Hyperthyroidism and fulminant myocarditis in an adolescent with iodine-induced hyperthyroidism: A case report

Abstract

This paper describes the case of a 15-year-old male patient who exhibited chest distress and pain following an upper respiratory tract infection. Upon admission, the patient exhibited elevated levels of myocardial enzymes and troponin I. Electrocardiography revealed an acute inferior myocardial infarction. Coronary computed tomography angiography ruled out coronary stenosis; however, cardiac magnetic resonance imaging revealed myocardial congestion and edema. Subsequent examinations revealed increased thyroid hormone levels and decreased thyroid-stimulating hormone levels, which is consistent with the manifestations of hyperthyroidism. The patient was diagnosed with acute fulminant myocarditis accompanied by iodine-induced hyperthyroidism. The patient received no pharmacologic treatment for hyperthyroidism but was prescribed a low-iodine diet, medication, and supportive treatment. His myocardial enzymes and troponin I levels gradually decreased, his electrocardiography and echocardiography results improved, and his cardiac function returned to normal. The patient was discharged and advised to maintain a low-iodine diet. At the 6-month follow-up, the patient’s thyroid function and cardiac indicators had returned to normal. This case demonstrates that myocardial injury can result from myocarditis and iodine-induced hyperthyroidism and highlights the importance of closely monitoring and assessing thyroid function during treatment.

Introduction

Myocarditis is a complex inflammatory disease usually resulting from viral infections that selectively involve the myocardium or autoimmune processes. ¹ Fulminant myocarditis (FM) is a rare syndrome characterized by sudden and severe diffuse cardiac inflammation that often leads to cardiogenic shock, ventricular arrhythmias, or death from multi-organ system failure.^2,3 Thyroid dysfunction is usually induced by similar underlying mechanisms. In particular, hyperthyroidism has significant and well-recognized effects on the cardiovascular system at the molecular and circulatory levels. Iodine-induced hyperthyroidism (IIH) often develops after exposure to large amounts of iodine or long-term use of amiodarone. ⁴ IIH and myocarditis are not linked by a direct cause-and-effect relationship; however, hyperthyroidism may have certain effects on the heart that indirectly affect the course and symptoms of myocarditis. Here, we report a rare case of FM accompanied by IIH.

Case presentation

A 15-year-old male patient was admitted to the hospital due to “chest distress and pain for 9 hours.” The patient had a history of staying up late and presented with symptoms of upper respiratory tract infection, such as nasal discharge and sore throat, 2 weeks prior. Vital signs were stable upon admission, and physical examination revealed no significant irregularities. Emergency laboratory tests showed creatine kinase isoenzyme (CK-MB) 69.3 U/L and cardiac troponin I (cTnI) 13.44 ng/mL. Electrocardiography (ECG) revealed ST-segment elevation of 0.3–0.6 mV in leads II, III, aVF, and V4–V6, which is indicative of acute inferior myocardial infarction. Thus, the patient was diagnosed with acute inferior–posterior wall myocardial infarction. An emergency coronary computed tomography angiography (CTA) revealed normal coronary development, a smooth endothelium, and no stenosis. Cardiac magnetic resonance imaging revealed high signal areas in the inferior wall of the left ventricle on T2-weighted imaging and focal enhancement on late gadolinium-enhanced imaging. Since the patient did not meet the criteria for acute inferior–posterior wall myocardial infarction, the diagnosis was revised to acute FM and cardiac catheterization was not performed. Treatment prescribed by the consultants that were brought on board to take care of the patient included bed rest, fosinopril and metoprolol, high-dose vitamin C, coenzyme Q10, 1,6-fructose diphosphate for myocardial nutrition support, and symptomatic relief. After 12 h, repeat laboratory examination showed lactate dehydrogenase (LDH) 502.7 U/L, LDH1 221.2 U/L; creatine kinase (CK) >2000 U/L; CK-MB 279 U/L; cTnI >20.64 ng/mL; α-hydroxybutyrate dehydrogenase (αHBDH) 499.3 U/L; aspartate aminotransferase (AST) 257.2 U/L; and hypersensitive C-reactive protein (hs-CRP) >10 mg/mL. The eosinophil count was 0.2 cells/μL (normal range, 0.02–0.5 cells/μL). No evidence of influenza, parainfluenza, or COVID-19 was observed in the conducted examinations.

On the first day of admission, a re-examination of CK, CK-MB, cTnI, and BNP levels revealed a continued increase, with BNP at 265.1 pg/mL. A thyroid panel revealed thyroid-stimulating hormone (TSH) 0.05 μIU/mL (reference range, 0.55–4.78 μIU/mL); triiodothyronine (T3) 5.61 nmol/L (reference range, 0.92–2.79 nmol/L); thyroxine (T4) 178.38 nmol/L (reference range, 58.1–140.6 nmol/L); free triiodothyronine (FT3) 21.14 pmol/L (reference range, 3.5–6.5 pmol/L); free thyroxine (FT4) 29.9 pmol/L (reference range, 11.5–22.5 pmol/L); anti-thyroglobulin antibody (TGAb) 1 IU/L (reference range, 0–1.75 IU/L); anti-thyroid peroxidase (TPOAb) 0.5 IU/L (reference range, 0–1.75 IU/L); and thyroglobulin (Tg) 2.29 ng/mL. Thyroid ultrasound showed no significant abnormalities. Echocardiography revealed a dilated left ventricular end-systolic diameter with reduced wall motion, mild regurgitation in the mitral, tricuspid, and aortic valves, and reduced left ventricular systolic function (ejection fraction (EF) 46%, fractional shortening (FS) 23%). A low-iodine diet was prescribed, and anti-thyroid medication was temporarily withheld (Tables 1 and 2).

Table 1.

Significant laboratory results and progress trends.

Tests	Reference range with units	Hour 12	Day 1	Day 3	Day 7
LDH	109–245 U/L	502.7	784.5	858.4	238.6
LDH1	17–96 U/L	221.2	403	475.4	186.7
CK	24–229 U/L	>2000	>2000	971.4	190.5
CK-MB	0–25 U/L	279	257.1	73.1	24
CTnI	0–1.5 ng/mL	>20.64	>20.64	>20.64	4.25
αHBDH	72–182 U/L	499.3	852.9	970.8	276.2
AST	10–40 U/L		257.2	93.8	36.4
hs-CRP	<2.0 mg/mL		8.14	>10	2.08

αHBDH: α-hydroxybutyrate dehydrogenase; AST: aspartate aminotransferase; CK: creatine kinase isoenzyme; CK-MB: creatine kinase isoenzyme; cTnI: cardiac troponin I; hs-CRP: hypersensitive C-reactive protein; LDH: lactate dehydrogenase.

Table 2.

Laboratory results of thyroid function and cardiac function-related indicators.

Tests	Reference range with units	Day 1	Day 3	Day 7
TSH	0.27–4.2 μIU/mL	0.05	0.03	0.045
T3	1.3–3.1 nmol/L	5.61	5.01	5.50
T4	66–181 nmol/L	178.38	164.32	158.72
FT3	3.1–6.8 pmol/L	21.14	19.08	17.60
FT4	12–22 pmol/L	29.9	28.9	26.34
TGAb	0–4 IU/L	1.0	1.12	1.30
TPOAb	0–9 IU/L	0.5	0.6	0.63
Tg	3.8–77 ng/mL	2.29	2.42	2.37
EF	50%–70%	46%	63%	64%
FS	25%–45%	23%	33%	35%

EF: ejection fraction; FS: fractional shortening; FT3: free triiodothyronine; FT4: free thyroxine; T3: triiodothyronine; T4: thyroxine; Tg: thyroglobulin; TGAb: anti-thyroglobulin antibody; TPOAb: anti-thyroid peroxidase; TSH: thyroid-stimulating hormone.

On the third day of hospitalization, a re-examination of CK, CK-MB, CTnI, hs-CRP, and BNP showed decreased levels, while thyroid function test indicators remained abnormal with no significant changes. ECG revealed a reduction in the range of ST-segment elevation in the related leads, while echocardiography revealed normal left ventricular systolic function (EF 55%, FS 33%) (Tables 1 and 2).

On the seventh day of hospitalization, the patient reported no discomfort. Re-examination of indicators showed LDH 138.6 U/L; LDH1 86.7 U/L; CK 180.5 U/L; CK-MB 24 U/L; CTnI 1.25 ng/mL; αHBDH 176.2 U/L; AST 36.4 U/L; hs-CRP 1.08 mg/mL; and BNP 65.1 ng/mL. The repeat thyroid panel showed TSH 0.045 μIU/mL; T3 5.50 nmol/L; T4 158.72 nmol/L; FT3 17.60 pmol/L; FT4 26.34 pmol/L; TGAb 1.30 IU/L; TPOAb 0.63 IU/L; and Tg 2.37 ng/mL. The repeat ECG indicated a sinus rhythm (Tables 1 and 2).

The patient’s condition improved with treatment, and he was discharged on the 10th day with instructions to adhere to a low-iodine diet. Follow-up at the outpatient clinic 3 months later showed normal liver function and myocardial enzyme and troponin I levels. Thyroid function tests had significantly improved. At the 6-month follow-up to date, the patient’s thyroid function had returned to normal, with no adverse events reported.

Discussion

Acute myocarditis is most commonly viral in nature. In the present case, the adolescent patient had developed an upper respiratory tract infection, which led to acute myocarditis. The patient exhibited persistent chest pain and ST-segment elevation in the inferior leads, along with abnormally high myocardial enzymes and troponin I levels. The absence of obstructive lesions on coronary CTA and myocardial edema and injury in the left ventricular region on cardiac magnetic resonance imaging confirmed the diagnosis of acute FM.

The changes in the patient’s ECG ST-segment indicated myocardial edema and injury, which worsened cell membrane permeability, caused the accumulation of biological products and reduced the energy supply and oxygenation of myocardial tissue. ⁵ With treatment, the patient’s ECG ST-segment returned to normal, the cardiac ventricular structure improved, valvular regurgitation diminished, and normal cardiac function was restored.

The patient did not exhibit symptoms of thyroid toxicity, such as fever, excessive sweating, or a significantly increased heart rate (>120 beats per minute). Thyroid examination and ultrasound showed no goiter, and no fine hand tremor was observed. Considering the patient’s age, exposure to iodinated contrast media (ICM) during the coronary CTA may have disrupted his thyroid hormone autoregulation, resulting in destructive thyroiditis associated with subsequent sporadic hyperthyroidism. Hyperthyroidism is characterized by increased T3 and T4 levels and decreased TSH levels. Furthermore, these symptoms are consistent with those of the Jod–Basedow phenomenon, which can lead to thyroid storm and severe cardiac complications, including arrhythmias and heart failure.^6–9 A previous report described the case of an elderly female patient who developed a Jod–Basedow phenomenon with subsequent atrial fibrillation and ventricular tachycardia after cervical CT imaging with iodinated contrast. Therefore, a comprehensive evaluation of a patient’s medical history can elucidate the correlation between cardiac and thyroid events and identify potential risk factors. ⁷

Acute myocarditis and hyperthyroidism typically occur in young, otherwise healthy patients. Autoimmunity is central to the pathogenesis of both, with thyroid dysfunction rarely associated with myocarditis. The diagnosis of myocarditis is based on magnetic resonance edema and troponin as a sign of myocardial necrosis. The patient did not undergo endomyocardial biopsy, which is the gold standard for diagnosing myocarditis. In its absence, we do not know the histotype of inflammation associated with hyperthyroidism. Is it an autoimmune myocarditis? Giant cell myocarditis? Lymphocytic myocarditis? ² Thyrotoxicosis often leads to cardiac consequences, and the prevalence of thyroid function abnormalities is related to that of myocarditis. Acute myocarditis is an autoimmune pathological process, often triggered by viral infections, which may be a risk factor for the development of IIH. Therefore, establishing a correlation between symptoms and exposure to ICM or other iodinated substances is crucial in obtaining an accurate diagnosis and providing suitable treatment.

Conclusion

This case demonstrated that myocarditis accompanied by IIH can be managed with a low-iodine diet, the use of β-adrenergic receptor blocker metoprolol, and close monitoring of thyroid function with regular follow-up assessments without requiring anti-hyperthyroid treatment and ECMO implantation. This treatment course showed good patient prognosis and complied with the requirements of relevant guidelines.

This case report describes a rare case of a juvenile patient with FM complicated by IIH. The limitations of the study were the lack of thyroid nuclear imaging and myocardial biopsy evaluation, the latter of which is the gold standard for myocarditis diagnosis. Nevertheless, the current case provides valuable insights into the complex interplay among myocarditis, hyperthyroidism, and ICM exposure in the pediatric population.