Parvovirus B19 Infection and Unusually High Troponin-I Levels in a Child with Duchenne Muscular Dystrophy: A Rare Coexistence or A Possible Association?

Introduction

Duchenne muscular dystrophy (DMD) is an X-linked progressive muscular disease, not a bone disease. Clinical manifestations of DMD are progressive cardiomyopathy, and muscle weakness (Mah JK et al., Neuromuscul Disord 2014; 24(6): 482–491). The molecular cause of DMD is a mutation in the dystrophin gene, which leads to disruption in the sarcolemma of both cardiomyocytes and skeletal myofibers, ultimately affecting muscle cell integrity [Bushby K et al., Lancet Neurol 2010; 9(1): 77–93]. The primary characterization of DMD is the rapid deterioration of the skeletal muscles. There have been many reported cases of co-occurrence of DMD and cardiac involvement. Cardiac involvement most commonly manifests as lateral wall fibrosis due to ongoing inflammation [Mavrogeni S et al., Int J Cardiol 2009; 132(3): e123–e124]. Acute myocarditis may mimic the early cardiac symptoms of cardiomyopathy, further complicating diagnosis in DMD patients [Veronese G et al., Anatol J Cardiol 2018]. Cardiomyopathy in DMD is a direct result of progressive myocardial fibrosis, not typically triggered by viral myocarditis [Karcic A, Conrad AR, N Engl J Med 2000; 343: 299–300]. However, acute myocarditis is rarely presented in DMD patients. The diagnosis of acute myocarditis can be made based on the findings of cardiac MRI and noninvasive tests. Chronic elevation of cardiac Troponin T has been observed in DMD patients, but Troponin I, a cardiac-specific biomarker, is typically not elevated in this population unless there is concurrent myocarditis (Barthel BL et al., Muscle Nerve 2021; 64(1): 43–49). Specifically, troponin T may be chronically elevated in DMD patients due to skeletal muscle involvement, while troponin I remains a specific marker for cardiac injury and is typically only elevated in cases of acute myocarditis or myocardial infarction. Elevated Troponin I in DMD patients may therefore indicate an underlying viral infection, which can contribute to myocarditis or other forms of cardiac stress.

Case Report

A 13-year-old boy with Duchenne muscular dystrophy (DMD) due to a deletion of exons 45 to 50 in the DMD gene was diagnosed in the Department of Medical Genetics at the age of eight years. The patient was admitted to the ED due to heavy chest pain. His physical examination in the ED revealed he was afebrile; his heart rate was 97 bpm, his blood pressure was 120/65 mm Hg, and he had 97% oxygen saturation on room air. His cardiac examination was normal, with no abnormal sound or murmur. His pulmonary examination revealed normal auscultation, his jugular venous pressure was normal, and no extremity edema was detected. A complete blood count revealed WBC: 13,400/mm³, Hemoglobin: 12.2 g/dL Hematocrit: 36.2%, Platelets: 354,000/mm³, CRP: 0.53 mg/dL (normal<5 mg/L), Troponin I: 7454.4 ng/mL (normal<0.04 ng/mL), CK-MB: 60 U/L, CK: 1088 U/L The patient was transferred to the Department of Pediatric Cardiology for further examination. ECG was normal. There was no pathology on the echocardiographic examination. Left ventricular ejection and shortening fraction were measured at 60% and 30, respectively. Even though the patient's general condition was normal, the patient was still monitored for rhythm abnormalities. Enterovirus RNA was identified by PCR. Other viral panels were unremarkable and thus omitted. Given his elevated Troponin I levels, the patient was admitted to the pediatric ward for close monitoring.

On the first day of hospitalization, Troponin I levels increased gradually to 36,950 ng/mL) ( the normal range should be between 0 and 0.04 ng/mL). Intravenous immunoglobulin (IVIG) treatment was administered at 400 mg/kg/dose over a 12-hour infusion. Following the infusion, Troponin I levels rose to 64,486 ng/mL. ([Tab. 1]). Cardiac magnetic resonance (MRI) was done on the patient to clarify the etiology. Cardiac MRI revealed anterior, anterolateral, and inferolateral wall myocardial edema with elevated T2 values and late gadolinium enhancement (LGE) in the basal to mid inferolateral walls consistent with acute myocarditis ([Fig. 1] [2]). Also, parvovirus B19 IgM was detected as positive. He was diagnosed with acute myocarditis due to clinical and laboratory findings. The same IVIG dose was continued for two more days, and non-steroid anti-inflammatory treatment (ibuprofen 2×400 mg) was started. No echocardiographic deterioration or arrhythmia occurred. A continuous decline in Troponin I was noted. By day 7, the patient was symptom-free. By day 10, he was discharged with Troponin I levels of 500 ng/mL and improved condition.

Fig. 1 Cardiac magnetic resonance (CMR) imaging revealed anterior, anterolateral, and inferolateral wall myocardial edema with elevated T2 values and the presence of late gadolinium enhancement (LGE) in the basal to mid inferolateral walls consistent with acute myocarditis.

Fig. 2 Cardiac magnetic resonance (CMR) imaging revealed anterior, anterolateral, and inferolateral wall myocardial edema with elevated T2 values and the presence of late gadolinium enhancement (LGE) in the basal to mid inferolateral walls consistent with acute myocarditis.

Tab. 1 The course of Troponin I and CK-MB levels during hospitalization:

Day Since Admission	Troponin I (ng/mL)	CK-MB (U/L)
0	7,454.4	60
1	36,950	75
2	64,486	90
3	50,000	70
7	3,000	50
10	500	40

Trend Summary: Troponin I peaked on Day 2 and declined progressively thereafter, correlating with clinical improvement. CK-MB followed a similar, though less dramatic, trend.

 

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Publication History

Article published online:
31 July 2025