It has been reported that fasting, especially depletion of carbohydrate intake, induces a low triiodothyronine (T
3) syndrome and that this low serum T
3 is the outcome of decreased conversion of thyroxine (T
4) to T
3 in the peripheral tissues. In the present study, the levels of serum T
3, T
4, reverse triiodothyronine (rT
3), and thyrotropin (TSH) and their changes during the clinical course of treatment of ketoacidosis (KA) in three female insulin-dependent diabetics were investigated, since the body is assumed to be under carbohydrate hunger in diabetic KA due to absolute insulin deficiency.
(1) In the KA state of the three cases (Case 1, 21 yrs; Case 2, 27 yrs; Case 3, 18 yrs, associated with chronic focal thyroiditis), extremely low levels of serum T3 of 34-35, 19-38, and 56-64 ng/dl (normal, 89-177), respectively, and low T4 concentrations of 3.5-4.0, 2.3-4.2, and 4.7-5.9 μg/dl (normal, 5.4-12.6), respectively, and slightly high rT
3 values of 20.5-22.8, 48.0-45.7, and 45.6-48.5 ng/dl (normal 15.4-38.2), respectively, were observed. Within one day after the disappearance of KA following treatment of low dose insulin, fluid, and electrolytes, these abnormalities in serum T
3, T
4, and rT
3 concentration still remained within almost the same ranges as those in the KA, although they tended slightly towards normal values.
(2) After 3 to 7 weeks of sustained good control (GC) of the diabetic state with insulin, all the abnormalities in T
3, T
4, and rT
3 in the cases disappeared and the values remained within normal limits.
(3) On the other hand, the levels of basal serum TSH were within the normal range in all diabetic states in all cases, and the TSH responses to TRH (500 μg, iv) in the GC state were also normal, except for a slightly exaggerated one in Case 3.
These results indicate that, during the diabetic KA and soon after improvement of the KA with treatment, there were markedly low T
3, low T
4, slightly high rT
3, and normal basal TSH values, and that these abnormalities were ameliorated in the GC state. Decrease in secretion and/or synthesis of hormones in the thyroid per se, probably concomitant with a temporary shift of the hypothalamic-pituitary axis, rather than decreased conversion of T
4 to T
3, may contribute to this phenomenon.
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