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Subclinical hyperthyroidism: 3 case reports In a case series, 3 patients (1 woman and 2 men) aged 58–66 years were described, who developed subclinical hyperthyroidism during treatment with levothyroxine-sodium (case 1 and case 3) for hypothyroidism and amiodarone (case 2) for ventricular tachycardia. Case 1: A 63-year-old woman went to the emergency room of hospital for palpitations, chest pains, and fainting in July 2016. She had Hashimoto’s thyroiditis. Over the last month, she was suffering from heat intolerance, shortness of breath, and easy fatigue. Electrocardiogram (ECG) revealed a tachycardia with supraventricular extrasystoles. Holter monitoring revealed ventricular extrasystoles. Transthoracic echocardiography revealed an enlarged left atrium and a severe mitral regurgitation. Blood tests revealed normal FT4, FT3, and TSH levels. She received levothyroxine-sodium 100 mcg/day for a month. Thus, initial iatrogenic hyperthyroidism was suspected, which was treated by reducing the dose of levothyroxine-sodium to 50 mcg/day and starting 2.5mg per day of bisoprolol. Four months later, she had a lower degree of mitral insufficiency, a slight reduction in palpitations and fatigue, and an increase in TSH to 1.36 mIU/L with FT3 2.58 pg/mL and FT4 1.21 ng/dL. Due to presence of consistent easy fatigue, the dose of levothyroxine-sodium was reduced to 25 mcg/day. Bisoprolol was replaced with metoprolol. After 8 months, she recovered and reported wellness. Holter monitoring revealed a repetitive supraventricular extrasystoles and monomorphic single ventricular extrasystoles. ECG revealed a small stretching of the papillary muscles, and a reduction of mitral regurgitation which became mild in the meantime. In this control, FT4 and FT3 were within the normal range and TSH value was close to the highest limit of the normal range. Case 2: A 58-year-old man was referred to unit for facial trauma which occurred during a syncope in 2014. He had no history of known drug intake or cardiovascular disease. On admission, ECG revealed sinus rhythm with frequent extrasystoles. Holter monitoring indicated ventricular extrasystoles. Biochemical tests were within normal limits, and thyroid function assessment by TSH assay was slightly below the reference value. A subcutaneous loop recorder was implanted. Two weeks later, he had blurred vision and palpitations with spontaneous regression of symptoms; a fast-synchronised ventricular tachycardia at 220 beats per minute was detected by loop recorder’s control. ECG showed significant dilatation of the right ventricle with global hypokinesia along with a bulging of the free wall of the outflow tract. Coronarographic angiography was normal. After cardiac MRI, he was diagnosed with arrhythmogenic dysplasia of the right ventricle. A single-chamber cardioverter-defibrillator was implanted. Therapy with bisoprolol was started. He was admitted to different cardiology units for recurrent episodes of sustained ventricular tachycardia, interrupted by DC shocks, and underwent numerous ablations.