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DIFFERENT HEPATIC RESPONSES TO THYROXINE REPLACEMENT IN SPONTANEOUS AND 131 I‐INDUCED PRIMARY HYPOTHYROIDISM
Author(s) -
GOW S. M.,
CALDWELL G.,
TOFT A. D.,
BECKETT G. J.
Publication year - 1989
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1989.tb01421.x
Subject(s) - medicine , endocrinology , hormone , thyroid , glutathione , alanine aminotransferase , group a , chemistry , enzyme , biochemistry
SUMMARY The serum levels of a range of analytes known to change with thyroid status were measured in two groups of patients with primary hypothyroidism commencing T4 replacement therapy. One group (group 1; n = 9) had spontaneous hypothyroidism whilst in the second (group 2; n = 10), hypothyroidism had resulted from radioiodine therapy. The replacement dose was increased in 50 μg increments each month to 200 μg/day; this produced similar serum concentrations of thyroid hormones and TSH in the two groups at each dose. Dose‐dependent increases in glutathione S‐transferase (GST) were seen in both groups but changes in alanine aminotransferase (ALT) and gamma glutamyltransferase (GGT) activities occurred only in group 1 patients. Group 1 patients had significantly higher levels of GST than group 2 at the 150 μg ( P > 0.01) and the 200 μg ( P > 0.005) doses of T4, and they had higher activities of ALT ( P > 0.01) and GGT ( P > 0.02) at the 200 μg dose. Seven patients in group 1 had abnormalities in GST and four had high levels of ALT, whereas three patients from group 2 had high GST concentrations and all had ALT activities within reference limits. The concentrations of the other analytes measured in serum showed the same response to T4 in the two groups, particularly the concentrations of certain transport proteins whose serum concentrations depend on hepatic protein synthesis. These data suggest that patients with spontaneous primary hypothyroidism are more susceptible to hepatocellular damage than patients who have radioiodine‐induced primary hypothyroidism when given oral doses of thyroxine < 150 μg/day.