Physical Medicine, and Internal Medicine Departments between May 2024 and July 2025. Conventional disease-modifying antirheumatic drugs and glucocorticoids were continued during the study period alongside the new biologic treatment. The investigators excluded anyone with clinical or laboratory evidence of thyroid disorder before enrollment, previous use of biologic or targeted synthetic DMARDs, or use of medications known to affect thyroid function, such as amiodarone or lithium.
Each participant underwent a comprehensive assessment at baseline and again after six months of anti-TNF therapy. The clinical evaluation included a thorough medical history, general physical and locomotor system examination, and disease activity scoring with DAPSA. Laboratory testing covered inflammatory biomarkers, specifically the erythrocyte sedimentation rate and C-reactive protein, alongside a thyroid panel comprising thyroid stimulating hormone, free T3, free T4, anti-thyroid peroxidase antibodies, and anti-thyroglobulin antibodies. Thyroid gland morphology was determined through ultrasonography. Data analysis was performed with SPSS version 25, using paired t-tests or Wilcoxon signed-rank tests depending on data distribution, and the McNemar test for categorical measures, with statistical significance set at a p-value of 0.05 or less. A single blinded experienced radiologist performed all ultrasound assessments to minimize inter-observer variability.
The cohort was predominantly female, at 68.3 percent, with a mean age of 50.12 years and a mean disease duration of 9.62 years. Most patients had peripheral joint involvement, while axial affection was present in only eleven patients, or 18.3 percent. Skin and/or nail psoriasis was found in 39 patients, representing 65.0 percent of the group. Disease activity was moderate in seventeen patients and severe in forty-three despite conventional therapy. All patients received anti-TNF treatment: 39 received adalimumab, 15 received golimumab, and 6 received etanercept. This distribution across three different anti-TNF agents allowed the researchers to compile a descriptive subgroup analysis of thyroid hormones, autoantibodies, and ultrasound findings by drug type, although the limited number of patients per subgroup meant no statistical testing was performed on those comparisons.
The central result was one of stability. Thyroid autoantibodies were positive in six patients, or 10 percent of the cohort, at baseline and remained positive after treatment, accompanied by modest, statistically non-significant reductions in mean serum levels. Anti-thyroid peroxidase antibody levels declined from 36.93 plus or minus 46.59 to 31.93 plus or minus 38.65, while anti-thyroglobulin antibody levels declined from 68.06 plus or minus 45.44 to 66.70 plus or minus 61.25. Among the six antibody-positive patients, five were female, all continued their conventional therapy together with anti-TNF treatment, four were on adalimumab, and two were on golimumab. Anti-thyroglobulin antibodies were much higher than anti-thyroid peroxidase antibodies in this subgroup, but both showed only minimal reduction after six months. Morphological changes were noted by ultrasound in four of the six antibody-positive patients, while two had unremarkable ultrasound studies.
Ultrasound examination at baseline revealed subclinical structural changes in a subset of patients even though their thyroid hormone levels were normal. These findings included increased gland size in 6.7 percent, hypoechogenicity in 11.7 percent, hypervascularity in 6.7 percent, and the presence of nodules in 13.3 percent. After six months of anti-TNF therapy, all of these ultrasound findings demonstrated only trivial, non-significant changes. The persistence of both autoantibody positivity and structural changes, without progression or meaningful regression, suggests that six months of cytokine blockade neither provoked new thyroid abnormalities nor resolved pre-existing subclinical ones within this observation window. The authors note that this study enabled the detection of psoriatic arthritis patients with subclinical positive thyroid autoantibodies who may be at risk of developing overt thyroid dysfunction, thereby warranting follow-up and underscoring the potential benefits of screening.
The mechanistic rationale for studying this question rests on the biology of tumor necrosis factor itself. TNF enhances cytotoxicity and proliferation of T cells, B lymphocytes, and natural killer cells, increases cytokine synthesis, and promotes expression of MHC class I and class II antigens, adhesion molecules, and chemokines crucial for immune cell trafficking to sites of inflammation. In thyroid tissue of patients with autoimmune thyroid disease, TNF-alpha and its messenger RNA are found in greater concentration than in people without these disorders, and thyroid cells themselves produce TNF-alpha. Receptors for TNF-alpha are found on the surface of thyroid cells, which clarifies how the cytokine participates in cytotoxic mechanisms and destruction of thyroid tissue in autoimmune thyroid disease. On this basis, anti-TNF therapy has even been explored as a treatment for autoimmune thyroid disease and thyroid-associated ophthalmopathy; in a pilot study by Paridaens and colleagues, ten patients with mild to moderate Graves’ disease were treated with etanercept for twelve weeks and 60 percent showed moderate to marked improvement.
The results of the new study align with several previous investigations. A 2018 study by Roman and colleagues found no substantial differences in mean TSH and T3 measurements in psoriasis patients receiving etanercept, although TSH was lower in that group compared with patients not receiving biological treatment. A study by Paschou and colleagues investigating anti-TNF therapy in patients with inflammatory bowel disease revealed no significant differences in T3 and TSH levels, although patients on anti-TNF showed a significant reduction of T4 compared with the non-biologically treated group. Raterman and colleagues identified amelioration of thyroid function among rheumatoid arthritis patients with hypothyroidism following six months of adalimumab, and in a study of 138 rheumatoid arthritis patients on adalimumab, observed a lower anti-thyroid peroxidase antibody concentration after therapy, from 267 to 201 IU per milliliter, with two patients with associated hypothyroidism returning to a euthyroid state. The 10 percent autoantibody positivity rate in the present cohort is consistent with work by Fallahi and colleagues, who found significantly higher anti-thyroglobulin and anti-thyroid peroxidase antibody levels in psoriatic arthritis patients compared with normal subjects, and with Elghandour and colleagues, who demonstrated significantly higher anti-thyroid peroxidase levels in psoriatic arthritis patients relative to those with subclinical psoriatic arthritis and patients with psoriasis alone.
The authors acknowledge important methodological limitations. The cohort was small and the follow-up duration limited to six months, and the small number of patients in each of the three anti-TNF subgroups precluded meaningful statistical comparisons between drugs. Although a single blinded experienced radiologist performed all ultrasound assessments, intra-observer variability cannot be excluded, and ultrasonography is inherently operator-dependent. Notably, none of the reported cases of subacute thyroiditis associated with anti-TNF therapy were encountered in this cohort, which the researchers attribute to the limited patient numbers and monitoring duration. The team concludes that extensive longitudinal studies incorporating significantly larger patient samples are required to more definitively assess the influence of anti-TNF therapy on thyroid disorders and to ascertain whether regular thyroid monitoring could yield favorable outcomes for psoriatic arthritis patients. For now, the practical message is reassuring: in this prospective cohort, six months of anti-TNF therapy left thyroid hormone levels, autoantibody status, and gland morphology essentially unchanged.
Subject of Research: The effect of anti-TNF therapy on thyroid function, autoantibodies, and thyroid gland morphology in psoriatic arthritis patients.
Article Title: Assessment of thyroid gland disorders in patients with psoriatic arthritis after anti-tumor necrosis factor therapy
Article References: Mahmoud Salem, R., Ahmed Almokadem, H., Elsaied Elkholy, R., F. Mansour, T., Fouad Mohamed Rashad, Y., & H Shalaby, R. (2026). Assessment of thyroid gland disorders in patients with psoriatic arthritis after anti-tumor necrosis factor therapy. Egyptian Rheumatology and Rehabilitation, 53(1), Article 71. https://doi.org/10.1186/s43166-026-00443-8
Image Credits: AI Generated
DOI: 10.1186/s43166-026-00443-8
Keywords: psoriatic arthritis, anti-TNF therapy, thyroid function, thyroid autoantibodies, thyroid ultrasound, tumor necrosis factor, autoimmune thyroid disease, adalimumab, golimumab, etanercept, prospective cohort study, rheumatology
News Source: Ophelia Keating. (October 30, 2026). Anti-TNF Therapy Leaves Thyroid Function Largely Unchanged in Psoriatic Arthritis Patients. Scienmag.
