Protective Role of Bilirubin Against Increase in hsCRP in Different Stages of Hypothyroidism.

In conjunction with thyroxine, bilirubin may play an important role for regulation of hsCRP level and a consequent pro-inflammatory condition in hypothyroidism. In present study we evaluated the dependence of hsCRP changes on total bilirubin (BT) and fT4 level in thirty overt (OH) and thirty subclinical hypothyroidism (SH). Serum BT, hsCRP, thyroxine and TSH were measured in both groups and compared with forty control subjects. Serum values of TSH, hsCRP showed raised (P < 0.001 for both) values with lower levels for fT4 and BT (P < 0.001 and 0.03 respectively) in hypothyroid patients compared to the controls. ANOVA showed significant increments in TSH and hsCRP values with decreases in fT4 among the control, SH and OH groups respectively (P < 0.001). BT values showed decrease in OH group only in comparison to controls (P = 0.04). Regression analysis revealed that hsCRP was negatively dependent on fT4 (β = -0.35, P = 0.002) and serum bilirubin (β = -0.40 and P < 0.001 respectively). Univariate general linear model analysis showed this dependence persisted even when carried out distinctly in SH and OH groups separately (P < 0.001). TSH did not show any significant predictive value on the hsCRP level in either of these two tests. From these analyses we suggest that serum hsCRP is closely integrated to a lowered synthesis of bilirubin and fT4 in hypothyroid patients. Furthermore, this causal relationship is not only limited to overt but also extends to the SH.