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Myxedema coma in a patient with subclinical hypothyroidism.

AbstractBACKGROUND:
Myxedema coma is the extreme manifestation of hypothyroidism, typically seen in patients with severe biochemical hypothyroidism. Its occurrence in association with subclinical hypothyroidism is extremely unusual. We describe a patient with subclinical hypothyroidism who developed clinical manifestations of myxedema coma.
SUMMARY:
A 47-year-old woman presented to our endocrine clinic with complaints of fatigue and biochemical findings of subclinical hypothyroidism. She was started on treatment with thyroxine (T4) but remained unwell and was later admitted to hospital with hormone profile showing persisting subclinical hypothyroidism (elevated thyrotropin and normal free T4 [FT4] and free triiodothyronine [FT3]): FT4 10.7 pmol/L (reference range 10.3-24.5), FT3 2.7 pmol/L (reference range 2.67-7.03), and thyrotropin 6.09 mU/L (reference range 0.4-4.0). She subsequently developed hypothermia (temperature 33.2°C), circulatory collapse, and coma. Biochemical profile showed hyponatremia, elevated creatinine phosphokinase, metabolic acidosis, and renal failure. An echocardiogram revealed a moderate-sized pericardial effusion. We diagnosed myxedema coma and started treatment with intravenous T3. She responded dramatically with improvement in level of consciousness and normalization of metabolic parameters. We found no explanation other than hypothyroidism to account for the presentation. Adrenocorticotrophic hormone (ACTH) stimulation tests excluded adrenal insufficiency, and serum gonadotrophins were within the normal reference range. FT4 estimation by equilibrium dialysis excluded analytical interference, and molecular analysis for the thyroid hormone receptor β gene associated with thyroid hormone resistance was negative.
CONCLUSIONS:
To the best of our knowledge this is the first report of myxedema coma in a patient with subclinical hypothyroidism. The reason for normal thyroid hormone levels is unclear but may reflect deviation from a higher pre-morbid set-point. The case highlights the importance of careful clinical evaluation in patients with disparate clinical and laboratory findings.
AuthorsAkhila Mallipedhi, Hamza Vali, Onyebuchi Okosieme
JournalThyroid : official journal of the American Thyroid Association (Thyroid) Vol. 21 Issue 1 Pg. 87-9 (Jan 2011) ISSN: 1557-9077 [Electronic] United States
PMID21058937 (Publication Type: Case Reports, Journal Article)
Chemical References
  • Thyroid Hormone Receptors beta
  • Thyroid Hormones
  • Triiodothyronine
  • Adrenocorticotropic Hormone
Topics
  • Adrenocorticotropic Hormone (blood)
  • Coma (complications, drug therapy)
  • Echocardiography (methods)
  • Female
  • Humans
  • Hypothyroidism (complications)
  • Middle Aged
  • Myxedema (complications, drug therapy)
  • Thyroid Function Tests
  • Thyroid Hormone Receptors beta (genetics)
  • Thyroid Hormones (blood)
  • Treatment Outcome
  • Triiodothyronine (therapeutic use)

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