Endocrine Abstracts (2019) 62 WH8 | DOI: 10.1530/endoabs.62.WH8

More than just a co-incidence? Hyponatremia as the first manifestation of profound Hypothyroidism

Ahmed Al-Sharefi, David Bishop & Ashwin Joshi

Sunderland Royal Hospital, City Hospitals and Sunderland NHS Foundation Trust, Sunderland, UK.

Background: Hyponatraemia is a frequent finding in medical inpatients, where a comprehensive evaluation is warranted to establish the underlying mechanism and guide further management. Whilst the role of confounding medications, syndrome of inappropriate anti-diuretic hormone (SIADH), adrenal insufficiency and polydipsia is well-established as causative factors in the development of hyponatremia, the link between hypothyroidism and hyponatremia is controversial in the medical literature and often described as merely ‘an association ‘rather than a direct causality.

Case Presentation: A 72- years old male was referred to the acute medical unit after a biochemical finding of hyponatraemia. Past medical history included chronic obstructive pulmonary disease (COPD), fibromyalgia, age-related macular degeneration and recent diagnosis of hypertension. He reported fatigue, muscle cramps, constipation, headaches and confusion over the last 6 weeks. His medications included amlodipine, Loratadine and citalopram. He was euvolemic on examination. His initial biochemical panel showed sodium of 125 mmol/l (NR 135–145), serum potassium of 4.2 mmol/l (NR 3.5–5.5), urea 4.0 mmol/l (NR 2.5–7.8), creatinine of 101 umol/l (NR 60–105). Citalopram was stopped and he was commenced on 1L fluid restriction. However, his biochemistry failed to improve after 3 days and an endocrinology referral was requested. Further investigations showed a 9.00 am cortisol of 307 nmol/l (NR of 172–497),thyroid stimulating hormone (TSH) of 85 mIU/l (NR 0.5–3 mIU/l), free Thyroxine (Free T4) of <3.0 pmol/l (NR 10–22) with undetectable Free T3 levels. His Thyroid peroxidase antibodies were raised at 83.6 kU/l (NR 0–34) confirming the diagnosis of primary autoimmune hypothyroidism. The patient was prescribed Levothyroxine at a starting dose of 50 mcg once daily and with further up titration of the dose, his symptoms and biochemistry normalised in 8 weeks’ time.

Conclusion: Though perceived as an incidental association, our case demonstrates that hyponatremia could be the first presenting sign of severe hypothyroidism. Serum TSH measurement is a reliable and rapid tool to screen for unrecognized hypothyroidism in the context of hyponatraemia with the potential (subjective to optimisation of all other confounding factors), to achieve normalisation of serum sodium with Levothyroxine therapy.

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