Hashimoto’s thyroiditis is an autoimmune condition where the immune system mistakenly attacks the thyroid gland, often leading to hypothyroidism. Hives (urticaria) are raised, itchy welts on the skin. When these welts recur for six weeks or more without a clear cause, the condition is called Chronic Spontaneous Urticaria (CSU). There is a significant association between Hashimoto’s disease and chronic hives, suggesting the underlying immune dysfunction can trigger skin reactions.
The Observed Clinical Link
The correlation between thyroid autoimmunity and recurring hives is established through clinical observations. Chronic Spontaneous Urticaria (CSU) frequently co-exists with autoimmune disorders like Hashimoto’s thyroiditis. Studies show that a large percentage of individuals with CSU test positive for thyroid autoantibodies.
The presence of thyroid peroxidase antibodies (TPOAb) is a strong indicator of thyroid autoimmunity. These antibodies are detected in approximately 25% to 30% of patients with chronic hives, increasing the likelihood of developing urticaria. This association holds true even if thyroid function tests are within the normal range.
This clinical relationship primarily involves CSU, which is often considered idiopathic (of unknown cause). However, the high co-occurrence suggests the cause is rooted in a shared autoimmune process. The risk of developing CSU is higher in patients with Hashimoto’s compared to the general population, particularly among female patients with autoimmune thyroid disease.
Shared Autoimmune Pathways
Both Hashimoto’s thyroiditis and chronic hives are considered autoimmune conditions, sharing common immunological roots. The immune system generates antibodies that target self-tissue in both disorders, a phenomenon known as polyautoimmunity.
In Hashimoto’s, the immune system produces IgG autoantibodies (TPOAb and TgAb) that attack thyroid cells. In many chronic hive cases, the body produces IgG autoantibodies that target components on the surface of mast cells, which are responsible for releasing histamine. These autoantibodies may bind to the high-affinity IgE receptor (FcεRI) or to the IgE antibody itself, triggering mast cells to release inflammatory chemicals.
The inflammation related to the thyroid condition can exacerbate or directly contribute to chronic hives. Thyroid autoantibodies may cross-react with components on the surface of mast cells, stimulating histamine release. Furthermore, both diseases involve dysregulation of immune cells, such as regulatory T cells, and elevated levels of inflammatory proteins like Interleukin-6 (IL-6), pointing to a shared systemic inflammatory background.
Management and Treatment Approaches
Managing hives in a patient with Hashimoto’s often requires a dual approach due to the strong autoimmune link. The first step involves careful diagnostic assessment, including a full thyroid panel (TSH and Free T4) and tests for thyroid antibodies (TPOAb and TgAb). Identifying thyroid autoimmunity is important even if hormone levels are currently normal.
Initial treatment for autoimmune-related hives focuses on blocking histamine effects, similar to most chronic urticaria cases. This typically involves non-sedating H1 antihistamines, often prescribed at higher-than-standard doses for symptom control. If standard antihistamine therapy is insufficient, next-line treatments are introduced.
Optimizing thyroid function is essential for patients with both conditions. If the patient is hypothyroid, treatment with thyroid hormone replacement (levothyroxine) can sometimes lead to significant improvement or complete remission of chronic hive symptoms. If initial treatments fail, a healthcare provider may consider advanced therapies, including immunosuppressants or biological medications like Omalizumab, which targets and neutralizes IgE to reduce mast cell activation.