Effect of Levothyroxine Replacement on Cognitive Function Impairment in a Sample of Egyptian Population with Subclinical Hypothyroidism

Introduction: Subclinical hypothyroidism (SHT) is characterized by a normal range of free thyroxin concentrations together with increased serum TSH levels. SHT is defined as serum thyroid-stimulating hormone (TSH) concentration above the upper limit of the reference range in the face of normal free FT4 and FT3 levels. The effect of SHT on cognitive function has been investigated in several preclinical studies, and a growing body of evidence has suggested a relevant link between thyroid hormones and the central nervous system. Objectives: This study aimed to investigate the effect of levothyroxine replacement on cognitive impairment in a sample of Egyptian patients with SHT. Methods: A prospective cohort study conducted on 30 patients with cognitive impairment and SHT attending an endocrine outpatient clinic at the Ain Shams University Hospital to study the effect of levothyroxine supplementation on cognitive impairment in patients with SHT. The study was conducted on 30 patients. All participants were subjected to a full history taking; thorough clinical examination; laboratory investigations including thyroid profile (FT3, FT4, TSH), anti-thyroid peroxidase antibodies, anti-thyroglobulin antibodies, and lipid profile; imaging tests as neck ultrasound, echocardiography, and carotid duplex; and finally Addenbrooke’s questionnaire used to diagnose mild cognitive impairment. Results: A highly statistically significant difference was found before, 3 months and 6 months after treatment with levothyroxine regarding all clinical data, TSH, LDL, T. cholesterol, FT3, FT4 and HDL, carotid intima-media thickness, and Addenbrooke’s questionnaire. Our study showed a statistically significant inverse correlation between TSH level and mild cognitive impairment before and after treatment with levothyroxine at 3 and 6 months intervals as when TSH increased, results of Addenbrooke’s questionnaire decreased and, so, cognitive impairment increased, while when TSH decreased in response to thyroxine replacement, cognitive impairment improved as detected by an increase in the patient’s score. Conclusion: SHT has a great effect on cognitive impairment, as normalization in TSH level results in improvement in cognitive function. Also, there was a significant reduction in carotid intima-media thickness, which may contribute to improvement of cognitive function in addition to a great improvement in lipid profile, which in turn positively affects cardiac and cognitive function.