Down-regulated resistin level in consequence of decreased neutrophil counts in untreated Grave's disease

Abstract

Resistin, belongs to cysteine-rich secretory protein, is mainly produced by circulating leukocytes, such as neutrophils monocytes and macrophages in humans. To date, few but controversial studies have reported about resistin concentrations in hyperthyroid patients, especially in Graves' disease (GD). We undertaked a controlled, prospective study to explore the serum resistin concentration in GD patients before and after -MMI treatment. In addition, we also investigated the main influencing factor on serum resistin level and discuessed the potential role of serum resistin plays in GD patients. 39 untreated GD (uGD) patients, including 8 males and 31 females, were enrolled in our investigation. All of these patients were prescribed with MMI treatment, in addition to 25 healthy controls. Anthropometric parameters and hormone assessment were measured. Enzyme-linked immunosorbent assay was used to detect serum resistin concentration in different stages of GD patients. Furthermore, neutrophil cell line NB4 with or without T3 treatment to detect the effect of thyroid hormones on resistin expression. The serum resistin level and neutrophil counts in untreated GD patients were significantly declined. And all of these parameters were recovered to normal after MMI treatment in ethyroid GD (eGD) and TRAb-negative conversion (nGD) patients. Resistin concentration exhibited a negative correlation with FT3 and FT4, but a positive correlation with absolute number of neutrophiles in uGD patients, whereas did not correlate with thyroid autoimmune antibodies and BMI. Neutrophile cell line, NB4, produced decreased expression of resistin when stimulated with T3. Our study showed a decrease of serum resistin level in GD patients and we suggested that the serum resistin might primarily secreted from circulating neutrophils and down-regulated by excessive thyroid hormones in GD patients.

Ascitic fluid regulates the local innate immune response of patients with cirrhosis

“…We detected resistin secretion by neutrophils, but not by monocytes, and this secretion increased upon activation. In line with our findings, resistin has been shown to be secreted by circulating neutrophils in patients with Graves’ disease and sepsis …”

“…We detected resistin secretion by neutrophils, but not by monocytes, 27,28 and this secretion increased be secreted by circulating neutrophils in patients with Graves' disease and sepsis. 29,30 To identify whether the factors responsible for resistin production were also responsible for IL-6 production, we analyzed whole blood cultures stimulated with different inflammatory cytokines.…”

Evaluation of neutrophil-to-lymphocyte ratio and hematologic parameters in patients with Graves’ disease

“…Van der Weerd K and et al reported that with fl ow cytometry method analysis, T and B lymphocyte counts were signifi cantly higher in Graves' disease than in healthy control group and in the same study there was a positive correlation between the levels of ft4 and B lymphocytes (14). Although antithyroid drugs are known to cause neutropenia as a side effect (15), Peng Y and et al, reported that compared with untreated Graves' patients, neutrophil counts increase in Graves patients who are euthyroid with treatment (16). In this study neutrophil count increased but not statistically signifi cantly.…”

Neutropenia in patients with hyperthyroidism: Systematic review and meta‐analysis

“…These studies were published between 1932 and 2019 by authors from USA, Scotland, New Zealand, Italy, Middle East (ie Turkey and Iran), Asia (ie Japan and China) and UK. They were monocentric, observational cohort studies, with retrospective design except for two which were prospective 13,17 . The total number of untreated hyperthyroid patients, whose baseline ANC values or neutropenic cases were available, was 1144 [including 991 affected by Graves’ disease and 153 with other causes of hyperthyroidism (ie toxic multinodular goitre and toxic adenoma)].…”