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secondary hyperaldosteronism

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secondary hyperaldosteronism,
excessive production of aldosterone caused by an extraadrenal disorder, such as heart failure, kidney disease, cirrhosis, or hypoproteinemia.


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The brain then triggers secondary hyperaldosteronism (increased secretion of aldosterone by the adrenal gland) to compensate; once the laxatives are stopped, this in turn can lead to reflex fluid retention with peripheral edema, a sense of feeling bloated, and weight gain.
Clinical studies do not show a loss of effect to laxatives (Muller Lissner, 1993) and studies carried out in rats also suggest that long-term sennoside treatment in diarrhogenic doses does not induce habituation in the sense of a reduced laxative effect and does not lead to secondary hyperaldosteronism (Leng-Peschlow et al.
 
 
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