Viscoelastic properties of human whole blood were measured in 338 subjects: 110 persons (75 F, 35 M) following total thyroidectomy but without substitution therapy over three weeks as well as 228 healthy control subjects (124 F, 104 M) were investigated in this study. Subjects with other variable factors were excluded. The viscous and the elastic portion of apparent whole blood viscosity -the latter subdivided into red cell aggregation and red cell rigidity were determined by using a newly developed oscillating capillary rheometer and densitymeter at the real hematocrit value and at a computed hematocrit of 40%. Serum viscosity, hematocrit (Hct), hemoglobin (Hb), mean corpuscular volume of red blood cells (MCV), free triiodothyronine (fT3), free thyroxine (fT4) and serum-thyrotropin (bTSH) were evaluated as well. In a further subgroup of 80 subjects (40 patients with hypothyroidism, 40 healthy control persons) additional plasma viscosity and sedimentation rate were determined. Red cell aggregation and blood viscosity especially at shear-rates below 10/sec increased significantly in hypothyroid patients. There was no significant difference of red cell rigidity, serum viscosity, plasma viscosity and sedimentation rate as against euthyroids. So new aspects of thyroid dysfunction could be described probably with consequences for therapy and for considerations about the development of atherosclerosis and ischemic disorders.
This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/ATSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.
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