Thyroid Function and Chronic Hepatosplenic Schistosomiasis: Peripheral Conversion of Thyroxine to 3,5,3′—Triiodothyronine and Pituitary—Thyroid Relationship

Publisher Website
Google Scholar
Abstract
The relationship between chronic hepatosplenic schistosomiaisis (CHES) and circulating thyroid hormones as well as the TSH response to TRH were investigated in 41 hospitalized CHES patients and compared to those in 11 patients with non-CHES cirrhosis with severe hepatic failure. CHES patients were subdivided into 3 groups depending on the severity of parenchymal dysfunction, based upon a composite clinical and laboratory index. Angiographic and hemodynamic studies of CHES patients revealed altered hepatic arteriograms, suggesting a decreased arterial blood flow associated with an increased venous blood flow from the portal system. A significantly reduced serum concentration of total T4 (but not free T4) was only found in the cirrhotic patients. Compared to CHES groups I and II, CHES group III patients and the non-CHES cirrhotics had significantly lower mean serum T3 levels of 80 ± 12 and 52 ± 8 ng/dl, respectively. The serum rT3 concentration was elevated (69 ± 6.2 ng/dl) only in the cirrhotic patients. Both basal and peak TSH levels after TRH were within the normal range for all 4 groups of patients. The basal (40.7 ± 8.3 ng/ml) and peak (85.5 ± 13.7 ng/ml) serum PRL levels T4-binding globulin after TRH administration were only elevated in the cirrhotic group. Although the mean Trbinding globulin values were lower in CHES group III (17.5 ± 3.2 μg/ml) and in the non-CHES cirrhotic group (18.3 ± 2.1 μg/ml) compared to those in groups I (21.8 ± 2.2 μg/ml) and II (20.4 ± 2.3 μg/ml), the differences between groups were not statistically significant. It was concluded that hemodynamic changes without parenchymal failure have little, if any, effect on the hepatic T4 5'-monodeiodination to T3, and that the low T3 and high rT3 state does not modify the pituitary secretion of TSH, presumably by a local (at the thyrotroph level) normal conversion of T4 to T3, even at very low peripheral T3 concentrations.