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• Adrenal function also needs to be evaluated in hypothyroidism-related pericardial effusion(revised version of my recent rapid response)
  oscar,m jolobe
  Published on: 7 April 2019

• Published on: 7 April 2019

  Adrenal function also needs to be evaluated in hypothyroidism-related pericardial effusion(revised version of my recent rapid response)

  • oscar,m jolobe, retired geriatrician manchester medical society

  Under the "diagnosis" heading the authors asserted that "hypothyroidism can be deemed the aetiology of pericardial effusion or cardiac tamponade if a high TSH level has been found, after excluding other secondary causes like a neoplastic, bacterial or an inflammatory process"(1).. I would add that, if the patient's hypothyroidism is of autoimmune aetiology, Addison's disease is a secondary cause that also requires urgent exclusion(2).
  In one report, a 21 year old man presented with cardiac tamponade, in association with a TSH level of 17.9 microUnits/L(normal range 0.35-5.0 microUnits/L), and serum thyroxine and serum tri-iodothyronine levels which were both at the lower limit of the normal range. Serum cortisol, however, was 0.5 micrograms/dl(normal range 3.0-23.0 mcd/dl). Tests for thyroid and adrenal autoantibodies were positive, thereby fulfilling the criteria for Type 2 autoimmune polyglandular syndrome(Type-2 APS).
  Comment
  On the basis of the above observations the work-up of patients with pericardial effusion of presumed hypothyroid aetiology should include evaluation of adrenal function, because Addison's disease can, in its own right, be the underlying cause of cardiac tamponade(3). Furthermore, irrespective of hormonal status, pericardial effusion in a patient with Type 2 APS may ultimately be attributable to the "serositis" component of that syndrome, rendering the effusion capable of relapsing...

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  Under the "diagnosis" heading the authors asserted that "hypothyroidism can be deemed the aetiology of pericardial effusion or cardiac tamponade if a high TSH level has been found, after excluding other secondary causes like a neoplastic, bacterial or an inflammatory process"(1).. I would add that, if the patient's hypothyroidism is of autoimmune aetiology, Addison's disease is a secondary cause that also requires urgent exclusion(2).
  In one report, a 21 year old man presented with cardiac tamponade, in association with a TSH level of 17.9 microUnits/L(normal range 0.35-5.0 microUnits/L), and serum thyroxine and serum tri-iodothyronine levels which were both at the lower limit of the normal range. Serum cortisol, however, was 0.5 micrograms/dl(normal range 3.0-23.0 mcd/dl). Tests for thyroid and adrenal autoantibodies were positive, thereby fulfilling the criteria for Type 2 autoimmune polyglandular syndrome(Type-2 APS).
  Comment
  On the basis of the above observations the work-up of patients with pericardial effusion of presumed hypothyroid aetiology should include evaluation of adrenal function, because Addison's disease can, in its own right, be the underlying cause of cardiac tamponade(3). Furthermore, irrespective of hormonal status, pericardial effusion in a patient with Type 2 APS may ultimately be attributable to the "serositis" component of that syndrome, rendering the effusion capable of relapsing or remitting irrespective of concurrent hormone replacement therapy(4).
  An important caveat to interpretation of raised TSH levels is that, in the presence of primary hypoadrenalism, a raised serum TSH does not necessarily signify coexistence of primary hypothyroidism. On its own, primary hypoadrenalism can cause elevation of serum TSH which reverts to the normal range during the course of corticosteroid replacement therapy(5). In the latter report a 26 year old man with Addison's disease had a documented pretreatment serum TSH of 32 microUnits/L. Over a 2 year period of corticosteroid replacement therapy his serum TSH progressively fell to 2.5 microUnits/L, without concomitant thyroid replacement therapy. During that period both his serum thyroxine and serum tri-iodothyronine levels remained well within the normal range(5).
  Finally, even in the presence of the coexistence of raised serum TSH and subnormal serum thyroxine clinicians should remain vigilant for type 2 APS, notwithstanding the fact that an identical biochemical scenario was depicted by the authors of the clinical vignette(1). In one case report a 24 year old man had a diagnosis of primary hypothyroidism characterised by serum thyroxine 40 nmol/L(normal 60-140 nmol/L), tri-iodothyronine 1.2 nmol/L(normal 1.6-3.0 nmol/L), and serum TSH 90 microUnits/L. However, he deteriorated after commencing thyroid replacement therapy, and this deterioration proved to be attributable to coexisting Addison's disease. Thyroxine was stopped, and he received corticosteroid replacement therapy instead. Over a period of 18 months of corticosteroid replacement therapy he experienced clinical improvement, and his thyroid function tests reverted to the normal range without the benefit of concomitant thyroid replacement therapy(6).
  References
  (1)Chahine J., Ala CK., Pantalone KM., Klein AL
  Pericardial diseases in patients with hypothyroidism
  Heart 2019;0:1-7,doi 10.1136/heartjnl-2018-314528
  (2) Bacal A., Mathew G., Pyle J., Pauwaa S., Kazi M
  Cardiac tamponade as initial presentation of autoimmune ployglandular syndrome type 2
  AACE Clinical Case Reports 2018;4:e195-e198
  (3) Torfoss D., von der Lippe E., Jacobsen D
  Cardiac tamponade preceding adrenal insufficiency-an unusual presentation of Addison's disease: a report of two cases
  Journal of Internal Medicine 1997;241:525-528
  (4) Tucker WS., Niblack GD., McLean RH., Alspaught MA., Wyatt RJ., Jordan SC et al
  Serositis with autoimmune endocrinopathy: Clinical and immunogenetic features
  Medicine 1987;66:138-147
  (5) Candrina R., Giustina G
  Addison's disease and corticosteroid-reversible hypothyroidism
  J Endocrinol Invest 1987;10:523-524
  (6) Burrows AW
  Reversible hypothyroidism after steroid replacement for Addison's disease
  Postgrad Med J 1981;57:368-370

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  Conflict of Interest:
  None declared.

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