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A rise in troponin is usually diagnostic of myocardial damage, but there are exceptions.
A man aged 51 attended the accident and emergency department after three days of right upper quadrant pain associated with nausea, vomiting and rigors. His stools had become pale and his urine was darker than normal. There was no chest pain and he had no risk factors for coronary artery disease. His temperature was 38.5°C. Cardiorespiratory examination was unremarkable and he was haemodynamically stable. The abdomen was tender with guarding in the right upper quadrant and Murphy's sign was positive. The clinical diagnosis was acute cholecystitis. Haemoglobin was 15.0 g/dL and white cell count 17.4 × 109/L (neutrophils 14.6). Renal function was normal. Alkaline phosphatase was raised at 356 IU/L (normal 70-330) and bilirubin at 34 μmol/L (0-22) but other liver function tests were normal. C-reactive protein was 165 mg/L (<5). Ultrasound of the abdomen revealed a thickened gallbladder full of echogenic debris; the liver, pancreas, spleen and kidneys were all normal. Peripheral blood cultures (two sets) taken at the time of admission were negative.
He was initially managed with intravenous antibiotics and fluids and made good progress. He then developed an expiratory wheeze. Chest radiography was unremarkable. To exclude a cardiac event serial electrocardiograms were also performed, despite the absence of chest pain, and these showed sinus rhythm without any signs of ischaemia. Troponin T, however, proved to be raised at 0.25 μg/L (normal <0.03)—a result that prompted transthoracic echocardiography, which was normal. Over the next forty-eight hours he improved, with all inflammatory markers and pyrexia subsiding. Coronary angiography was then undertaken, which showed no abnormality; left ventricular function was also normal.
The raised troponin T in this patient was not a consequence of myocardial ischaemia and there was no clear evidence of myocarditis. Probably, therefore, it was related to his cholecystitis. We have found only one previous report of such a case,1 on that occasion with troponin I.
Cardiac troponins T and I are the most sensitive and specific serum markers of myocardial cell injury and have revolutionized the diagnosis of myocardial infarction and acute coronary syndromes. They have now superseded creatine kinase and creatine kinase MB as the gold standard for the detection of non-ST segment elevation acute coronary syndromes.2 Both the American College of Cardiology3 and European Society of Cardiology4 have accepted troponin measurements as a key part of the diagnostic work-up in such patients. Increases in troponin are most commonly related to ischaemic myocardial cell injury/necrosis caused by acute coronary syndromes, and are now one of the commonest indications for urgent coronary angiography. The other documented causes of troponin increases can be broken down into two groups. Non-ischaemic cardiac causes include myocarditis and myopericarditis, pulmonary embolism (troponin rise secondary to acute right heart strain), acute heart failure, cardiotoxic drugs (e.g. doxorubicin), radiofrequency ablation, prolonged tachycardia and septicaemia/septic shock. Increases without apparent cardiac injury are seen in some patients with established chronic renal failure. In one recent study a raised troponin concentration in end-stage renal disease was an independent risk factor for mortality.5
In this case the patient had cholecystitis but no evidence of septic shock, and blood cultures were negative. He seemed in good cardiac health. Both ST segment depression and T wave inversion have been recorded in acute cholecystitis,6 but these were absent here. We surmise that the cholecystitis itself, or the systemic inflammation (which may have been associated with transient bacteraemia despite the negative blood cultures), led to release of troponin from the myocardium.