[Hyperthyroxinemia and clinical euthyroidism. Report of one case]

Area of Science:

• Endocrinology
• Genetics
• Clinical Chemistry

Background:

• Euthyroid hyperthyroxinemia, characterized by elevated thyroxin with normal thyroid-stimulating hormone (TSH) and no clinical hyperthyroid signs, is a recognized clinical entity.
• This condition often involves alterations in thyroid hormone transport proteins.
• Understanding the underlying causes is crucial for accurate diagnosis and management.

Observation:

• A case report of an asymptomatic 28-year-old male with significantly elevated serum total thyroxin (18.5 µg/dL) and free thyroxin (2.9 ng/dL).
• Thyroid-stimulating hormone (TSH) levels were within the normal range (3.4 µIU/mL), and triiodothyronine was 128 ng/dL.
• Standard laboratory tests ruled out high thyroxin-binding globulin, albumin, prealbumin, or antithyroxin antibodies.

Findings:

• The patient exhibited an elevated thyroxin-binding capacity of albumin (58.2 µg/dL), significantly exceeding the normal range (11.5–34.1 µg/dL).
• Thyroid-stimulating hormone (TSH) demonstrated normal responsiveness to thyrotropin-releasing hormone (TRH) stimulation.
• Exogenous triiodothyronine administration suppressed TSH and induced a hyperthyroid syndrome, confirming the thyroid axis's integrity.

Implications:

• The findings strongly suggest familial dysalbuminemia as the cause of the observed euthyroid hyperthyroxinemia.
• This case underscores the necessity of evaluating thyroid hormone-binding proteins in patients presenting with unexplained elevations in thyroxin levels.
• Accurate identification of familial dysalbuminemia prevents misdiagnosis of hyperthyroidism and unnecessary treatment.