Department of Medical and Surgical Science, University Magna Grecia of Catanzaro, 88100 Catanzaro, Italy.
Department of Clinical and Experimental Medicine, University Magna Grecia of Catanzaro, 88100 Catanzaro, Italy.
Medicina (Kaunas). 2022 Jul 18;58(7):946. doi: 10.3390/medicina58070946.
Background and Objectives: Thyroid dysfunction is associated with non-alcoholic fatty liver disease, but its role in the progression of liver damage in obese patients remains unclear. In addition, several case reports have suggested the existence of a levothyroxine-induced liver injury, which has been poorly investigated. Our aim was to verify whether a difference in the prevalence of liver fibrosis exists in a population of obese individuals taking Levothyroxine. Materials and Methods: We conducted a cross-sectional study on a population of 137 obese individuals, of which 49 were on replacement therapy with Levothyroxine. We excluded those who had hypertriglyceridemia and diabetes mellitus. All participants underwent a liver stiffness assessment by transient elastography as well as biochemical measurements. In subjects with liver fibrosis, other cause of liver fibrosis were ruled out. Results: Participants taking Levothyroxine had a higher prevalence of liver fibrosis than those not taking Levothyroxine (30.6% vs. 2.3%; p < 0.001), and these results were obtained after we made an adjustment for age (Exp(B) = 18.9; 95% CI = 4.1−87.4; p < 0.001). The liver stiffness value differed significantly between groups (6.0 ± 3.6 and 5.1 ± 1.2, p = 0.033). Of those subjects taking Levothyroxine, there were no significant differences in the dose of medication (1.21 ± 0.36 vs. 1.07 ± 0.42; p = 0.240) and treatment duration (13.7 ± 7.43 vs. 11.13 ± 6.23; p = 0.380) between those with and without liver fibrosis. Conclusions: We found, for the first time, a greater prevalence of liver fibrosis in obese individuals taking Levothyroxine than in those not taking this medication. This finding needs to be confirmed by longitudinal population studies as well as by cellular studies.
甲状腺功能障碍与非酒精性脂肪性肝病有关，但在肥胖患者中，其在肝损伤进展中的作用尚不清楚。此外，有几项病例报告表明存在左旋甲状腺素诱导的肝损伤，但对此研究甚少。我们的目的是验证在服用左甲状腺素的肥胖人群中，是否存在肝纤维化患病率的差异。
我们对 137 名肥胖个体进行了一项横断面研究，其中 49 名正在接受左甲状腺素替代治疗。我们排除了那些患有高甘油三酯血症和糖尿病的患者。所有参与者均接受了瞬时弹性成像的肝硬度评估以及生化测量。对于存在肝纤维化的患者，排除了其他原因引起的肝纤维化。
服用左甲状腺素的患者肝纤维化的患病率高于未服用左甲状腺素的患者（30.6% vs. 2.3%；p<0.001），并且在我们对年龄进行调整后仍得到了这一结果（Exp(B)=18.9；95%CI=4.1-87.4；p<0.001）。两组之间的肝硬度值差异具有统计学意义（6.0±3.6 和 5.1±1.2，p=0.033）。在服用左甲状腺素的患者中，药物剂量（1.21±0.36 vs. 1.07±0.42；p=0.240）和治疗持续时间（13.7±7.43 vs. 11.13±6.23；p=0.380）在有肝纤维化和无肝纤维化的患者之间没有显著差异。
我们首次发现，服用左甲状腺素的肥胖患者肝纤维化的患病率高于未服用该药的患者。这一发现需要通过纵向人群研究和细胞研究来进一步证实。
