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Abstract
Background Association between the heart and the thyroid gland has been well-known for 200 years, from hyperthyroidism leading to cardiac arrhythmias and high-output heart failure to cardiovascular diseases in hypothyroidism through accelerated atherosclerosis and endothelial dysfunction. We present a case which demonstrates another conjunction between the heart and the thyroid.
Case Presentation A 32-year-old female presented to the A&E department with chest pain, vomiting, and generalized unwellness. She has been well previously, without any underlying medical disease. Her EWS score was 7 with tachycardia and high fever. Blood results showed microcytic anaemia, leucocytosis and raised C-reactive protein. She was treated for sepsis which later turned out to be infective endocarditis. Blood culture was positive for Staph aureus. The subsequent echocardiogram showed a vegetation of 1.2cm x 0.8cm at the posterior mitral valve (figure 1). Interestingly, she was found to be hyperthyroid from thyroid screening prompted by tachycardia presentation. Thyroid stimulation hormone (TSH) was high <0.01 (0.5–5 μIU/mL). TSH receptor antibodies and thyroid peroxidase (TPO) antibodies were also high. Carbimazole and beta-blocker were initiated. Despite antibiotic therapy, the patient required mitral valve replacement because of the vegetation size, persistently raised inflammatory markers and incompetent mitral valve. Surgical findings include large vegetation on P2 segment of the mitral valve, with deep abscess cavity underneath. She was discharged without further complications and her thyroid status normalized 3 months later with carbimazole.
Discussion Although thyrotoxicosis together with infective endocarditis is a rare presentation, any organ involvement is possible with endocarditis. There have been a few case reports of suppurative thyroiditis or thyroid abscess in infective endocarditis. In our case, there have been no symptoms such as neck pain or swelling and thyroid gland appears normal from CT scan. Presence of TSH receptor antibodies and TPO antibodies suggest autoimmune thyroiditis nature.
Association between autoimmune thyroiditis and infected cardiac valves can be explained by several mechanisms. In Graves’ disease, circulating TSH receptor autoantibodies activate mucopolysaccharide-secreting endothelial cells leading to thickening and myxomatous changes with likelihood of endocarditis in transient bacteremia. Conversely, various infections are suggested to trigger autoimmune thyroid disorders due to the release of sequestered antigens from inflammation and molecular mimicry of the infective organisms. Psychological stress is also a factor known to precipitate autoimmunity. Infective endocarditis reflects both.
Conclusion This case highlights the importance of thyroid investigation in the management of infective endocarditis. It also illustrates the possible association between autoimmune thyroid disease and infective endocarditis.
Conflict of Interest None