Why Do You Need to Take Conn's Syndrome Seriously?
Because too much aldosterone is very toxic. Too high aldosterone levels lead to toxic effects called Target Organ Damage). Furthermore, we are passionate to educate patinets and doctors because today only a fraction of all patients (< 5%) are being diagnosed, and an even smaller fraction are being offered curative surgery. This toxic (and very silent) disease can often be cured by a 20-30-minute Mini-Back Scope Adrenalectomy (MBSA) operation. Primary aldosteronism is important not only because of its high prevalence (very common disease), but also because patients with primary aldosteronism have a very high cardiovascular morbidity and mortality. It is very silent and deadly. The risk of stroke, heart attack and heart arrhythmias are increased 10-fold; 1,000%) compared to age-, sex- and blood pressure matched patients with essential hypertension (high blood pressure NOT related to an adrenal tumor). Why is primary aldosteronism so important, and why are we so eager to get patients treated? Treating primary hyperaldosteronism by surgery Mini-Back Scope Adrenalectomy (MBSA) cures hypokalemia, lowers blood pressure, reduces the number of antihypertensive medications required, and improves parameters of impaired cardiac and renal function. Even if you decide surgery is not for you (maybe you are at a very advanced age, and have multiple comorbidities, and your heart is not strong enough for a 30-minute procedure), we want you to be diagnosed accurately because there are some medications (albeit not as good or cost-effective as surgery) that may be beneficial to you. These include mineralcorticoid receptor antagonists.What is the Role of Too Much Aldosterone in Target Organ Damage?
Complications of primary hyperaldosteronism (Conn’s syndrome): The consequences of undiagnosed and untreated Conn’s syndrome.
Remember, too much aldosterone (often from a bad aldosterone-producing adrenal adenoma) is toxic to your body. This toxicity is called Target Organ Damage. Traditionally, aldosterone has been considered the main regulator of water and electrolyte homeostasis due to its effects on epithelial cells, particularly in the collecting ducts of the kidney and distal colon. The physiological actions of aldosterone in other tissues were much less evident, but over the last 15 years, studies both in humans and animal models have gained new insights on its effects, that are mainly targeted in the heart, blood vessels, kidney, and central nervous system (CNS). Please note that the below discussion is technical and reviews some of the latest science on primary hyperaldosteronism.
Too much aldosterone is toxic to the inner lining of blood vessels called the endothelium, leading to increased risk of stroke, heart attack, arrhythmia, kidney failure, and premature death.
Vascular and perivascular inflammation via by too much aldosterone in myocardium (heart muscle cells) can also be observed in other vascular areas, with similar mechanisms of endothelial activation, leukocyte accumulation, and pro-fibrogenic cytokine production (this is bad inflammation in your vessels; the arteries, and veins responsible for transporting blood throughout your body). Aldosterone cause problems with relaxation of your vessels due to effect of the inner lining of vessel (this is called endothelial dysfunction). Also, aldosterone causes increased vascular stiffness. In patients with primary hyperaldosteronism, research has proven that blood vessels have a higher level of fibrosis (scar formation) in the walls of small resistance arteries.