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Kinetics of the pituitary-thyroid axis and the peripheral thyroid hormones in 2 children with thyroxine intoxication
1Pediatric Endocrinology Unit, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Insights
Thyroxine (T4) intoxication in children is generally benign. This study tracked two girls who ingested a large dose, revealing their bodies primarily combat excess T4 by increasing T3 hormone production and degradation.
Area of Science:
- Pediatric Endocrinology
- Clinical Pharmacology
- Toxicology
Background:
- Thyroxine (T4) intoxication is a common, non-fatal pediatric condition.
- Understanding the hormonal response to T4 overdose is crucial for effective management.
Observation:
- Two healthy girls inadvertently ingested 2,500 micrograms of L-thyroxine.
- Thyroid hormones (T4, T3, rT3, Tg) and TSH were monitored for 20 days post-ingestion.
- Patients received ipecac, gastric lavage, propranolol, prednisone, cholestyramine, and propyl-thiouracil.
Findings:
- Serum T4 levels peaked within 2 hours and normalized after 13 days.
- Thyroid-stimulating hormone (TSH) levels decreased significantly for 4 days.
- T3 production and degradation increased, while rT3 levels showed decreased production and degradation.
- The T3/rT3 ratio fluctuated, indicating complex hormonal regulation.
- Thyroglobulin (Tg) levels dropped and then began to rise.
Implications:
- Pediatric T4 intoxication is managed through enhanced T3 metabolism.
- The body actively regulates thyroid hormone levels to mitigate overdose effects.
- This case study provides valuable kinetic data for T4 intoxication in children.
Abstract:
Thyroxine intoxication is a benign, nonfatal condition, relatively common in the pediatric age group. We present here a detailed laboratory follow-up of all thyroidal hormones in 2 healthy girls who inadvertently ingested 2,500 micrograms of L-thyroxine. The two girls were hospitalized and treated with ipecac, gastric lavage, propranolol, prednisone, cholestyramin and propyl-thiouracil. All physical signs were normal and no symptoms were reported. All thyroidal hormones were measured 12 times from 2 h to 20 days after the ingestion. For T4, T3, rT3 and thyroglobulin (Tg) a one-compartment kinetic model was formulated and fitted to the empirical data. The kinetic data constants of production and elimination were calculated, as well as the metabolic clearance rate. All laboratory values were similar in both girls. T4 serum levels were already high 2 h after the intoxication and returned to normal values only after 13 days. Fitting the T4 serum levels with a one-compartment model resulted in absorption and degradation constants similar to those in normal adult subjects. Thyroid-stimulating hormone (TSH) levels decreased reaching their lowest concentration 14 h after the intoxication. They remained low till the 4th day, after which they rose gradually. Twenty days after the intoxication, TSH levels were still below their initial values. T3 reached its peak levels 11 h after the ingestion and decreased to normal values after 3 days. Both T3 production constants and T3 degradation constants were significantly increased. rT3 reached its peak level on the 2nd day after the intoxication and decreased to normal values on the 4th day. Its production and degradation constants were somewhat below normal levels. The T3/rT3 ratio decreased from a normal level of around 3 to as low as 1 and rose again after 13 days to extremely high levels (as high as 8). Tg serum levels dropped continuously with a half-life of 1-5 days and started rising again after 2-13 days. In conclusion, T4 intoxication in the child is combated primarily by a significant increase in T3 production and degradation, while meticulously maintaining relatively low T3 levels.
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