Journal of Hematology & Thromboembolic Diseases
Open Access

lood Cell Abnormalities and Coagulation Factors in Autoimmune Thyroid Diseases

Claudia Rehnberg^{* *}Correspondence: Claudia Rehnberg, Department of Hemostasis and Thrombosis, University of Sao Paulo, Sao Paulo, Brazil, Email:

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Description

Autoimmune Thyroid Diseases (AITDs), including Hashimoto’s thyroiditis and Graves’ disease, represent a significant portion of thyroid disorders with complex pathophysiological mechanisms. AITDs are characterized by immune system dysfunction, where the body's immune system mistakenly targets thyroid cells, leading to either hypo or hyperthyroidism. This autoimmune attack on thyroid cells often results in various systemic manifestations and abnormalities, particularly in hematological parameters. Hematological changes in autoimmune thyroid diseases have been widely studied in clinical settings, revealing distinct alterations in blood cell counts, clotting factors, and other markers of inflammation. Understanding the link between hematology parameters and autoimmune thyroid diseases is essential for better patient management, early diagnosis, and predicting disease outcomes.

This article explores the relationship between hematological parameters and autoimmune thyroid diseases, focusing on blood cell abnormalities, coagulation factors, inflammatory markers, and their clinical relevance in disease diagnosis and management.

Autoimmune thyroid diseases

AITDs encompass two major conditions like Hashimoto’s thyroiditis and Graves’ disease. Both conditions involve the immune system attacking thyroid cells, but the clinical manifestations and outcomes differ.

Hashimoto’s thyroiditis: This is the most common cause of hypothyroidism worldwide. In Hashimoto's thyroiditis, the immune system produces antibodies against Thyroid Peroxidase (TPO) and Thyroglobulin (TG), leading to thyroid cell destruction. Patients with Hashimoto's may present with fatigue, weight gain, depression, and other hypothyroid symptoms.

Graves’ disease: In contrast, Graves' disease is the most common cause of hyperthyroidism. It occurs when the immune system produces stimulating antibodies against the Thyroid-Stimulating Hormone Receptor (TSHR), leading to excessive thyroid hormone production. Symptoms of hyperthyroidism include weight loss, palpitations, tremors, and anxiety.

Despite their different clinical presentations, both diseases can influence various physiological systems, including the hematologic system.

Hematology parameters in autoimmune thyroid diseases

The immune dysregulation seen in autoimmune thyroid diseases often extends beyond the thyroid gland, influencing the hematologic system. The most commonly observed hematological alterations include changes in the number and function of blood cells, as well as abnormalities in coagulation markers.

Anemia: One of the most frequent hematologic abnormalities in AITDs is anemia. The mechanism behind anemia in autoimmune thyroid diseases is multifactorial. Hypothyroidism, as seen in Hashimoto’s thyroiditis, can lead to Anemia of Chronic Disease (ACD), characterized by low serum iron levels and low reticulocyte counts. This occurs due to the inflammatory cytokines, such as Interleukin-6 (IL-6), which affect iron metabolism and erythropoiesis in the bone marrow. Additionally, hypothyroidism can lead to macrocytic anemia due to impaired vitamin B12 absorption or folate deficiency, which is commonly observed in patients with thyroid dysfunction.

Conversely, in hyperthyroidism, there is an increased metabolic demand that may also impair erythropoiesis, contributing to mild anemia in some cases. However, anemia in Graves’ disease may be less frequent than in Hashimoto’s thyroiditis and is typically associated with other comorbidities, such as autoimmune hemolytic anemia or iron deficiency due to gastrointestinal losses.

Leukocyte alterations: Hematologic analysis often reveals the leukocytosis or leukopenia in patients with AITDs. Elevated White Blood Cell (WBC) counts are more commonly observed in Graves' disease due to the heightened inflammatory state and autoimmune activation. In some patients, this increase in WBCs can be due to concurrent infections or an exaggerated inflammatory response to thyroid hormone excess. On the other hand, leukopenia has been reported in patients with Hashimoto’s thyroiditis, possibly due to the effects of autoimmune antibodies on the bone marrow or the presence of other autoimmune conditions, such as lupus or rheumatoid arthritis, which often co-exist with Hashimoto’s thyroiditis.

Thrombocytopenia and thrombocytosis: Alterations in platelet counts are another significant hematologic finding in AITDs. Thrombocytopenia (low platelet count) has been observed in patients with Hashimoto’s thyroiditis and is often linked to the presence of autoimmune antibodies against platelets or bone marrow suppression. Thrombocytopenia may also be a secondary manifestation of hypothyroid-associated anemia or associated with the development of splenomegaly, a known complication in some autoimmune thyroid disease patients.

Coagulation factors: Changes in coagulation markers are another important aspect of hematological findings in AITDs. Studies have shown that patients with Graves’ disease tend to have procoagulant states due to the increased levels of thyroid hormones, which enhance the synthesis of clotting factors, such as fibrinogen, prothrombin, and factor VIII. This elevated clotting activity can increase the risk of thrombosis and cardiovascular complications. On the other hand, Hashimoto’s thyroiditis is generally associated with a mild hypo coagulant state, as hypothyroidism is known to decrease clotting factor synthesis, leading to an increased bleeding tendency in some cases.

Inflammatory markers: Since autoimmune thyroid diseases are characterized by systemic inflammation, markers of inflammation often show significant alterations in blood tests. In both Hashimoto’s thyroiditis and Graves' disease, C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR) may be elevated, reflecting the immune response and inflammatory state. These markers can be used as adjunctive diagnostic tools, helping to identify the activity and severity of autoimmune thyroid diseases.

Conclusion

In summary, autoimmune thyroid diseases significantly impact hematology parameters through complex mechanisms involving autoimmune dysregulation, thyroid hormone imbalances, and systemic inflammation. Anemia, leukocyte alterations, thrombocytosis, and coagulation abnormalities are commonly observed in patients with these disorders, reflecting the broader systemic effects of thyroid dysfunction. Clinicians should remain vigilant in monitoring these parameters to optimize patient care, improve outcomes, and prevent complications associated with AITDs. Understanding the intricate links between hematology parameters and autoimmune thyroid diseases is essential for advancing both diagnostic and therapeutic strategies in the management of these disorders.