COVID and Thyroid: Impacts on Hormones and Recovery

COVID-19 affects more than just the respiratory system—it also has significant implications for endocrine function, including thyroid health. Research suggests that both direct viral effects and immune responses can disrupt thyroid hormone levels, leading to temporary or lasting changes.

Understanding how COVID-19 interacts with the thyroid is key to recognizing complications and guiding recovery strategies.

Virus-Related Thyroid Inflammatory Conditions

SARS-CoV-2 has been linked to inflammatory thyroid conditions, with subacute thyroiditis being one of the most frequently reported. Also known as De Quervain’s thyroiditis, it typically presents with neck pain, fever, and transient thyrotoxicosis due to thyroid follicular cell destruction. A study in The Journal of Clinical Endocrinology & Metabolism (2021) found that COVID-19-associated subacute thyroiditis often involves elevated inflammatory markers like C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), distinguishing it from other thyroid dysfunctions. Unlike classic viral thyroiditis triggered by enteroviruses or adenoviruses, SARS-CoV-2 induces a more aggressive inflammatory response, potentially prolonging recovery.

Beyond subacute thyroiditis, COVID-19 has been associated with non-thyroidal illness syndrome (NTIS), also known as euthyroid sick syndrome. This condition is marked by low triiodothyronine (T3) levels with normal or slightly reduced thyroxine (T4) and thyroid-stimulating hormone (TSH). A retrospective analysis in Thyroid (2022) found that hospitalized COVID-19 patients with severe illness frequently exhibited NTIS-like patterns, correlating with worse outcomes. Unlike primary thyroid disorders, NTIS results from systemic illness affecting peripheral thyroid hormone metabolism, with severity proportional to disease progression.

Some cases of COVID-19-related thyroid dysfunction have progressed to long-term hypothyroidism. A multicenter study in The Lancet Diabetes & Endocrinology (2023) reported that some patients who developed thyroiditis during infection failed to regain normal thyroid function, requiring long-term levothyroxine therapy. This suggests SARS-CoV-2 may trigger autoimmune thyroid diseases, such as Hashimoto’s thyroiditis, in genetically predisposed individuals. Follow-up studies indicate that some patients develop thyroid peroxidase (TPO) antibodies post-infection, signifying a potential shift toward autoimmunity.

Endocrine Mechanisms Involving Thyroid Gland

SARS-CoV-2 disrupts thyroid function through multiple endocrine pathways, including alterations in hypothalamic-pituitary-thyroid (HPT) axis regulation. In severe cases, disruptions in TSH secretion have been observed, with the hypothalamus and pituitary gland affected by inflammatory and metabolic changes. Studies in The Journal of Clinical Endocrinology & Metabolism (2022) report that critically ill COVID-19 patients often exhibit suppressed TSH levels, a hallmark of NTIS.

Another key factor is the altered peripheral conversion of T4 to the biologically active T3. This process, mediated by deiodinase enzymes, is highly sensitive to metabolic stress. A systematic review in Thyroid Research (2023) found that hospitalized COVID-19 patients frequently displayed reduced T3 levels with normal or slightly decreased T4, suggesting an adaptive response to systemic inflammation. Downregulation of deiodinase type 1 (D1) and upregulation of deiodinase type 3 (D3), which inactivates T3, contribute to these changes. While this may help conserve energy during severe illness, prolonged suppression of T3 can lead to complications such as impaired thermoregulation and delayed recovery.

SARS-CoV-2 may also interfere with thyroid hormone transport and receptor sensitivity. Thyroid hormones rely on transport proteins like thyroxine-binding globulin (TBG) to circulate, and disruptions in these proteins can affect hormone bioavailability. A study in Endocrine Reviews (2023) noted that COVID-19-related systemic inflammation alters TBG levels, leading to fluctuations in free T4 and free T3. Additionally, cytokine-mediated changes in thyroid hormone receptors could impair the body’s ability to respond to circulating hormones, further complicating endocrine balance.

Patterns of Hormone Fluctuations

Thyroid hormone levels in COVID-19 patients fluctuate based on infection severity, health status, and recovery trajectory. Early in the disease, some individuals experience elevated free thyroxine (FT4) and free triiodothyronine (FT3) due to systemic stress, cellular damage, or hormone-binding protein dysregulation. However, this phase is short-lived, often followed by a decline in thyroid hormone levels.

As infection severity increases, FT3 levels tend to drop while FT4 remains stable or slightly decreased. This “low T3 syndrome” reflects a metabolic shift aimed at energy conservation. Unlike primary hypothyroidism, where TSH rises in response to low thyroid hormones, COVID-19 patients often exhibit inappropriately low or normal TSH despite diminished FT3, indicating a disruption in the HPT axis.

Recovery does not always restore thyroid hormone levels immediately. Some individuals experience prolonged FT3 suppression, leading to persistent fatigue, cognitive sluggishness, and thermoregulatory disturbances. Others may have a temporary TSH rebound before stabilization. This variability underscores the need for ongoing thyroid function monitoring, especially in those with preexisting endocrine disorders.

Laboratory Parameters and Clinical Indicators

Assessing thyroid function in COVID-19 patients requires careful interpretation of laboratory results, as standard thyroid hormone assays may not fully capture dynamic changes. Suppressed or inappropriately normal TSH with low FT3 and normal or slightly reduced FT4 is a common pattern, often resembling NTIS. Distinguishing NTIS from true thyroid dysfunction is critical, as the former typically resolves with overall health improvement, while the latter may require treatment.

Beyond standard thyroid panels, additional biomarkers provide insight into thyroid involvement. Reverse T3 (rT3), an inactive T4 metabolite, is frequently elevated in hospitalized patients, reflecting altered thyroid hormone metabolism. High rT3 with low FT3 suggests an energy-conserving shift rather than intrinsic thyroid failure. Fluctuations in thyroid-binding proteins like TBG, influenced by systemic inflammation or liver function changes, further complicate hormone interpretation. Considering broader biochemical markers, including albumin and cortisol, can help clarify thyroid hormone availability and metabolism.

Thyroid Considerations in Post-Infection Recovery

Lingering thyroid dysfunction can complicate COVID-19 recovery, with some patients experiencing persistent fatigue, weight fluctuations, or cognitive sluggishness due to prolonged T3 imbalances. Unlike transient thyroiditis, which typically resolves within weeks, post-COVID thyroid dysregulation can persist for months, necessitating follow-up. Endocrinologists recommend periodic thyroid function testing, especially for individuals with preexisting conditions or significant abnormalities during illness.

For those with prolonged hypothyroid-like symptoms, thyroid hormone replacement therapy may be necessary if lab abnormalities persist. Some patients, particularly those with autoimmune predispositions, transition from temporary dysfunction to long-term hypothyroidism requiring levothyroxine. Others with lingering NTIS-like patterns often recover without medication as systemic health improves. Dietary and lifestyle modifications, including adequate iodine intake and stress management, may aid thyroid recovery, though research on post-COVID thyroid rehabilitation remains limited. Given the variability in recovery, personalized management strategies are essential.