Hyperthyroidism and fulminant myocarditis in an adolescent with iodine-induced hyperthyroidism: A case report.
Study Goal
The researchers aimed to investigate the relationship between iodine-induced hyperthyroidism and acute myocarditis in a patient with elevated thyroid hormone levels.
Results Summary
The study found that iodine-induced hyperthyroidism contributed to myocardial injury in the patient, but a low-iodine diet and supportive treatment led to recovery of cardiac and thyroid function. No pharmacologic intervention for hyperthyroidism was required.
Population
15-year-old male with acute fulminant myocarditis and iodine-induced hyperthyroidism.
Effective Dosage
Not specified (low-iodine diet advised).
Duration
6-month follow-up (intervention duration not specified).
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
low-iodine diet, medication, and supportive treatment | decrease | myocardial enzymes and troponin I levels | 15-year-old male patient with acute fulminant myocarditis and iodine-induced hyperthyroidism | - | gradually decreased | #1 |
low-iodine diet, medication, and supportive treatment | increase | electrocardiography and echocardiography results | 15-year-old male patient with acute fulminant myocarditis and iodine-induced hyperthyroidism | - | improved | #2 |
low-iodine diet, medication, and supportive treatment | increase | cardiac function | 15-year-old male patient with acute fulminant myocarditis and iodine-induced hyperthyroidism | - | returned to normal | #3 |
low-iodine diet | increase | thyroid function and cardiac indicators | 15-year-old male patient with acute fulminant myocarditis and iodine-induced hyperthyroidism | - | returned to normal | #4 |
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.