• 대한영상의학회지
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• 제85권2호
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• pp.456-462
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• 2024

원발성 알도스테론증은 자율신경계에 의한 알도스테론 분비조절의 장애로 고혈압 및 저칼륨혈증과 관련이 있다. 원발성 알도스테론증에서 편측성을 결정하는 것이 매우 중요한 이유는 그에 따라 치료 방법이 달라지기 때문이다. 부신정맥채혈술은 원발성 알도스테론증에서 편측성을 평가하는 가장 신뢰성 있는 방법으로 알려져 있다. 부신정맥채혈술은 부신 정맥이 크기가 매우 작으며 그 해부학적 위치가 다양하기 때문에 기술적으로 어려운 시술이다. 따라서 성공적인 시술을 위해서는 해부학적 변이를 잘 이해하고 시술 전 영상 검사를 면밀히 검토하는 것이 중요하다. 부신정맥채혈술 중에 발견된 세 가지 해부학적 변이를 보고하고자 한다.

• Endocrinology and Metabolism
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• 제33권4호
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• pp.485-492
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• 2018

Background: Increasing evidence supports interplay between aldosterone and parathyroid hormone (PTH), which may aggravate cardiovascular complications in various heart diseases. Negative structural cardiovascular remodeling by primary aldosteronism (PA) is also suspected to be associated with changes in calcium levels. However, to date, few clinical studies have examined how changes in calcium and PTH levels influence cardiovascular outcomes in PA patients. Therefore, we investigated the impact of altered calcium homeostasis caused by excessive aldosterone on cardiovascular parameters in patients with PA. Methods: Forty-two patients (mean age $48.8{\pm}10.9$ years; 1:1, male:female) whose plasma aldosterone concentration/plasma renin activity ratio was more than 30 were selected among those who had visited Severance Hospital from 2010 to 2014. All patients underwent adrenal venous sampling with complete access to both adrenal veins. Results: The prevalence of unilateral adrenal adenoma (54.8%) was similar to that of bilateral adrenal hyperplasia. Mean serum corrected calcium level was $8.9{\pm}0.3mg/dL$ (range, 8.3 to 9.9). The corrected calcium level had a negative linear correlation with left ventricular end-diastolic diameter (LVEDD, ${\rho}=-0.424$, P=0.031). Moreover, multivariable regression analysis showed that the corrected calcium level was marginally associated with the LVEDD and corrected QT (QTc) interval (${\beta}=-0.366$, P=0.068 and ${\beta}=-0.252$, P=0.070, respectively). Conclusion: Aldosterone-mediated hypercalciuria and subsequent hypocalcemia may be partly involved in the development of cardiac remodeling as well as a prolonged QTc interval, in subjects with PA, thereby triggering deleterious effects on target organs additively.