Blood Levels of Thyroid Hormones and Sugar in Acute Carbon Monoxide Poisoning.
- Author:
Ok Jun KIM
1
;
Il Saing CHOI
;
Ki Hwan KIM
Author Information
1. Department of Neurology, Yonsei University College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Acute CO Poisoning;
T3;
T4;
TSH;
Sugar
- MeSH:
Blood Glucose;
Carbon Monoxide Poisoning*;
Carbon Monoxide*;
Carbon*;
Compensation and Redress;
Consciousness;
Humans;
Physiology;
Poisoning;
Reference Values;
Thyroid Gland*;
Thyroid Hormones*;
Thyrotropin
- From:Journal of the Korean Neurological Association
1995;13(1):67-76
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study was performed to observe the changes of blood sugar levels in 200 cases with acute Carbon monoxide (CO) poisoning. Successive tests of blood sugar on the day of onset and the lst, 2nd, 3rd & 4th day after anoxic insult were done in 12 patients with acute CO poisoning. In addition, to determine the derangement of thyroid function, blood levels of triiodothyronine(T3), tetraiodothyronine(T4), thyroid-stimulating hormone (TSH) were measured on the day of admission in 29 with C0 poisoning. The blood levels of T3, T4 and TSH were within normal ranges, but over two-thirds were distributed in lower range of normal mean values. This lower tendency within normal range was especially prominent in the blood level of T3. The blood level of sugar was increased, and 79.5% was higher than the upper limit of normal range. The blood levels of T3 and T4 were significantly decreased as CO exposure time period- prolonged. There was significant negative correlation between blood T3 levels and consciousness levels. Blood TSH levels were not significantly affected in acute CO poisoning. As consciousness levels were depressed and exposure time period were prolonged, blood sugar was increased. There found a rapid increase in blood sugar, followed by a abrupt dropping, and then progressive decrease to normal level over a period of 5 days after exposure to CO. In conclusion, acute CO poisoning obviously changes the thyroidal physiology. Even though blood TSH levels were variable, there was an obvious decrease in T3. The assumed CO-induced decrease in thyroid hormone secretion is seemingly not mediated by depressed TSH secretion but thyroid hormone metabolic dysfunction or extrathyroidal cotiverslon defect The alterations of blood sugar were also found to be acute and temporal which may be the result of physiologic compensation to hypoxic state caused by CO poisoning.
