Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 19 P365

York Hospital, York, UK.

Context: Respiratory failure as a component of severe hypothyroidism has high mortality and a number of pathological mechanisms have been proposed. These range from cerebral causes to neuromuscualr and pulmonary factors. Changes due to mucopolysacharide deposition in the lungs is another postulated mechanism, but radiological changes are hitherto not clinically demonstrated.

Objective: A case of hypothyroidism with hypoxia associated with CT features suggestive of pulmonary fibrosis that resolved with correction of hypothyroidism.

Case summary: Case 1 (HW) is a 68-year-old lady with symptomatic severe hypothyroidism (free T4 (fT4) of 0.54 ng/dl (7.0 pmol/l, normal 10–30 pmol/l) and thyroid stimulating hormone (TSH) above measurable limits (> 50 mU/l, Normal=0.40–4.00 mU/l with high titres of anti-TPO antibody (212 IU/ml, normal 0–100 IU/ml)) associated with respiratory failure. Having presented with classic hypothyroid symptoms, her chest X-ray and CT Thorax organised to investigate hypoxia (PO2 of 47.36 mmHg (6.3 kPA), PCO2 of 28.64 mmHg (3.81 kPa)) showed appearances suggestive of pulmonary fibrosis. There were no signs of infection or cardiac failure.

Replacement therapy with levothyroxine led to correction of hypoxia and radiological abnormalities. Follow-up CT scan at four months showed resolution of fibrotic appearance. She remains clinically and biochemically euthyroid on levothyroxine replacement therapy and has normal oxygen saturations on room air.

Conclusions: Respiratory failure in myxoedema is multi-factorial. Radiological pulmonary abnormalities suggestive of fibrotic disease could be associated with severe hypothyroidism. Invasive investigations like lung biopsy could be deferred until the response to thyroxine replacement is assessed.

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