Endocrine Abstracts

Introduction: Myxedema coma is the end stage of untreated or inadequately treated hypothyroidism. It has an estimated incidence of 0.22 per million per year. The clinical picture is often that of an elderly obese female, presenting in midwinter with increased lethargy, somnolence and confusion. The presentation is one of severe hypothyroidism, with or without coma.

Such cases are predominantly based on a primary thyroid disorder such as Hashimoto′s thyroiditis. However, the underlying cause in approximately 5% of myxedema cases is hypothalamic or pituitary disease, where the patient usually lacks multiple anterior pituitary hormones, including thyroid-stimulating hormones (TSH).

Case study: A 69 years old male presents to the ER with dizziness, headache, postural instability, bradylalia and bradypsyhia symptoms that appeared 1 week prior. A stroke diagnosis was suspected and a cerebral CT scan was made showing a 22/21/38 mm pituitary adenoma with suprasellar extension. Laboratory tests showed high creatine kinase (4459 U/l) and LDH (591 U/l) and low natrium (122 mmol/l). He was then transferred to our clinic.

General examination revealed bradylalia, bradypsyhia, dry, coarse skin, hoarse voice, thin scalp and eyebrow hair with little to no body hair. Laboratory tests showed low values for FT4 (<0.3 ng/dl), TT3 (<40 ng/dl) low values for IGF1 (43.92 ng/ml), FSH (0.683 mIU/ml), LH (<0.1 mIU/ml), morning cortisol (1.06 microg/dl), ACTH not available and high prolactin (1772 ng/ml) but high thyroglobulin antibodies (>4000 IU/ml), and less than predicted high TSH (41.8 microUI/ml), TPO antibodies not available. The patient had prolonged QT interval on ECG and minimal pericardial effusion and minimal ventricular dyskinesia on cardiac ultrasonography.

We started treatment with L-thyroxine, corticotherapy and cabergoline with clinical improvement.

Conclusion: A male patient diagnosed with myxedema coma of both primary (Hashimoto′s thyroiditis) and secondary origin (macroprolactinoma with associated panhypopituarism) with high creatin kinase and non-classical presentation is treated with hormonal replacement therapy and dopamine receptor agonist with favorable evolution.

Key words: myxedema coma, primary and secondary origin, prolactinoma