Endocrine Abstracts

Introduction: Malabsorption of levothyroxine is an important clinical problem. Changes in gastric pH due to various medical conditions might cause challenges in maintaning normal TSH values.

Case: A forty-nine years old female who has been followed up with a diagnosis of primary hypothyroidism for 12 years admitted to our outpatient clinic with a complaint of unachievement of euthyroidism despite increasing the levothyroxine dose up to 200 mg. He did not have any other chronic disease and was not using any other medication. In laboratory examination, free T3 was 1.14 ng/l (2.3 - 4.2), free T4 was 0.32 ng/dl (0.89 – 1.76) and TSH was 129 mU/l (0.55 – 4.78). Thyroid autoantibodies were markedly high (antithyroglobulin >1000 IU/ml and antithyroid peroxidase antibody >13000 U/ml) and thyroglobulin was <0.20 µg/l Tthyroid ultrasonography showed heterogeneous parenchyma with widespread patchy hypoechoic areas and thin-thick fibrous bands. Free T4 was was measured just before and after the administration of oral levothyroxine 200 mg. Basal, first hour and second hour free T4 were 0.23 ng/dl, 0.29 ng/dl and 0.29 ng/dl, respectively. A malabsorption test was performed with 500 mg levothyroxine. Accordingly, free T4 was 0.40 ng/dl at basal state, 0.41 ng/dl in the first hour, 0.50 ng/dl in the second hour and 0.47 ng/dl in the fourth hour. Thus, free T4 level increased by a maximum of 25%. The patient’s celiac and anti-pariatel cell antibodies were negative. Helicobacter Pylori antigen tested in the stool was detected positive. The patient’s upper gastrointestinal endoscopy revealed antral gastritis and colonoscopy revealed Grade 1 internal hemorrhoids, He was given 1000 mg/day vitamin C. At the third day of vitamin C, serial free T4 levels were measured after ingestion of 250 mg levothyroxine. While basal TSH was 112 mU/l and free T4 was 0.5 ng/dl, free T4 increased to 0.71 ng/dl at the first, 0.80 ng/dl at the second and 0.80 ng/dl at the fourth hour. A maximum increase of 60% in free T4 value was detected.

Conclusion: There are publications in the literature showing that vitamin C corrects abnormalities in serum free T4, T3 and TSH in patients with hypothyroidism and gastrointestinal pathology. Although the mechanism was not explained clearly, it was suggested that decreasing pH via vitamin C might increase the absorption of the drug. Co-administration of vitamin C with L-T4 may be useful in the treatment of patients with high TSH values despite high doses of L-T4.