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. Author manuscript; available in PMC: 2025 Sep 17.
Published in final edited form as: Exp Clin Endocrinol Diabetes. 2014 Jun 11;122(9):540–543. doi: 10.1055/s-0034-1376965

High Ghrelin Levels in Post-treatment Euthyroid Patients with Hashimoto’s Thyroiditis: a Case-control Preliminary Study

N Malandrino 1, A Miceli 2, L Leggio 3, G Mingrone 1, E Capristo 1
PMCID: PMC12440139  NIHMSID: NIHMS2107582  PMID: 24918532

Abstract

Rationale:

Hashimoto’s thyroiditis is a chronic inflammatory condition often associated with changes in appetite and body composition. Ghrelin is an orexigenic peptide involved in the regulation of appetite and food intake. A possible role of ghrelin in mediating inflammation has been suggested. A few contrasting published data are available on the relationship between thyroid status and circulating ghrelin in patients affected by Hashimoto’s thyroiditis. The aim of the present case-control study was to provide additional evidence on the relationship between thyroid status and plasma ghrelin levels in post-treatment euthyroid female patients with Hashimoto’s thyroiditis, compared to healthy controls.

Methods:

25 women [age 46.6 ± 10.6 years; Body Mass Index 26.3 ± 3.8 kg/m2] affected by overt hypothyroidism due to Hashimoto’s thyroiditis were studied after thyroid hormones and body weight were already normalized for at least 2 months following L-thyroxine replacement. 25 healthy women (age 40.2 ± 6.4 years; Body Mass Index 26.2 ± 4.0 kg/m2) served as the control group. Blood levels of thyroid hormones, thyroid peroxidase antibodies, thyroglobulin antibodies and ghrelin were determined. Fat mass, fat-free mass and high-density lipoprotein cholesterol were also assessed.

Results:

Circulating ghrelin levels were significantly higher in patients vs. control subjects (p < 0.001). No differences were found in metabolic parameters (body mass index, fat mass, fat-free mass, high-density lipoprotein cholesterol) between groups.

Conclusion:

The present study provides additional evidence of hyperghrelinemia status in post-treatment euthyroid patients affected by Hashimoto’s thyroiditis.

Keywords: ghrelin, thyroid hormones, Hashimoto’s thyroiditis, inflammation, metabolism

Introduction

Hashimoto’s thyroiditis (HT) is a chronic inflammatory medical condition characterized by lymphocytic infiltration, destruction of the thyroid follicles and subsequent hypothyroidism due to the production of thyroid auto-antibodies. Hashimoto’s thyroiditis is responsible for several symptoms, including changes in appetite, food intake and body composition [1,2].

Ghrelin, the endogenous ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a), is a 28 amino acid orexigenic peptide predominantly produced by the entero-endocrine cells of the gastric mucosa [3]. However, ghrelin is also expressed in other tissues, such as the hypothalamus [3], pituitary, adrenal and thyroid [4, 5], heart [6], placenta [7], pancreas [8], kidney [9] and testes [10]. Ghrelin plays a main role in the regulation of appetite, food intake and control of energy expenditure [11–15].

A role for ghrelin in modulating the immune system and mediating inflammatory processes has also been suggested. Together with its receptor, ghrelin is expressed in cell lines of human T and B lymphocytes and neutrophils [16]. Ghrelin inhibits the expression of pro-inflammatory anorexigenic cytokines, such as interleukin-1β, interleukin-6 and tumor necrosis factor-α [17]. Consistent with observations made in other medical conditions [18–22], ghrelin might be involved in the modulation of inflammatory response in HT.

A few conflicting data are available on the relationship between thyroid status and ghrelin signalling in both animal models of and patients with HT. In rodents, increases in both gastric ghrelin mRNA expression and blood ghrelin levels were found in hypothyroid vs. euthyroid rats [23, 24]. In humans, reduced ghrelin levels have been reported in untreated euthyroid HT [25], in subclinical hypothyroidism before thyroid hormone replacement [26] and in overt hypothyroidism due to HT before and after replacement treatment [27]. Another study reported no difference in plasma ghrelin concentrations between hypothyroid patients and healthy controls, either before or after L-thyroxine (LT-4) treatment [28]. Tanda et al. observed a non-significant trend toward increased plasma ghrelin levels in patients with overt hypothyroidism [29]. More recently, a few human studies reported increased blood ghrelin levels in hypothyroid patients, which became normalized after LT-4 treatment, as compared to controls [30–33].

The aim of the present study was to provide additional evidence on the relationship between thyroid status and ghrelin signalling by comparing plasma ghrelin levels in post-treatment euthyroid HT patients vs. healthy controls.

Materials and Methods

This was a retrospective study with 25 women [age 46.6 ± 10.6 years; Body Mass Index (BMI) 26.3 ± 3.8 kg/m2] affected by overt hypothyroidism due to HT and studied after thyroid hormones and body weight were already normalized for at least 2 months following LT-4 replacement. This sample was selected among patients referred to the Metabolic Diseases Outpatient Unit, Department of Internal Medicine, Catholic University of Rome, Italy. The exclusion criteria were: pregnancy or breast feeding; cardiac, liver, pulmonary, and/or kidney failure; neoplastic diseases; chronic non-thyroidal inflammatory disorders; gastrointestinal atrophy; diabetes mellitus and/or other endocrine disorders; use of drugs potentially influencing metabolism; recent fever and/or intense physical activity. A group of 25 healthy women (age 40.2 ± 6.4 years; BMI 26.2 ± 4.0 kg/m2) served as the control group.

In all subjects, blood samples were collected, after an overnight fasting, between 8:00 and 9:00 AM. Samples were immediately centrifuged and stored at −80 °C until analysis. Free T4 (fT4), free T3 (fT3) and thyroid-stimulating hormone (TSH) were determined by immunofluorescence. Thyroid peroxidase (TPOAb) and thyroglobulin antibodies (TGAb) titres were assessed by chemiluminescence. Plasma total ghrelin levels were measured by a commercial radioimmunoassay kit (Linco, St. Charles, MO). High-density lipoprotein cholesterol (HDL-C) was enzymatically measured after precipitation of very low-density lipoproteins and low-density lipoproteins with heparin-magnesium.

Body weight was measured to the nearest 0.1 kg with a beam scale, and height was measured to the nearest 0.5 cm with a wall-mounted stadiometer while the subjects were wearing light clothes and no shoes. BMI was computed as the ratio between body weight (kg) and height (m2). Body composition was assessed by dual-energy X-ray absorptiometry, using a whole-body densitometer (Lunar DPX-L, Madison, WI, USA; software version 3.65) in order to estimate fat mass (FM) and fat-free mass (FFM), as previously described [18].

Given that TPOAb represent a marker of thyroid inflammatory status [34] and taking into account the emerging role of ghrelin in inflammation [16, 17], HT patients were divided in 2 subgroups according to their TPOAb titre, i.e., HT patients with low TPOAb titre (< 100 IU/mL; n = 10) or high TPOAb titre (≥ 100 IU/mL, n = 15). No subgroups were generated based on the TGAb titre, given that this was always lower than 100 IU/mL in all HT patients enrolled in this study.

The study protocol fully complied with the guidelines of the Ethics Committee of the Catholic University of Rome (Italy) and was conducted according to the Declaration of Helsinki of 1975, as revised in 1983.

Statistics

All data were reported as mean (M) ± standard deviation (SD). Kolmogorov-Smirnov test was used to test data for normal distribution. Skewed variables were logarithmically transformed to obtain a normal distribution. Differences among groups were compared with the analysis of variance test (ANOVA) with Bonferroni correction where appropriate for continuous variables. P-values < 0.05 were considered statistically significant. Statistical analysis was performed using SPSS Version 15 (SPSS Inc., Chicago, IL, USA).

Results

Circulating ghrelin levels were significantly higher in both HT patients with TPOAb titre < 100 IU/mL and with TPOAb titre ≥ 100 IU/mL, compared to control subjects (1.1 ± 0.5 ng/ml vs. 0.70 ± 0.2 ng/ml; 1.4 ± 0.5 ng/ml vs. 0.70 ± 0.2 ng/ml; p < 0.001). TSH levels were within the normal range but significantly lower in HT patients with TPOAb titre < 100 IU/mL compared to controls. Both fT3 and fT4 were within their normal ranges of reference and no significantly different between HT patients and controls. No differences were found in other metabolic parameters (BMI, FM, FFM, HDL-C) among the 3 groups. Table 1 outlines the overall findings of this study.

Table 1.

Biochemical and metabolic variables in patients with Hashimoto’s thyroiditis (HT) compared to healthy controls.

HT patients with TPOAb < 100 IU/ml (n = 10) HT patients with TPOAb ≥ 100 IU/ml (n = 15) Healthy controls (n = 25)
age (years) 42.7 ± 11.2 49.3 ± 9.6* 40.2 ± 6.4
ghrelin (ng/ml) 1.1 ± 0.5* 1.4 ± 0.5* 0.70 ± 0.2
TSH (μIU/ml) 1.3 ± 0.8* 1.6 ± 0.8 2.1 ± 0.9
fT3 (pg/ml) 2.9 ± 0.4 3.2 ± 0.5 3.1 ± 0.2
fT4 (pg/ml) 12.4 ± 2.0 13.5 ± 3.0 12.0 ± 1.0
TPOAb (IU/ml) 32.2 ± 21.0 2305.9 ± 2939.5* 15.8 ± 5.6
TGAb (IU/ml) 26.4 ± 15.7 55.8 ± 33.5* 10.4 ± 2.3
BMI (kg/m2) 26.6 ± 3.0 26.2 ± 4.3 26.2 ± 4.0
FM (kg) 26.0 ± 8.8 26.0 ± 8.5 18.4 ± 13.6
FFM (kg) 44.9 ± 6.6 43.7 ± 5.1 46.3 ± 7.3
HDL-C (mg/dl) 54.9 ± 15.6 59.7 ± 11.7 51.0 ±9.8
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*

p < 0.05 compared to healthy controls

BMI, Body Mass Index; FM, Fat Mass; FFM, Fat-Free Mass; HDL-C, high-density lipoprotein cholesterol; TSH, thyroid-stimulating hormone (normal range: 0.35–2.80 μIU/ml); fT3, free triiodothyronine (normal range: 2.3–4.2 pg/ml); fT4, free thyroxine (normal range: 8.5–15.5 pg/ml); TPOAb, thyroid peroxidase antibody (normal range: < 20 IU/ml); TGAb, thyroglobulin antibody (normal range: < 80 IU/ml)

Discussion and Conclusions

In the present study, we reported higher ghrelin levels in patients affected by HT already under LT-4 replacement therapy vs. healthy controls. Compared to previous studies, these findings could be explained, at least in part, by differences in some of the patients’ characteristics, such as etiology of hypothyroidism, gender, and HDL-C levels, as detailed next.

Some of the previous studies that analyzed blood ghrelin levels in hypothyroidism included subjects with different etiologies, i.e., HT, post-surgery hypothyroidism for goiter or thyroid cancer, and radioiodine treatment [28, 29, 31–33]. By contrast, here we only enrolled patients with HT diagnosis. Notably, HT is an inflammatory chronic disease and most patients maintain a subclinical inflammatory status even after clinical and biochemical recovery of their thyroid function [34]. A role for ghrelin in the modulation of inflammatory response has been suggested in several medical conditions [18–22]. Therefore, in this study the presence of significantly higher ghrelin levels in HT patients, compared to controls, may be due to the persistence of inflammatory processes in our HT patients. This suggests that ghrelin may be involved or at least modulate the chronic inflammatory status present in post-treatment euthyroid patients. Furthermore, after treatment with LT-4, TPOAb levels may decline, but become negative only in a small number of patients [34]. In our study, we observed that, although not statistically significant (probably due to the small sample), ghrelin levels were higher in patients with high TPOAb titre compared to those with low TPOAb titre. This observation provides additional evidence on the possible role of ghrelin in the inflammatory status of HT patients after pharmacological treatment. Future clinical studies should also include inflammatory biomarkers in order to shed light on the role of ghrelin in modulating inflammation in HT.

Our sample included only women, while in previous studies both men and women were included [30]. Notably, females may have blood ghrelin levels 3 times higher than males [35] and this could further explain the difference between our study and previous findings. However, future larger studies powered to detect possible gender-based differences are required in order to draw any definitive conclusion.

Our patients showed a trend toward increased HDL-C levels compared to controls. Beaumont and colleagues demonstrated that the HDL-C fraction binds ghrelin in vitro [36]. Also, a positive correlation between the mean residence time of ghrelin in the body and HDL-C has been reported, suggesting that HDL-C levels might be an independent biological determinant of ghrelin bioavailability in humans [37]. Altogether, these findings suggest that the higher HDL-C levels present in HT patients, compared to controls, may represent another explanation of the higher blood ghrelin levels in our sample.

Hypothyroid patients usually gain weight even if their appetite is often lowered [38]. Even after replacement therapy with LT-4, some patients still report hypothyroid symptoms, in particular increased weight, despite serum TSH levels within the normal laboratory reference range [39]. In a large cross-sectional study group, a significantly higher BMI was reported in euthyroid subjects treated with LT-4 compared with subjects not taking LT-4, and these findings were independent from blood TSH levels [40]. Also, a small decline in mean body weight over the first 6 months of treatment with LT-4, with a return to pre-treatment weight by 24 months, has been described in hypothyroid individuals [41]. In patients who lost weight after Roux-en-Y gastric bypass surgery, higher ghrelin levels have been associated with weight regain, which consisted primarily of FM [42]. In our study, BMI did not significantly differ in HT patients compared to controls. On the other hand, a trend toward increased FM was observed in HT patients compared to controls. Thus, we may hypothesize that increased ghrelin levels could influence some of the metabolic changes, especially weight gain and/or increased FM, observed in hypothyroid patients before and after LT-4 treatment.

This study has important limitations that need to be taken into account, i.e., the retrospective design, the lack of pre-treatment data, and the small sample. On the other hand, given the conflicting data generated to date, this study provides additional information on the potential role of ghrelin in patients affected by thyroid disorders, and does so by enrolling a pure sample of HT patients with no other causes of thyroid disease.

In conclusion, the present study provides evidence on the presence of a hyperghrelinemia status in post-treatment euthyroid HT patients. Additional longitudinal large studies are needed in order to further investigate the role of ghrelin in HT patients.

Acknowledgments

The authors would like to thank Anna Caprodossi, B.S., for performing the laboratory testing.

Footnotes

Conflict of interest: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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