Endocrine Abstracts

Case-1: Nineteen years old nursing student with primary hypothyroidism, despite thyroxine (T₄) at 200 μg/day and subsequent trial of T₄+T₃, remained significantly symptomatically hypothyroid. Over 4 years worsening hypothyroidism was evident (TSH: 19.1 to >200 and fT₄ 2.1–6.8) despite dose/regime changes. Investigations for malabsorption: normal coeliac screen, B12, ferritin, FBC, kidney and liver function, autoimmune profile, hydrogen breath test, upper-GI endoscopy/D2-biopsy, and barium meal/follow-through, with folate and vitamin-D deficiency (20 nmol/l). Through this period, she completed her degree. Later fulltime work marred by several periods of illness requiring time off.

Assay interference with heterophile antibodies was excluded. A ‘thyroid absorption test’ (TAT) – baseline TFTs, supervised administration of oral thyroxine 200 μg, and post-dose TFTs (see Table) all repeated a week later with T₄ 1000 μg – demonstrated poor absorption and need for high doses to achieve adequate serum levels.

Thyroxine 600–1000 μg daily, then alternate days caused hyperthyroidism (fT₄=27–95). Consequent dose reduction (any dose <500 μg) caused hypothyroidism. She is now having parenteral thyroxine 200 μg i.m. every 3 days with significantly improved quality of life and TFTs. Of note is a strong family history of hypothyroidism and maternal grandmother also being on parenteral thyroxine.

Case-2: Thirty years old Ex-army chef, primary hypothyroidism diagnosed during pregnancy 9 years prior. Gradually increasing dose of T₄ to 1000 μg with suboptimal TFTs. Tests for malabsorption negative. TAT showed good absorption for both 200 and 1000 μg doses. Advised to reduce T₄ to 200 μg/day.

Conclusions: ‘TAT’ is useful in selected cases of hypothyroidism. We have demonstrated that selective thyroxine malabsorption can occur. The exact underlying defect is currently unknown and treatment can prove challenging.