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Liver Stiffness in Obese Hypothyroid Patients Taking Levothyroxine

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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.
Title: Liver Stiffness in Obese Hypothyroid Patients Taking Levothyroxine
Description:
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.

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