Subject(s)
Humans , Diabetes Mellitus , Hypertension/complications , Blood Glucose , Blood Pressure , Brain Diseases/etiology , Brazil , Diabetes Complications/therapy , Diabetes Mellitus/therapy , Dyslipidemias/drug therapy , Heart Diseases/etiology , Hypertension/therapy , Kidney Diseases/etiology , Peripheral Arterial Disease/etiology , Risk Factors , Societies, MedicalABSTRACT
A 24 year-old man was admitted with hypertensive crises and diagnosis hypothesis of neurofibromathosis and pheochromocytoma with blood pressure of 150 x 110mmHg and in use of anti-hypertensive drugs. The electrocardiogram (EKG) showed left ventricle hypertrophy. An echocardiogram showed interventricular septum (IVS) thickness of 16mm, posterior wall (PW) thickness of 11mm (ratio IVS/PW was 1.4). Diastolic ventricular diameter was 39mm with gradient of 52mmHg and mild mitral-valve murmur by pulsate Doppler. Increased vanillylmandelic acid and metanephrines in a 24-hour sample of urine has confirmed diagnosis of pheochromocytoma within was localized by 131I metaiodobenzyl-guanidine scan and computerized axial tomography. The patient was submitted to right adrenalectomy. Blood pressure was normalized. Evaluation an year later revealed a healthy man with normal laboratory exams, EKG and echocardiogram. It seems that the hypertrophy was consequence of the hypertension and pheochromocytoma, was not hypertrophic cardiomyopathy.
Homem de 24 anos foi admitido com hipótese diagnóstica de neurofibromatose e feocromocitoma, com pressão arterial (PA) de 150 x 110 mmHg e em uso de medicação anti-hipertensiva. O eletrocardiograma mostrava sobrecarga de ventrículo esquerda. O ecocardiograma relatado com diagnóstico de miocardiopatia hipertrófica assimétrica, mostrava a espessura de septo interventricular de 16mm, parede posterior de 11mm, diâmetro diastólico de 39mm, com gradiente intra-ventricular de 52mmHg e discreta regurgitação proto-sistólica valvar mitral ao doppler pulsátil. As dosagens de ácido vanilmandélico e de metanefrina urinárias confirmaram a suspeita clínica de feocromocitoma, localizado através da cintilografia com metaiodobenzilguanidina e tomografia axial computadorizada. Um ano após adrenalectomia direita se encontra assintomático, com PA, alterações laboratoriais, eletrocardiográficas e ecocardiográficas normais, evidenciando assim, que a hipertrofia de ventrículo esquerdo (HVE) era conseqüência da hipertensão arterial do feocromocitoma e não da miocardiopatia hipertrófica. Esta regressão da HVE excluiu, assim, o falso diagnóstico de micardiopatia hipertrófica