| pubmed-article:2484874 | pubmed:abstractText | In order to improve understanding of factors that may contribute to reduced serum T4 in non-thyroidal illnesses, we have studied baseline thyroid function, serum TSH response to thyrotropin-releasing hormone (TRH), and/or increase in thyroidal radioiodine uptake and serum T4 after parenteral administration of TSH in 12 patients with decompensated liver cirrhosis. Ten age and sex matched normal volunteer subjects served as controls. Compared to control subjects, patients with hepatic cirrhosis had significantly lower mean serum total T3 (ng/dl, mean +/- SD, 56 +/- 31 vs. 147 +/- 25, P less than 0.001), total T4 (microgram/dl, 4.3 +/- 1.5 vs. 8.8 +/- 0.74, P less than 0.001), and higher TSH (microU/ml, 3.0 +/- 1.2 vs. 1.6 +/- 0.73, P less than 0.05). Serum TSH response to TRH (400 micrograms I.V.) was abnormal in seven of 12 patients so studied. The peak TSH post-TRH was subnormal in one patient and normal but delayed in six patients. The mean baseline 24 h thyroid 131I uptake was not significantly different between the two groups under study (17 +/- 12% in cirrhosis patients vs. 25 +/- 10% in normal subjects). However, six patients with hepatic cirrhosis had clearly subnormal (less than 15%) 24 h thyroid radioiodine uptake (normal range 15-47%). The mean increase in 24 h thyroid radioiodine uptake and serum T4 at about 40 h after exogenous TSH (0.1 U/kg body weight i.m.) was lower in liver cirrhosis patients than that in normal subjects, but the difference was not significant statistically.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
