[Carotid intima-media thickness as a marker of cardiovascular risk in patients with subclinical hypothyroidism]. / Espessura íntima-média carotídea como marcador de risco cardiovascular em pacientes com hipotireoidismo subclínico.

Subclinical hypothyroidism (SH) has been associated with an increased risk for coronary disease. Carotid intima-media thickness (IMT), as assessed by ultrasonography, is a precise marker of atherosclerotic changes and can be used as an endpoint for cardiovascular events. Aims of this study were to determine carotid IMT in a group of patients with SH and its possible association with an increase in cardiovascular risk. There were no significant differences in mean carotid IMT between patients and controls. Results of both groups were, respectively: common carotid arteries, 0.573 +/- 0.070 mm and 0.576 +/- 0.068 mm (p= 0.904); carotid bifurcation, 0.602 +/- 0.079 mm and 0.617 +/- 0.102 mm (p= 0.714). Similar results were obtained when analyzing subgroups with serum TSH < or > 8 mIU/L and with positive or negative titers of TPOAb. The mean carotid IMT in these subgroups were: TSH 4-8 mIU/L: 0.579 +/- 0.070 mm and 0.586 +/- 0.063 mm; TSH > 8 mIU/L: 0.569 +/- 0.073 mm and 0.616 +/- 0.091 mm; TPOAb+: 0.585 +/- 0.070 mm and 0.621 +/- 0.085 mm; TPOAb-: 0.554 +/- 0.072 mm and 0.571 +/- 0.066 mm. No differences in the lipid profile and in the apoprotein B and lipoprotein (a) levels between the groups were found. These findings suggest that mild SH with no related metabolic changes is not associated with an increase in cardiovascular risk, as assessed by carotid IMT.

Espessura íntima-média carotídea como marcador de risco cardiovascular em pacientes com hipotireoidismo subclínico / Carotid intima-media thickness as a marker of cardiovascular risk in patients with subclinical hypothyroidism

O hipotireoidismo subclínico (HS) já foi associado a aumento do risco cardiovascular. Na avaliação desse risco, a medida da espessura íntima-média (EIM) carotídea por ultra-sonografia é capaz de detectar alterações iniciais da aterosclerose. O objetivo deste estudo foi avaliar a EIM carotídea em pacientes com HS e sua associação com um provável aumento do risco cardiovascular. Não foi encontrada diferença significativa nas medidas da EIM das pacientes com HS e das controles. Os resultados encontrados nos dois grupos estudados foram, respectivamente: 0,573 ± 0,070 mm vs. 0,576 ± 0,068 mm para as carótidas comuns (p= 0,904) e 0,602 ± 0,079 mm vs. 0,617 ± 0,102 mm para as bifurcações (p= 0,714). Mesmo após estratificação das pacientes de acordo com o TSH e com a presença ou não de auto-imunidade, a diferença entre os sub-grupos permaneceu sem significância estatística. As medidas da EIM nesses grupos nos sítios avaliados foram: TSH 4-8 mUI/L: 0,579 ± 0,070 mm e 0,586 ± 0,063 mm; TSH > 8 mUI/L: 0,569 ± 0,073 mm e 0,616 ± 0,091 mm; anti-TPO+: 0,585 ± 0,070 mm e 0,621 ± 0,085 mm; anti-TPO-: 0,554 ± 0,072 mm e 0,571 ± 0,066 mm. Também não houve diferença no lipidograma e nas dosagens de apoproteína B e de lipoproteína (a). Este fato sugere que o HS, quando leve, sem alterações metabólicas associadas, não promove aumento do risco cardiovascular.

Subclinical hypothyroidism (SH) has been associated with an increased risk for coronary disease. Carotid intima-media thickness (IMT), as assessed by ultrasonography, is a precise marker of atherosclerotic changes and can be used as an endpoint for cardiovascular events. Aims of this study were to determine carotid IMT in a group of patients with SH and its possible association with an increase in cardiovascular risk. There were no significant differences in mean carotid IMT between patients and controls. Results of both groups were, respectively: common carotid arteries, 0.573 ± 0.070 mm and 0.576 ± 0.068 mm (p= 0.904); carotid bifurcation, 0.602 ± 0.079 mm and 0.617 ± 0.102 mm (p= 0.714). Similar results were obtained when analyzing subgroups with serum TSH < or > 8 mIU/L and with positive or negative titers of TPOAb. The mean carotid IMT in these subgroups were: TSH 4-8 mIU/L: 0.579 ± 0.070 mm and 0.586 ± 0.063 mm; TSH > 8 mIU/L: 0.569 ± 0.073 mm and 0.616 ± 0.091 mm; TPOAb+: 0.585 ± 0.070 mm and 0.621 ± 0.085 mm; TPOAb-: 0.554 ± 0.072 mm and 0.571 ± 0.066 mm. No differences in the lipid profile and in the apoprotein B and lipoprotein (a) levels between the groups were found. These findings suggest that mild SH with no related metabolic changes is not associated with an increase in cardiovascular risk, as assessed by carotid IMT.

Angina pectoris em paciente com hipertireoidismo e coronárias angiograficamente normais / Angina pectoris in patient with hyperthyroidism and normal angiography coronary

A presença de angina pectoris em mulher pré-menopausa sem outros fatores de risco para doença arterial coronariana, obriga-nos a descartar outras causas de lesão coronariana não aterosclerótica. A relação entre o hipertireoidismo e as alterações no sistema cardiovascular está bem estabelecida, contudo o hipertireoidismo responde por menos de 5 por cento dos casos de dor torácica. Apresenta-se um caso de uma mulher, 47 anos, com sintomas de precordialgia típica e eletrocardiograma (ECG) sugestivo de isquemia coronariana, mas sem alteração laboratorial sugestiva de lesão miocárdica. Anamnese, exame físico e resultados laboratoriais permitiram firmar o diagnóstico de hipertireoidismo. Investigação subseqüente com o cateterismo cardíaco não demonstrou lesões obstrutivas. Após tratamento com iodo radioativo e retorno ao eutireoidismo, a paciente manteve-se assintomática e o ECG e a cintilografia miocárdica foram negativos para isquemia. Esses resultados sugerem uma interação entre hiperatividade tireoidiana e isquemia miocárdica, tendo o hipertireoidismo como provável etiologia dos achados clínicos e eletrocardiográficos.

In the presence of angina pectoris in a premenopausal woman without significant risk factors for coronary disease, we have to rule out other causes of coronary lesion of non atherosclerotic origin. The relations between hyperthyroidism and the cardiovascular system are well known, but hyperthyroidism is responsable for less than 5 percent of all causes of chest pain. We present a clinical case of a 47 year old woman with typical chest pain and eletrocardiogram (EKG) suggesting coronary ischemia but with normal laboratory data. Anamnesis, clinical and the laboratory data confirmed the diagnosis of hyperthyroidism. Further investigation showed a normal coronary angiography. After treatment with radioiodine and the establishment of euthyroidism, the patient remained asymptomatic and EKG and myocardial scintilography were negative for ischemia. These results suggest a cause and effect relationship between thyroid overactivity and myocardial ischemia, implying a probable etiological role for hyperthyroidism in the clinical and EKG findings.

Angina pectoris in patient with hyperthyroidism and normal angiography coronary.

In the presence of angina pectoris in a premenopausal woman without significant risk factors for coronary disease, we have to rule out other causes of coronary lesion of non atherosclerotic origin. The relations between hyperthyroidism and the cardiovascular system are well known, but hyperthyroidism is responsable for less than 5% of all causes of chest pain. We present a clinical case of a 47 year old woman with typical chest pain and eletrocardiogram (EKG) suggesting coronary ischemia but with normal laboratory data. Anamnesis, clinical and the laboratory data confirmed the diagnosis of hyperthyroidism. Further investigation showed a normal coronary angiography. After treatment with radioiodine and the establishment of euthyroidism, the patient remained asymptomatic and EKG and myocardial scintilography were negative for ischemia. These results suggest a cause and effect relationship between thyroid overactivity and myocardial ischemia, implying a probable etiological role for hyperthyroidism in the clinical and EKG findings.

Norbixin ingestion did not induce any detectable DNA breakage in liver and kidney but caused a considerable impairment in plasma glucose levels of rats and mice.

From the seeds of Bixa orellana are extracted the carotenoids bixin and norbixin that have been widely used for coloring food. In this study, the toxicity of norbixin, purified or not (annatto extract containing 50% norbixin), was investigated in mice and rats after 21 days of ingestion through drinking water. Mice were exposed to doses of 56 and 351 mg/kg (annatto extract) and 0.8, 7.6, 66 and 274 mg/kg (norbixin). Rats were exposed to doses of 0.8, 7.5 and 68 mg/kg (annatto extract) and 0.8, 8.5 and 74 mg/kg (norbixin). In rats, no toxicity was detected by plasma chemistry. In mice, norbixin induced an increase in plasma alanine aminotransferase activity (ALT) while both norbixin and annatto extract induced a decrease in plasma total protein and globulins (P < 0.05). However, no signs of toxicity were detected in liver by histopathological analysis. No enhancement in DNA breakage was detected in liver or kidney from mice treated with annatto pigments, as evaluated by the comet assay. Nevertheless, there was a remarkable effect of norbixin on the glycemia of both rodent species. In rats, norbixin induced hyperglycemia that ranged from 26.9% (8.5 mg/kg norbixin, to 52.6% (74 mg/kg norbixin, P < 0.01) above control levels. In mice, norbixin induced hypoglycemia that ranged from 14.4% (0.8 mg/kg norbixin, P < 0.05) to 21.5% (66 mg/kg norbixin, P < 0.001) below control levels. Rats and mice treated with annatto pigments showed hyperinsulinemia and hypoinsulinemia, respectively indicating that pancreatic beta-cells were functional. More studies should be performed to fully understand of how species-related differences influences the biological fate of norbixin.