Macro- and micronutrients in African-Americans with heart failure

被引:25
作者
Bhattacharya, Syamal K.
Ahokas, Robert A.
Carbone, Laura D.
Newman, Kevin P.
Gerling, Ivan C.
Sun, Yao
Weber, Karl T. [1 ]
机构
[1] Univ Tennessee, Ctr Hlth Sci, Div Cardiovasc Dis, Memphis, TN 38163 USA
[2] Univ Tennessee, Ctr Hlth Sci, Dept Obstet & Gynecol, Memphis, TN 38163 USA
[3] Univ Tennessee, Ctr Hlth Sci, Div Connect Tissue Dis, Memphis, TN 38163 USA
[4] Univ Tennessee, Ctr Hlth Sci, Dept Surg, Memphis, TN 38163 USA
[5] Univ Tennessee, Ctr Hlth Sci, Div Endocrinol, Memphis, TN 38163 USA
[6] Vet Affairs Med Ctr, Memphis, TN USA
关键词
calcium; magnesium; zinc; selenium; hypovitaminosis D; secondary hyperparathyroidism;
D O I
10.1007/s10741-006-9192-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
An emerging body of evidence suggests secondary hyperparathyroidism (SHPT) may be an important covariant of congestive heart failure (CHF), especially in African-Americans (AA) where hypovitaminosis D is prevalent given that melanin, a natural sunscreen, mandates prolonged exposure of skin to sunlight and where a housebound lifestyle imposed by symptomatic CHF limits outdoor activities and hence sunlight exposure. In addition to the role of hypovitaminosis D in contributing to SHPT is the increased urinary and fecal losses of macronutrients Ca2+ and Mg2+ associated with the aldosteronism of CHF and their heightened urinary losses with furosemide treatment of CHF. Thus, a precarious Ca2+ balance seen with reduced serum 25(OH)D is further compromised when AA develop CHF with circulating RAAS activation and are then treated with a loop diuretic. SHPT accounts for a paradoxical Ca2+ overloading of diverse tissues and the induction of oxidative stress at these sites which spills over to the systemic circulation. In addition to SHPT, hypozincemia and hyposelenemia have been found in AA with compensated and decompensated heart failure and where an insufficiency of these micronutrients may have its origins in inadequate dietary intake, altered rates of absorption or excretion and/or tissue redistribution, and treatment with an ACE inhibitor or AT(1) receptor antagonist. Zn and Se deficiencies, which compromise the activity of several endogenous antioxidant defenses, could prove contributory to the severity of heart failure and its progressive nature. These findings call into question the need for nutriceutical treatment of heart failure and which is complementary to today's pharmaceuticals, especially in AA.
引用
收藏
页码:45 / 55
页数:11
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