title: Which thyroid-stimulating hormone level should be sought in hypothyroid patients under L-thyroxine replacement therapy?
abstract: We sought to determine whether relationships exist between level of thyroid-stimulating hormone (TSH) suppression and cardiovascular risk parameters such as plasma homocysteine, C-reactive protein (CRP), fibrinogen, D-dimer and serum cholesterol in patients taking L-thyroxine-replacement therapy (LT4-RT). Four hundred and two hypothyroid patients under LT4-RT were cross-sectionally evaluated. Patients were grouped according to their achieved TSH (mIU/l) levels under LT4-RT on an arbitrary manner. Those patients having a TSH value 0.4-2 were defined as group 1 (n = 154), a TSH level of 2 to less than 5.5 were defined as group 2 (n = 176) and a TSH level of 5.5 to less than 20 with a normal free T3 and free T4 level were defined as group 3 (n = 72). The three groups of patients were also compared with overt hypothyroid patients (n = 71) and healthy controls (n = 97). Homocysteine levels (micromol/l) were significantly different between the three groups (10.4 +/- 4 for group 1, 11.3 +/- 3.7 for group 2 and 13.5 +/- 4.7 for group 3; p < 0.01 for all groups). Significant differences in CRP (mg /l) levels were present between the three groups (2.6 +/- 2.6 for group 1, 3.3 +/- 2.9 for group 2 and 4.8 +/- 4.1 for group 3; p < 0.01 for all groups). Univariate analysis showed that both homocysteine and CRP levels significantly correlated with free T4 and TSH level (p < 0.01 for both groups). No statistically significant differences were noticed in respect to fibrinogen and d-dimer levels between three groups. In examining the effect of LT4-RT on lipid parameters, a tendency towards beneficial effects without achieving statistical significance was observed. Practically speaking, a target TSH level of less than 2 might be advisable to lower CRP levels and homocysteine levels, and possibly lipid parameters.
authors.affiliation: Department of Endocrinology and Metabolic Diseases, Ankara University, School of Medicine, Ankara, Turkey. alptekingursoy@hotmail.com
authors.forename: A
authors.initials: A
authors.lastname: Gursoy
authors.forename: M
authors.initials: M
authors.lastname: Ozduman Cin
authors.forename: N
authors.initials: N
authors.lastname: Kamel
authors.forename: S
authors.initials: S
authors.lastname: Gullu
mesh_terms: D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000139:chemically induced*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007037:Hypothyroidism / Q000188:drug therapy*; D008875:Middle Aged; D012307:Risk Factors; D013972:Thyrotropin / Q000097:blood*; D013974:Thyroxine / Q000627:therapeutic use*
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D006710:Homocysteine; D005340:Fibrinogen; D013972:Thyrotropin; D002097:C-Reactive Protein; D013974:Thyroxine