Cardiomyopahty is one of complications of thyrotoxicosis. About 6% of thyrotoxic patients develop heart failure, but less than 1% of the patients progress dilated cardiomyopathy with systolic left ventricular dysthnct...Cardiomyopahty is one of complications of thyrotoxicosis. About 6% of thyrotoxic patients develop heart failure, but less than 1% of the patients progress dilated cardiomyopathy with systolic left ventricular dysthnction.展开更多
BACKGROUND Acute myocarditis is an acute myocardium injury that manifests as arrhythmia,dyspnea,and elevated cardiac enzymes.Acute myocarditis is usually caused by a viral infection but can sometimes be caused by auto...BACKGROUND Acute myocarditis is an acute myocardium injury that manifests as arrhythmia,dyspnea,and elevated cardiac enzymes.Acute myocarditis is usually caused by a viral infection but can sometimes be caused by autoimmunity.Graves’disease is an autoimmune disease that is a rare etiology of acute myocarditis.Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults.CASE SUMMARY A rare case of new-onset Graves’disease combined with acute myocarditis and thyrotoxic periodic paralysis is reported.The patient was a 25-year-old young man who suddenly became paralyzed and felt palpitations and dyspnea.He was then sent to our emergency department(ED).Upon arrival,electrocardiography revealed an accelerated junctional rhythm and ST-segment depression in all leads,and laboratory findings showed extreme hypokalemia and elevated troponin I,with the troponin I level being 0.32 ng/mL(reference range,0-0.06 ng/mL).Coronary computer tomography angiography was performed,and there were no abnormal findings in the coronary arteries.Subsequently,the patient was admitted to the ED ward,where further testing revealed Graves’disease,along with continued elevated cardiac enzyme levels and B-type natriuretic peptide(BNP)levels.The troponin I level was 0.24 ng/mL after admission.All of the echocardiography results were normal:Left atrium 35 mm,left ventricle 48 mm,end-diastolic volume 102 mL,right atrium 39 mm×47 mm,right ventricle 25 mm,and ejection fraction 60%.Cardiac magnetic resonance was performed on the fifth day of admission,revealing myocardial edema in the lateral wall and intramyocardial and subepicardial late gadolinium enhancement in the lateral apex,anterior lateral,and inferior lateral segments of the ventricle.The patient refused to undergo an endomyocardial biopsy.After 6 d,the patient’s cardiac enzymes,BNP,potassium,and electrocardiography returned to normal.After the patient’s symptoms were relieved,he was discharged from the hospital.During a 6-mo follow-up,the patient was asymptomatic and subjected to thyroid function,liver function,kidney function,troponin I,and electrocardiograph routine tests for medicine adjustments.The hyperthyroid state was controlled.CONCLUSION Acute myocarditis is a rare manifestation of Graves’disease.Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults.When the reason for hypokalemia and elevated cardiac enzymes in patients is unknown,cardiologists should consider Graves’disease and also pay attention to accelerated junctional rhythm.展开更多
Along with hereditary myopathies, there are many exogenic (the same a not hereditary) muscle affections due to the pathology of endocrine gland’s functioning. These forms of muscle pathology are called endocrine myop...Along with hereditary myopathies, there are many exogenic (the same a not hereditary) muscle affections due to the pathology of endocrine gland’s functioning. These forms of muscle pathology are called endocrine myopathies. In the cases of thyroid gland hyperfunction (the same a thyrotoxicosis), different regions of neuromuscular system may be involved in the pathological process. Thyrotoxic myopathy (TM) which is a subject of this investigation, occupies one of the first places between thyrotoxic (the same a thyrotoxicosis) neuromuscular affections. Meanwhile, for a long time in literature there was no clarity about the degree of muscle weakness and atrophy to diagnose TM in a patient. It’s because of the fact that the majority of patients complain of increased fatigue and general weakness due to thyrotoxicosis. In present time TM diagnostics is very rare. TM is a phenocopy (the clinical similar) of many neuromuscular diseases. However in literature, the data about peculiarities of clinical picture of TM is almost completely absent, it isn’t known about the frequency of affection of the isolated muscles or muscle groups, the topography of muscle weakness and successive involvement of isolated muscles in the pathological process during different stages of thyrotoxicosis and myopathy. The questions of differential diagnosis with similar neuromuscular disorders are described very poorly. In present article, we accent our attention at the clinical differentiation of the TM with other neuromuscular diseases, namely muscular dystrophy, myasthenia gravis, polymyositis, Addison’s disease, proximal spinal muscular atrophy, steroid myopathy and neurosis. In our opinion, the early diagnosis of TM may help the diagnosis of thyrotoxicosis in patients who have no classical clinical signs of this disease, i.e. in patients with latent thyrotoxicosis.展开更多
文摘Cardiomyopahty is one of complications of thyrotoxicosis. About 6% of thyrotoxic patients develop heart failure, but less than 1% of the patients progress dilated cardiomyopathy with systolic left ventricular dysthnction.
文摘BACKGROUND Acute myocarditis is an acute myocardium injury that manifests as arrhythmia,dyspnea,and elevated cardiac enzymes.Acute myocarditis is usually caused by a viral infection but can sometimes be caused by autoimmunity.Graves’disease is an autoimmune disease that is a rare etiology of acute myocarditis.Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults.CASE SUMMARY A rare case of new-onset Graves’disease combined with acute myocarditis and thyrotoxic periodic paralysis is reported.The patient was a 25-year-old young man who suddenly became paralyzed and felt palpitations and dyspnea.He was then sent to our emergency department(ED).Upon arrival,electrocardiography revealed an accelerated junctional rhythm and ST-segment depression in all leads,and laboratory findings showed extreme hypokalemia and elevated troponin I,with the troponin I level being 0.32 ng/mL(reference range,0-0.06 ng/mL).Coronary computer tomography angiography was performed,and there were no abnormal findings in the coronary arteries.Subsequently,the patient was admitted to the ED ward,where further testing revealed Graves’disease,along with continued elevated cardiac enzyme levels and B-type natriuretic peptide(BNP)levels.The troponin I level was 0.24 ng/mL after admission.All of the echocardiography results were normal:Left atrium 35 mm,left ventricle 48 mm,end-diastolic volume 102 mL,right atrium 39 mm×47 mm,right ventricle 25 mm,and ejection fraction 60%.Cardiac magnetic resonance was performed on the fifth day of admission,revealing myocardial edema in the lateral wall and intramyocardial and subepicardial late gadolinium enhancement in the lateral apex,anterior lateral,and inferior lateral segments of the ventricle.The patient refused to undergo an endomyocardial biopsy.After 6 d,the patient’s cardiac enzymes,BNP,potassium,and electrocardiography returned to normal.After the patient’s symptoms were relieved,he was discharged from the hospital.During a 6-mo follow-up,the patient was asymptomatic and subjected to thyroid function,liver function,kidney function,troponin I,and electrocardiograph routine tests for medicine adjustments.The hyperthyroid state was controlled.CONCLUSION Acute myocarditis is a rare manifestation of Graves’disease.Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults.When the reason for hypokalemia and elevated cardiac enzymes in patients is unknown,cardiologists should consider Graves’disease and also pay attention to accelerated junctional rhythm.
文摘Along with hereditary myopathies, there are many exogenic (the same a not hereditary) muscle affections due to the pathology of endocrine gland’s functioning. These forms of muscle pathology are called endocrine myopathies. In the cases of thyroid gland hyperfunction (the same a thyrotoxicosis), different regions of neuromuscular system may be involved in the pathological process. Thyrotoxic myopathy (TM) which is a subject of this investigation, occupies one of the first places between thyrotoxic (the same a thyrotoxicosis) neuromuscular affections. Meanwhile, for a long time in literature there was no clarity about the degree of muscle weakness and atrophy to diagnose TM in a patient. It’s because of the fact that the majority of patients complain of increased fatigue and general weakness due to thyrotoxicosis. In present time TM diagnostics is very rare. TM is a phenocopy (the clinical similar) of many neuromuscular diseases. However in literature, the data about peculiarities of clinical picture of TM is almost completely absent, it isn’t known about the frequency of affection of the isolated muscles or muscle groups, the topography of muscle weakness and successive involvement of isolated muscles in the pathological process during different stages of thyrotoxicosis and myopathy. The questions of differential diagnosis with similar neuromuscular disorders are described very poorly. In present article, we accent our attention at the clinical differentiation of the TM with other neuromuscular diseases, namely muscular dystrophy, myasthenia gravis, polymyositis, Addison’s disease, proximal spinal muscular atrophy, steroid myopathy and neurosis. In our opinion, the early diagnosis of TM may help the diagnosis of thyrotoxicosis in patients who have no classical clinical signs of this disease, i.e. in patients with latent thyrotoxicosis.