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一名患有肾硬化症儿童的地塞米松可抑制性醛固酮增多症

Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis.

作者信息

Lee S M, Lightner E, Witte M, Oberfield S, Levine L, New M I

出版信息

Acta Endocrinol (Copenh). 1982 Feb;99(2):251-5. doi: 10.1530/acta.0.0990251.

DOI:10.1530/acta.0.0990251
PMID:6277130
Abstract

A 9 year old Mexican boy presented with severe hypertension, hypokalaemia and features suggesting acute glomerulonephritis. Nephrosclerosis was present on renal biopsy. Aldosterone levels were unresponsive to variations in dietary salt intake and plasma renin activity was suppressed. Following oral dexamethasone therapy (2 mg/day), plasma aldosterone decreased to undetectable levels, serum potassium normalized and plasma renin activity gradually increased. Dexamethasone also restored the normal responsiveness of the renin-aldosterone system to postural stimuli. The patient exhibited a marked response to a single dose of ACTH with a rise in plasma aldosterone. Long-term blood pressure control and normal potassium levels have been achieved with oral prednisone therapy (5 mg/day) for a period of one year. This case of dexamethasone suppressible hyperaldosteronism (DSH) illustrates that the degree of hypertension in this syndrome may produce severe renal microvascular lesions. DSH should be considered in all children who present with low renin hypertension.

摘要

一名9岁墨西哥男孩出现严重高血压、低钾血症及提示急性肾小球肾炎的特征。肾活检显示存在肾硬化。醛固酮水平对饮食中盐摄入量的变化无反应,血浆肾素活性受抑制。口服地塞米松治疗(2毫克/天)后,血浆醛固酮降至无法检测水平,血钾恢复正常,血浆肾素活性逐渐升高。地塞米松还恢复了肾素-醛固酮系统对体位刺激的正常反应性。患者对单剂量促肾上腺皮质激素有明显反应,血浆醛固酮升高。口服泼尼松治疗(5毫克/天)一年来实现了长期血压控制和血钾正常。这例地塞米松可抑制性醛固酮增多症(DSH)表明,该综合征的高血压程度可能会导致严重的肾微血管病变。所有表现为低肾素性高血压的儿童都应考虑DSH。

相似文献

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Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis.一名患有肾硬化症儿童的地塞米松可抑制性醛固酮增多症
Acta Endocrinol (Copenh). 1982 Feb;99(2):251-5. doi: 10.1530/acta.0.0990251.
2
Hypertension corrected and aldosterone responsiveness to renin-angiotensin restored by long-term dexamethasone in glucocorticoid-suppressible hyperaldosteronism.长期使用地塞米松可纠正糖皮质激素可抑制性醛固酮增多症患者的高血压,并恢复醛固酮对肾素-血管紧张素的反应性。
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Long term evolution of glucocorticoid-suppressible hyperaldosteronism.糖皮质激素可抑制性醛固酮增多症的长期演变
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Familial, dexamethasone-suppressible, normokalemic hyperaldosteronism.家族性、地塞米松可抑制性、正常血钾性醛固酮增多症。
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Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia?地塞米松可抑制性醛固酮增多症。肾上腺过渡细胞增生?
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Study on clinical and endocrine characteristics of dexamethasone-suppressible hyperaldosteronism compared with those in primary aldosteronism owing to aldosterone-producing adenoma.
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引用本文的文献

1
Rapid diagnosis of glucocorticoid suppressible hyperaldosteronism in infants and adolescents.婴幼儿及青少年糖皮质激素可抑制性醛固酮增多症的快速诊断
Arch Dis Child. 1994 Jul;71(1):40-3. doi: 10.1136/adc.71.1.40.
2
Dexamethasone-suppressible hyperaldosteronism: pathophysiology, clinical aspects, and new insights into the pathogenesis.地塞米松可抑制性醛固酮增多症:病理生理学、临床特点及发病机制的新见解
Klin Wochenschr. 1987 May 15;65(10):437-44. doi: 10.1007/BF01712834.