BackgroundIn recent years, more and

Background
In recent years, more and more evidence has demonstrated that hypothyroidism is associated with the increased prevalence of CHD [1,2]. This association is partly due to decreased levels of thyroid hormones, which lead to an atherogenic lipid profile characterized by increased levels of total cholesterol (TC) and lowdensity lipoprotein cholesterol (LDL-C) [3]. In the past decades, some studies indicate that subclinical hypothyroidism (SCH), which is defined as normal levels of serum free triiodothyronine (FT3) and free thyroxine (FT4) as well as elevated levels of thyrotropin (TSH), is also associated with a moderate increase in the risk of CHD [4,5]. Moreover, some researchers indicate that variations of serum TSH levels within the normal reference range are related to the TC, TG, and LDL-C [6,7], although not all investigations confirm these associations [8,9]. These findings imply that the association between lipid levels and thyroid function cannot be fully explained by the effects of FT3 and FT4 alone. We assumed that TSH, the most sensitive parameter reflecting the abnormal thyroid function in the early stage, might participate in the regulation of lipid profile to some extent. TSH responds significantly and precisely to minor changes in the concentrations of circulating thyroid hormones. A considerable amount of researches on the possible extrathyroidal effects of TSH has been published. For example, positive associations between the TSH level and waist circumference, body mass index and blood pressure have been described [10-12]. Regarding lipid metabolism, our previous study [13] indicated that TSH might up-regulate hepatic 3-hydroxy-3- methyl-glutaryl coenzyme A reductase (HMGCR) expression, which suggested a potential direct role of TSH in the cholesterol biosynthesis in the liver. In addition, most studies concerning the relationship between thyroid function and either CHD or the lipid profile had included both smokers and non-smokers. However, it is well known th t smoking is also a risk factor for CHD [14]. Furthermore, some populationbased study has indicated that smokers have lower levels of TSH [15]. Thus, in this study, we mainly focused on the possible association between TSH and the lipid profiles in euthyroid non-smokers with newly diagnosed asymptomatic CHD.

Hasil (Bahasa Indonesia) 1:

Latar belakangIn recent years, more and more evidence has demonstrated that hypothyroidism is associated with the increased prevalence of CHD [1,2]. This association is partly due to decreased levels of thyroid hormones, which lead to an atherogenic lipid profile characterized by increased levels of total cholesterol (TC) and lowdensity lipoprotein cholesterol (LDL-C) [3]. In the past decades, some studies indicate that subclinical hypothyroidism (SCH), which is defined as normal levels of serum free triiodothyronine (FT3) and free thyroxine (FT4) as well as elevated levels of thyrotropin (TSH), is also associated with a moderate increase in the risk of CHD [4,5]. Moreover, some researchers indicate that variations of serum TSH levels within the normal reference range are related to the TC, TG, and LDL-C [6,7], although not all investigations confirm these associations [8,9]. These findings imply that the association between lipid levels and thyroid function cannot be fully explained by the effects of FT3 and FT4 alone. We assumed that TSH, the most sensitive parameter reflecting the abnormal thyroid function in the early stage, might participate in the regulation of lipid profile to some extent. TSH responds significantly and precisely to minor changes in the concentrations of circulating thyroid hormones. A considerable amount of researches on the possible extrathyroidal effects of TSH has been published. For example, positive associations between the TSH level and waist circumference, body mass index and blood pressure have been described [10-12]. Regarding lipid metabolism, our previous study [13] indicated that TSH might up-regulate hepatic 3-hydroxy-3- methyl-glutaryl coenzyme A reductase (HMGCR) expression, which suggested a potential direct role of TSH in the cholesterol biosynthesis in the liver. In addition, most studies concerning the relationship between thyroid function and either CHD or the lipid profile had included both smokers and non-smokers. However, it is well known th t smoking is also a risk factor for CHD [14]. Furthermore, some populationbased study has indicated that smokers have lower levels of TSH [15]. Thus, in this study, we mainly focused on the possible association between TSH and the lipid profiles in euthyroid non-smokers with newly diagnosed asymptomatic CHD.

Hasil (Bahasa Indonesia) 2:

Latar Belakang
Dalam beberapa tahun terakhir, semakin banyak bukti menunjukkan bahwa hipotiroidisme dikaitkan dengan peningkatan prevalensi PJK [1,2]. Asosiasi ini sebagian disebabkan oleh penurunan kadar hormon tiroid, yang mengarah ke profil lipid aterogenik yang ditandai dengan peningkatan kadar kolesterol total (TC) dan lowdensity lipoprotein kolesterol (LDL-C) [3]. Dalam beberapa dekade terakhir, beberapa studi menunjukkan bahwa hipotiroidisme subklinis (SCH), yang didefinisikan sebagai tingkat normal serum triiodothyronine bebas (FT3) dan tiroksin bebas (FT4) serta peningkatan kadar thyrotropin (TSH), juga terkait dengan Kenaikan moderat dalam risiko PJK [4,5]. Selain itu, beberapa peneliti menunjukkan bahwa variasi kadar TSH serum dalam kisaran referensi yang normal terkait dengan TC, TG, dan LDL-C [6,7], meskipun tidak semua investigasi mengkonfirmasi asosiasi ini [8,9]. Temuan ini menyiratkan bahwa hubungan antara tingkat lipid dan fungsi tiroid tidak dapat sepenuhnya dijelaskan oleh efek F3 dan F4 sendiri. Kami berasumsi bahwa TSH, parameter yang paling sensitif yang mencerminkan fungsi tiroid normal pada tahap awal, mungkin berpartisipasi dalam regulasi profil lipid sampai batas tertentu. TSH merespon secara signifikan dan tepat untuk perubahan kecil pada konsentrasi sirkulasi hormon tiroid. Sejumlah besar penelitian tentang efek extrathyroidal kemungkinan TSH telah diterbitkan. Sebagai contoh, asosiasi positif antara tingkat TSH dan lingkar pinggang, indeks massa tubuh dan tekanan darah telah dijelaskan [10-12]. Mengenai metabolisme lipid, studi kami sebelumnya [13] menunjukkan bahwa TSH mungkin up-mengatur hati 3-hidroksi-3- metil-glutaryl koenzim A reduktase (HMGCR) ekspresi, yang menunjukkan peran langsung potensi TSH dalam biosintesis kolesterol dalam hati . Selain itu, kebanyakan studi mengenai hubungan antara fungsi tiroid dan baik PJK atau profil lipid telah termasuk baik perokok dan non-perokok. Namun, hal ini juga diketahui th t merokok juga merupakan faktor risiko untuk penyakit jantung koroner [14]. Selain itu, beberapa studi telah menunjukkan bahwa populationbased perokok memiliki tingkat TSH [15]. Dengan demikian, dalam penelitian ini, kami terutama berfokus pada hubungan yang mungkin antara TSH dan profil lipid pada eutiroid non-perokok dengan yang baru didiagnosis PJK tanpa gejala.