Objective[|]To investigate the influence of thyroid hormones, beta human chorionic gonadotropin (β-HCG), and free β-HCG (fβ-HCG) in the etiology of hyperemesis gravidarum (HG) and to determine the main hormone that is responsible for the exacerbation of symptoms.[¤]Materials and Methods[|]Serum thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4), β-HCG, and fβ-HCG levels were measured twice (before and after hospitalization) in 55 patients with HG and measured once in 64 healthy controls. Serum hormone levels were determined using enzyme-linked immunosorbent assay.[¤]Results[|]Decreased mean TSH and increased mean fT4 levels were found in the pre-treatment serum samples of the HG group compared with the control group. Both differences were statistically significant (p=0.020 and p=0.007, respectively). However, there was no statistically significant difference in mean fT3, β-HCG, and fβ-HCG levels between the pre treatment serum samples of the HG group and control group. We could not demonstrate any correlation between the levels of β-HCG and thyroid hormones in the HG group; however, fβ-HCG moderately correlated with fT4 levels (r=0.494).[¤]Conclusion[|]The presence of hyperthyroidism was observed as the leading alteration in HG. In this study, fβ-HCG was demonstrated to have no direct effect on the etiology of HG; however, a possible indirect effect of fβ-HCG in relation with thyroid hormones was indicated. Hyperthyroidism was assessed to be primarily responsible for the symptoms in HG.[¤]