Endocrine Abstracts

Introduction: Hypothyroidism remains a global problem with prevalence of 1–2% in iodine replete areas of the world. Primary or Autoimmune Hypothyroidism remains the most common type of hypothyroidism worldwide. Central (secondary) hypothyroidism (CH) because of pituitary/hypothalamic disorders is a rare cause of hypothyroidism with reported prevalence of 1:20.000 to 1:80.000 in the general population¹. This makes CH about 1000 fold rarer than primary hypothyroidism. We present an interesting case of a young female who initially presented with biochemical features of autoimmune primary hypothyroidism and subsequently developed isolated central hypothyroidism (ICH) with concomitant Thyroxine malabsorption.

Case report: A 45-year old female patient presented with clinical features of hypothyroidism. Biochemistry showed TSH 5.29 mIU/l & free T4 11.4 pmol/l with strongly positive TPO antibodies (> 1000) suggesting primary autoimmune hypothyroidism. Despite being on increasing doses of Levothyroxine, she remained symptomatic. Serial TFTs showed suppressed value of both TSH & free T4. The results were cross checked by sandwich Delfia assay in a different laboratory which showed consistent pattern of TFTs ruling out assay interference. Further investigations, including full pituitary hormones profile, Short Synacthen Test and MRI pituitary were normal apart from suppressed TSH and low T4 which is indicative of Isolated Central Hypothyroidism. Despite adequate Thyroxine replacement, her free T4 level remained low. Her Coeliac and malabsorption screens were normal. She had supervised Oral Thyroxine absorption test (with 700 mg of Levothyroxine) but subsequent serial measurements of free T4 levels failed to rise above 8.7 pmol/l (Normal range 12–22 pmol/l). As a consequence, patient was offered even higher dose Thyroxine replacement and planned for trial of intravenous thyroxine but she chose to move her care to a different hospital.

Discussion: This is a very rare case of primary hypothyroidism which later transformed into central hypothyroidism of unknown aetiology and also developed Thyroxine malabsorption. If relied solely on the TSH level, the primary care practitioners can be caught out by the persistently low TSH being perceived as Thyroxine over replacement and potentially inadvertently reducing the Thyroxine dose and delay in diagnosis of central hypothyroidism. This leads to a question whether T4 should be routinely tested even for diagnosis and monitoring of all patients with suspected hypothyroidism.

Reference

1. Price A, Weetman AP, Screening for central hypothyroidism is unjustified. BMJ 2001 322 798.