Q J Med 2002; 95: 188-189
© 2002 Association of Physicians
Correspondence |
Pericardial disease associated with Grave's thyrotoxicosis
Cardiology Department, John Radcliffe Hospital, Oxford
Cardiology Department, Milton Keynes General Hospital, Milton Keynes
Derbyshire Royal Infirmary, Derby
Sir,
Cardiac complications may dominate the clinical picture in the middle-aged and older patient with thyrotoxicosis. A cardiomyopathy with poor resting systolic function, which may or may not be reversible following return to the euthyroid state, has occasionally been described.1,2 Other poorly-understood complications include atrioventricular block and acute ischaemic syndromes, including myocardial infarction in the absence of coronary disease. Transient widespread ST/T wave changes and atrial fibrillation are common in hyperthyroidism. We suggest that pericardial disease may be an unrecognized complication of hyperthyroidism.
Patient 1, a 53-year-old man, presented with clinical features of cardiac tamponade and a pyrexia of 38 °C. Following drainage of a large bloodstained pericardial effusion, a CT scan demonstrated marked thickening of the visceral and parietal pericardium, and cardiac catheterization revealed pericardial constriction. Thyrotoxicosis was suggested by a history of a recent tendency to anxiety and heat intolerance. Carbimazole was commenced in addition to frusemide following biochemical confirmation, and euthyroidism was restored after 2 months. He later underwent successful pericardectomy.
Patient 2, a 35-year-old woman, presented with a 2-month history of pericarditic and pleuritic chest pain, recent breathlessness and a weight loss of 12 kg. Carbimaxole and propranolol had recently been commenced following diagnosis of thyrotoxicosis. Examination revealed breathlessness at rest, emaciation, marked lid lag but no goitre, signs of cardiac tamponade, a pericardial rub, bilateral pleural effusions, an enlarged liver and marked peripheral oedema. Severe Grave's thyrotoxicosis was confirmed and a large pericardial effusion was drained. Anti-thyroid medication was discontinued at 18 months following radio-iodine therapy. Subsequently she remains euthyroid with no recurrence of the pericardial or pleural effusions.
Patient 3, a 54-year-old woman, presented with severe acute anterior pleuritic chest pain, and night sweats for 2 months. Examination revealed pyrexia of 38 °C, fine tremor, rapid atrial fibrillation, third heart sound gallop and a pericardial rub. There was anterolateral concave ST segment elevation on the electrocardiogram. Echocardiography was normal apart from a global pericardial effusion of 1.0 cm. Following confirmation of hyperthyroidism, carbimazole was commenced. After 1 week the flicking pyrexia persisted and the effusion had grown globally to 2.0 cm. There was pericardial thickening, but no features of tamponade. A pericardial biopsy via a mini-thoracotomy revealed thickened fibrotic tissue with areas of marked non-specific granulation tissue. The pericardial fluid was unremarkable. The pericardial effusion and fever resolved following the commencement of indomethacin. Biochemical euthyroidism was achieved 6 weeks after treatment initiation and antithyroid medication was discontinued 10 months later.
Patient 4, a 47-year-old woman, presented with a 2-week history of lethargy and weakness. Examination revealed a listless appearance, pyrexia of 38 °C, fine tremor, small goitre and rapid atrial fibrillation. Blood tests confirmed Grave's thyrotoxicosis, raised inflammatory markers with a low albumin and a corrected calcium of 2.87 mM. Initial treatment included full dose heparin, propranolol and carbimaxole. Anticoagulation was discontinued on the third day following spontaneous reversion to sinus rhythm. At 2 weeks the flicking pyrexia persisted and a pericardial rub was noted. Echocardiography revealed a global 2 cm pericardial effusion, with normal cardiac function and no features of tamponade. The hypercalcaemia and pericardial effusion resolved within 2 months and the carbimazole was successfully discontinued after 12 months.
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All patients were comprehensively investigated for an alternative aetiology of the pericardial disease. Negative or unremarkable results for the following investigations were recorded: multiple blood cultures, urine culture, Mantoux test including culture for tuberculosis of pericardial fluid, pericardial fluid cytology, acute and convalescent serology, antinuclear antibody, anti-neutrophil cytoplasmic antibody and rheumatoid factor.
Grave's disease is the most likely aetiology of the hyperthyroid state in this case series. DeQuervain's thyroiditis is unlikely because of the absence of a markedly raised ESR or thyroid pain. Grave's disease is a multisystem autoimmune disease with occasional complications including diffuse lymphadenopathy and splenomegaly in addition to its association with other autoimmune diseases.
We propose that pericardial disease may be a rare unrecognized complication of Grave's thyrotoxicosis. If so, the pericardial disease may have a similar aetiology to pretibial myxoedema or ophthalmic myopathy. This raises the possibility of steroids as a potential treatment. The severity of the pericardial and systemic illness in these patients and the documentation of signs or symptoms of thyrotoxicosis at the initial presentation makes a chance association unlikely. Occasional cases of pericardial disease have been documented in Grave's disease. Two cases have been described of widespread ST segment elevation with normal coronary arteries, one associated with a pericardial rub.3,4 Another report described two cases of painful pericarditis accompanied by pericardial tamponade, pleural effusions and fever in Grave's disease.5 The authors felt that this was only a coincidence, because of a lack of any previous reports, despite the fact that the principal reason for presentation was aggressive thyrotoxicosis.
Our patients presented either with symptoms of pericardial disease, or non-specific symptoms of fatigue and weakness. In addition to worsening control of angina, heart failure and arrhythmias, presentation with pericardial syndromes should raise the diagnostic suspicion of thyrotoxicosis. Similarly a thyrotoxic patient who is making poor progress on treatment should have an echocardiogram to exclude haemodynamically significant pericardial disease.
References
1. Umpierrez GE, Challapalli S, Patterson C. Congestive heart failure due to reversible cardiomyopathy in patients with hyperthyroidism. Am J Med Sci1995; 310:99–102.[Web of Science][Medline]
2. Ebisawa K, Ikeda U, Murata M, et al. Irreversible cardiomyopathy due to thyrotoxicosis. Cardiology1994; 84:274–7.[Medline]
3.
Sugar SJ. Pericarditis as a complication of thyrotoxicosis. Arch Intern Med1981; 141:1242.
4. Simon D, Boutonnet G, Luton JP, et al. Myocardite d'origine endocrinienne et metabolique a propos de l'observation d'une jeune femme hyperthyroidienne et diabetique. Ann Med Interne1979; 130:703–8.[Medline]
5. Tourniare J, Sassolas G, Touboul P, et al. Tamponade par percardite subaigue au cours de la malade de Basedow. Presse Med1983; 12:1989–90.
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