# The COX Pathway Alters Hematopoiesis in Hashimoto’s Thyroiditis

**Authors:** Karolina Wrońska, Maciej Ziętek, Magdalena Marciniak, Małgorzata Szczuko

PMC · DOI: 10.3390/cells14221796 · 2025-11-15

## TL;DR

This study shows that COX pathway products are linked to blood cell changes and immune markers in Hashimoto’s Thyroiditis.

## Contribution

It is the first to demonstrate a strong correlation between anti-tTG and ATG antibodies in Hashimoto’s Thyroiditis.

## Key findings

- NLR and PLR are correlated with PGE2 and TXB2 levels in Hashimoto’s Thyroiditis patients.
- A strong correlation (r = 0.781) was found between anti-tTG and ATG antibodies.
- TSH levels are significantly associated with increased monocyte counts in these patients.

## Abstract

What are the main findings?
The association was noted between the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) with prostaglandin E2 (PGE2) and thromboxane B2 (TXB2).Furthermore, a very strong correlation was demonstrated for the first time between antibodies against tissue transglutaminase (anti-tTG) and antibodies against thyroglobulin (ATG) (r = 0.781 and p = 0.007).

The association was noted between the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) with prostaglandin E2 (PGE2) and thromboxane B2 (TXB2).

Furthermore, a very strong correlation was demonstrated for the first time between antibodies against tissue transglutaminase (anti-tTG) and antibodies against thyroglobulin (ATG) (r = 0.781 and p = 0.007).

What are the implications of the main findings?
The results suggest the involvement of cyclooxygenase (COX) products in the pathogenesis of Hashimoto’s Thyroiditis (HT) and hematopoiesis.This study may contribute to developing new guidelines for diagnosing and treating autoimmune diseases.

The results suggest the involvement of cyclooxygenase (COX) products in the pathogenesis of Hashimoto’s Thyroiditis (HT) and hematopoiesis.

This study may contribute to developing new guidelines for diagnosing and treating autoimmune diseases.

Introduction: There is limited data in the literature on the effect of prostaglandins (PG) and thromboxanes (TX) on the development and severity of Hashimoto’s Thyroiditis (HT). This article aimed to analyze the association between blood count and the cyclooxygenase (COX) pathway in 39 women with HT. Methods: Biochemical analysis of PGE2 and TXB2 was performed using liquid chromatography (HPLC). Results: Morphological abnormalities were found in the women studied, particularly with regard to white blood cell parameters. An increase in thyroid-stimulating hormone (TSH) was associated with significantly higher levels of monocytes (p = 0.041). Correlations were also noted between the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) with TXB2 and PGE2. Furthermore, a very strong correlation was demonstrated for the first time between antibodies against tissue transglutaminase (anti-tTG) and antibodies against thyroglobulin (ATG) (r = 0.781; p = 0.007). Correlations between blood count and eicosanoids were also demonstrated. Conclusions: The results suggest the involvement of COX products in the pathogenesis of HT and hematopoiesis; therefore, this study may contribute not only to advancing knowledge, but also to developing new guidelines for diagnosing and treating autoimmune diseases.

## Linked entities

- **Chemicals:** prostaglandin E2 (PubChem CID 5280360), thromboxane B2 (PubChem CID 5283137)
- **Diseases:** Hashimoto’s Thyroiditis (MONDO:0007699)

## Full-text entities

- **Genes:** TGM2 (transglutaminase 2) [NCBI Gene 7052] {aka G(h), TG(C), TGC, hTG2, tTG}, TG (thyroglobulin) [NCBI Gene 7038] {aka AITD3, TGN}
- **Diseases:** HT (MESH:D050031), autoimmune diseases (MESH:D001327)
- **Chemicals:** TXB2 (MESH:D013929), PG (MESH:D011453), TX (MESH:D013931), PGE2 (MESH:D015232), eicosanoids (MESH:D015777)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12650877/full.md

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Source: https://tomesphere.com/paper/PMC12650877