Acute pericarditis associated to onset of diabetes mellitus

Acute pericarditis, an inflammatory process involving the pericardium, is a common condition occurring in association with other diseases and may be the first sign of an underlying systemic disease. In the United States, acute pericarditis occurs in approximately 1 out of each 1000 hospital admissions and in 1% of all patients admitted to the emergency room with chest pain and elevated ST in the electrocardiogram (ECG).¹ A number of infectious and non-infectious causes, including systemic diseases, may be responsible for this condition.² Acute pericarditis is more common in males than in females, and in adults as compared to children.³ The case of a patient diagnosed with acute pericarditis at the onset of diabetes mellitus is reported below.

A 31-year-old male patient with an unremarkable medical history reported polydipsia, polyuria, and asthenia over the preceeding 20 days. In the previous week he had also experienced palpitations and stabbing chest pains unaffected by changes in posture and of increasing severity, which led him to attend the emergency room. Physical examination revealed blood pressure levels of 120/75 mmHg and a heart rate of 85 beats per minute. Cardiopulmonary auscultation revealed no cardiac murmurs or pericardial rub. Laboratory tests showed leukocytosis without neutrophilia (WBCs 14,000, with 68% neutrophils). Venous glucose level was 480 mg/dL, and the results of all other laboratory tests were as follows: creatinine 1.3 mg/dL, creatinine kinase (CK) 4020 IU/L (normal range 55–170 IU/L), CK-MB 2.42 ng/mL (normal value less than 3.6 ng/mL), and troponin I < 0.012 ng/mL (cut-off value for myocardial infarction < 0.12 ng/mL). Venous blood gas test results included: pH 6.93, pCO₂ 29 mmHg, pO₂ 19 mmHg, and bicarbonate 6.1 mEq/L (normal range 20–24 mEq/L). Urine examination revealed ketone bodies. Based on a diagnosis of onset of diabetes mellitus with ketoacidosis, treatment was started with continuous insulin infusion and intravenous hydration, which improved blood glucose levels and metabolic acidosis. ECG showed sinus rhythm with left axis deviation and diffuse concave ST segment elevation. Chest X-rays showed no changes in pulmonary fields or the mediastinum. Because of the findings of elevated CK in laboratory tests and ECG changes, an echocardiogram was performed, which showed a non-dilated left ventricle with a 60% ejection fraction. No pericardial effusion was found, but pericardial refringence was seen. The patient was diagnosed with acute pericarditis associated with diabetic ketoacidosis and, after evaluation by the cardiology department, treatment was started with colchicine and ibuprofen, which led to a clinical improvement. A gradual improvement was seen in kidney function, and the creatinine level at discharge was 0.7 mg/dL. The results of other biochemical tests performed were glycosylated hemoglobin 10.7% and negative insulin, tyrosine phosphatase IA2 and Langerhans cell antibodies. Thyroid function was normal. The patient was treated with a basal-bolus insulin scheme, and once stable was discharged on this same insulin scheme and ibuprofen 800 mg every eight hours for one week, in a tapering scheme, and colchicine 1 mg daily for three months. In the first outpatient visit after admission, an improvement was seen in blood glucose level, and rapid action insulin was therefore discontinued. A repeat echocardiogram showed no changes, and an ECG revealed sinus rhythm with 60° axis, normal PR interval, narrow QRS, and early repolarization (dolphin back elevation in the inferior aspect, normal precordial leads). Acute pericarditis was considered to be resolved, and colchicine treatment was therefore discontinued. To date, the patient has not re-experienced cardiac symptoms.

Acute pericarditis may be associated with a number of systemic diseases or may occur as an isolated condition. Its most common etiologies include viruses (adenovirus, enterovirus, cytomegalovirus, and influenza, hepatitis B, and herpes simplex viruses), tuberculosis, uremia, tumors, and autoimmunity.

The most common clinical symptoms and signs of pericarditis include chest pain, pericardial rub, ECG changes (ST segment elevation in all leads or shortening of the PR interval), and pericardial effusion. It is generally considered that at least two of these symptoms or signs should be present before acute pericarditis is diagnosed.⁴

In 1971, Bennet and Blake⁵ first reported seven cases of pericarditis associated with diabetic ketoacidosis. Few cases have been reported in the literature since then. None of the patients reported by Bennet had chest pains, unlike the patient reported here, who had complained of chest pains over the previous week.

ECG changes seen in diabetic ketoacidosis include ST depression, prolongation of the QT interval, T wave changes, and prominent U waves. The reason for these changes has not been fully elucidated, but they are thought to be secondary to metabolic changes and changes in plasma potassium levels,^6,7 which cause dehydration of the pericardial layers.⁸

Medical treatment of acute pericarditis associated with the onset of diabetes mellitus includes water and electrolyte replacement, insulin treatment, and analgesics. Once the internal environment is stable, ECG changes persist for 48–72 h, and this type of pericarditis is therefore considered to be benign in nature.³