药物所致假性醛固酮增多症的诊断与治疗

药物所致假性醛固酮增多症的诊断与治疗,谢 红,文献阅读报告,报告内容,文献来源,文献内容简介,文献分析与评论,结论与启示,4,1,2,3,文献来源,王继伟,苏海.假性醛固酮增多症J.中华高血压杂志, 2009, 17(2): 187-190.刘然.甘草及甘草酸制剂引起的假性醛固酮增多症及防治J.药物不良反应杂志,2009,11(6):416-419.Decio Armanini,Lorenzo Calo,Andrea Semplicini. Pseudohyperaldosteronism:Pathogenetic Mechanisms.Critical Reviews in Clinical Laboratory Sciences,2003,40(3):295-335.Bruno Sontia,Jan Mooney,Lise Gaudet,et. Pseudohyper- aldosteronism,Liquorice,and Hypertension.The Journal of Clinical Hypertension(Greenwich),2008,10(2):153-157.,甘草及其制剂简要介绍,王继伟,苏海.假性醛固酮增多症J.中华高血压杂志, 2009,17(2): 187-190.,甘草为豆科植物甘草、胀果甘草或光果甘草的干燥根及根茎，其主要成分为甘草甜素（甘草酸）、甘草次酸及黄酮类化合物。甘草味甘、性平，具有抗菌、抗病毒、保肝、祛痰、解毒和类激素样作用，广泛用于肝脏疾患、胃及十二指肠溃疡、阿狄森氏病等的治疗。,甘草甜素比砂糖甜250倍，常作为糖料或食物添加剂制备糖果、蜜饯、口香糖、巧克力和饮料。有的患者食用大量的天然甘草引起PHA，导致高血压。,临床上常用复方甘草片、复方甘草合剂、甘草甜素片、甘草甜素注射剂、甘草酸单胺等，不良反应有：过敏反应，PHA消化系统、神经精神系统、内分泌系统、生殖系统等，其中PHA是其主要不良反应之一。,PHA？,血醛固酮水平增高,醛固酮增多症,真性醛固酮增多症,假性醛固酮增多症（PHA）,血醛固酮水平不高原因： 药物：最常见是甘草酸类药物，其次是黄酮类和多元酚类；遗传性PHA：Liddle综合征，表象性盐皮质激素过多综合征，糖皮质激素可治性高血压；内分泌疾病如Cushing综合征。,临床表现：高血压、低血钾,文献1,王继伟,苏海.假性醛固酮增多症J.中华高血压杂志, 2009,17(2): 187-190.,1、首要措施：停用甘草及其制剂以及含甘草的食品和保健品，甘草的洗脱期约2周，最长可达4月。2、采取低钠饮食、补钾、降压等对症处理；醛固酮受体拮抗剂螺内酯具有良好的降压效果；肾小管上皮钠通道抑制剂氨苯蝶啶或阿米洛利也有一定作用；3、对严重的低钾患者，可考虑给予地塞米松，抑制内源性皮质醇的产生，减少皮质醇对盐皮质激素受体的激活作用。,文献2,甘草制剂所致PHA,刘然.甘草及甘草酸制剂引起的假性醛固酮增多症及防治J.药物不良反应杂志,2009,11(6):416-419.,文献2,刘然.甘草及甘草酸制剂引起的假性醛固酮增多症及防治J.药物不良反应杂志,2009,11(6):416-419.,1、立即停药；2、适当补充钾盐，一般每天给予氯化钾3.0g；氨苯蝶啶剂量每天8-10mg/kg，口服3个月可纠正电解质紊乱并使血压降低；用药过程中监测血钾、钠、氯，及时调整剂量。以免发生高血钾、低血钠和高氯性酸中毒；注意肾功能状态：每日尿量700ml，每小时30ml补钾安全，一般需补钾4-6天，严重者10-20天；3、低钠饮食，每天饮食最多给予2g氯化钠。,文献3内容介绍,甘草制剂所致PHA,Decio Armanini,Lorenzo Calo,Andrea Semplicini. pseudohyperaldosteronism: Pathogenetic Mechanisms.Critical Reviews in Clinical Laboratory Sciences, 2003, 40(3): 295-335.,the requirement of some functional adrenal tissue or of the presence of glucocorticoids to show the effect of licorice.Licorice alone is inactive in patients with Addisons disease or after bilateral adrenalectomy.Its effects are evident only when cortisone is added.,所需条件,文献3,文献3,文献3,文献3,文献4 病例报道,55-year-old woman, hypertension 2 years, enalapril , amlodopine and 12.5 mg thiazide diuretic, BP148-180/80-90mmHg, a positive family history for hypertension, postmenopause status, and ex-smoker status, denied excessive alcohol intake, ahealthy diet.,introduction,casual sitting BP 151/85(automatic BPmonitor) and 158/82mmHg(manual) normal except for a left carotid bruit. thiazide diuretic increased to 25mg/d.,examination and measurement,Bruno Sontia,Jan Mooney,Lise Gaudet,et. Pseudohyperaldosteronism,Liquorice,and Hypertension.The Journal of Clinical Hypertension(Greenwich),2008,10(2):153-157.,文献4 病例报道,laboratory investigation and measurement,K 2.4, Na 148, Cl 99, CO2 33, anion gap 14mmol/l diuretic therapy discontinued,K-rich diet, K supplements,2 weeks later,K 2.7, Na 145 mmol/l，BP150/100mmHg，plasma aldosterone31pmol/l, plasma renin 4,2ng/L.,diagnosis of PHA,in light of hypokalemia, hypernatremia, and reduced plasma aldosterone levels. detailed dietary history revealed that sher consumed 200 to 250g of black liquorice daily since quitting smoking 4 years ago.,therapy,stop eating liquorice and continue the K-rich diet and K supplementation,3 months later, K 3.8, K supplements stopped.18 months, BP controlled 123/77 on low doses of perindo