Plaque Psoriasis and Thyroid Disorders: How They’re Linked

Plaque Psoriasis is a chronic inflammatory skin disease that produces red, scaly plaques, most often on elbows, knees, and scalp. It is driven by an over‑active immune system and affects roughly 2‑3% of the UK population. While skin symptoms dominate the conversation, researchers increasingly recognise that plaque psoriasis often co‑exists with internal conditions, especially thyroid disorders. Understanding why these seemingly separate ailments overlap can help patients and clinicians catch problems early and tailor treatment.

Quick Take

• Both plaque psoriasis and many thyroid disorders are autoimmune diseases.
• Shared cytokines - especially IL‑17 and TNF‑α - drive inflammation in skin and thyroid.
• People with psoriasis are 1.5‑2× more likely to develop Hashimoto thyroiditis or Graves disease.
• Screening thyroid function at diagnosis and during biologic therapy improves outcomes.
• Biologics that block IL‑17 or TNF‑α can stabilize thyroid autoimmunity, but monitoring is essential.

What Is Plaque Psoriasis?

Plaque psoriasis belongs to the broader family of autoimmune diseases. In these conditions, the body’s own immune cells mistakenly attack healthy tissue. In psoriasis, T‑cells release pro‑inflammatory cytokines such as interleukin‑17 (IL‑17) and tumor necrosis factor‑alpha (TNF‑α). These molecules trigger rapid skin cell turnover, producing the characteristic thick plaques.

Genetic susceptibility plays a big role; the HLA‑Cw6 allele is the most strongly linked gene. Yet not everyone with the gene develops the disease - environmental triggers like stress, infection, or smoking often tip the balance.

Thyroid Disorders: An Overview

The thyroid gland regulates metabolism via hormones thyroxine (T4) and triiodothyronine (T3). Disorders fall into two main categories: hypothyroidism (under‑active) and hyperthyroidism (over‑active). The two most common autoimmune forms are Hashimoto thyroiditis and Graves disease. Both involve autoantibodies that mistakenly target thyroid proteins, but their clinical pictures differ.

In Hashimoto, antibodies (anti‑TPO and anti‑TG) destroy thyroid cells, leading to low T4/T3 and elevated thyroid‑stimulating hormone (TSH). In Graves, stimulating antibodies (TRAb) push the gland to over‑produce hormones, causing low TSH and high T4/T3. Both conditions are estimated to affect about 5% of the UK population, with a clear female predominance.

Shared Autoimmune Mechanisms

Why do skin and thyroid inflammation often appear together? The answer lies in overlapping immune pathways. The cytokines IL‑17 and TNF‑α, central to plaque psoriasis, are also active in thyroid autoimmunity. Studies show elevated IL‑17 levels in patients with Hashimoto, suggesting a common inflammatory driver.

Another link is the presence of shared genetic risk loci. The PTPN22 gene, which regulates T‑cell activity, is associated with both psoriasis and autoimmune thyroid disease. This gene‑environment‑immune triad explains the higher co‑occurrence rate.

Finally, systemic inflammation increases oxidative stress, which can damage thyroid follicular cells, further fueling autoimmunity. In short, the immune system’s mis‑fire in one organ can spill over to another.

Epidemiological Evidence

Large‑scale cohort studies from the UK, Scandinavia, and the US consistently report a 1.5‑ to 2‑fold increase in thyroid disorder prevalence among people with plaque psoriasis. For instance, a 2023 British Dermatology Journal analysis of 12,000 psoriasis patients found that 12% had a documented thyroid disorder, compared with 5% in matched controls.

Age and gender matter. Women with psoriasis over the age of 40 are especially prone to Hashimoto, while younger men show a slightly higher rate of Graves disease. The risk also rises with disease severity - patients with a Psoriasis Area Severity Index (PASI) above 10 have a 30% higher odds of thyroid autoimmunity.

Clinical Implications: Screening and Diagnosis

Given the strong link, clinicians should adopt a low threshold for thyroid screening in psoriasis patients. Baseline tests include:

1. Serum TSH (sensitive marker for both hypo‑ and hyper‑thyroidism).
2. Free T4 and Free T3 (to confirm hormonal status).
3. Anti‑TPO and anti‑TG antibodies (detect Hashimoto).
4. TRAb (thyroid‑stimulating receptor antibodies) when hyperthyroidism is suspected.

Repeating the panel annually, or whenever psoriasis therapy changes, helps catch subclinical disease before symptoms develop.

Therapeutic Overlap: Biologics and Thyroid Health

Modern psoriasis treatment often involves biologic agents that specifically block IL‑17 (e.g., secukinumab, ixekizumab) or TNF‑α (e.g., etanercept, adalimumab). Because these cytokines are also implicated in thyroid autoimmunity, biologics can have a dual effect.

Clinical observations suggest that IL‑17 inhibitors may reduce anti‑TPO titres in some patients, potentially slowing Hashimoto progression. Conversely, TNF‑α blockers have been linked to rare cases of new‑onset Graves disease, possibly by altering immune regulation. The takeaway? Regular thyroid function monitoring is advised after initiating any biologic.

For patients already diagnosed with a thyroid disorder, coordination between dermatologists and endocrinologists is vital. Adjusting levothyroxine dosage may be necessary when systemic inflammation improves, as metabolism normalises.

Practical Checklist for Patients and Clinicians

• At diagnosis: Order baseline TSH, free T4, and thyroid antibody panel.
• When disease is severe (PASI >10): Flag for more frequent (6‑month) thyroid review.
• Before starting biologics: Confirm stable thyroid status; document any existing antibodies.
• During biologic therapy: Repeat TSH and antibodies every 12 months, or sooner if symptoms arise.
• If new thyroid symptoms appear: Conduct full panel immediately; consider endocrinology referral.

Related Concepts and Next Steps

Beyond the direct psoriasis‑thyroid link, several adjacent topics are worth exploring:

• Metabolic syndrome - often co‑exists with both conditions, amplifying cardiovascular risk.
• Vitamin D deficiency - influences immune tolerance and may exacerbate both skin and thyroid autoimmunity.
• Stress management - chronic stress drives cytokine release, worsening plaques and thyroid imbalance.
• Future research: Novel dual‑target agents that modulate both IL‑17 and thyroid‑specific pathways.

Readers interested in the broader autoimmune landscape might next dive into "Autoimmune Disease Clusters: Why One Condition Often Sparks Another" or "Biologic Therapies: Balancing Efficacy and Endocrine Safety".