Minerals in the News Vol. 9, No. 9 (September 2011)

Naeder NT A, et al.

J Am Coll Cardiol; 2011 Jul 26; 58(5):474-80.

 

This study tries to evaluate the pathophysiological connection anemia and the severity of congestive heart disease. Anemia often accompanies advanced heart failure. However, the connection between the two remains uncertain. It has been hypothesized that a depletion of myocardial iron content may be the link. Complementary clinical and basic studies were performed. Hemodynamic, biochemical, and echocardiographic investigations were performed in 9 healthy controls and 25 patients with advanced HF (left ventricular ejection fraction: 23 ± 10%). Tissue iron content and type 1 transferrin receptor (Tfr1) expression were assessed in human myocardial tissue, and the regulation of Tfr1 expression was studied in isolated cardiomyocytes. HF patients displayed evidence of iron deficiency as measured by lower serum iron (p < 0.05) and transferrin saturation (TFS) (p < 0.05). When subclassified according to the presence of anemia, TFS was lower in anemic compared with nonanemic HF patients, whereas TFS in nonanemic HF patients was intermediate. In association, myocardial iron content was reduced in HF versus non-HF samples (0.49 ± 0.07 ?g/g vs. 0.58 ± 0.09 ?g/g, p < 0.05), and there was a significant reduction (p < 0.05) in the myocardial mRNA expression of Tfr1, which plays a key role in cellular iron transport. In the context of HF, catecholamines and aldosterone both down-regulated Tfr1 expression in isolated cardiomyocytes. This study suggests the presence of iron depletion in the failing human heart, providing a potential link for the association between anemia and adverse prognosis in HF.

 

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Takaya J, et al.

J Pregnancy; 2011:2011:270474. Epub 2010 December 28.

 

Magnesium deficiency in pregnancy frequently occurs because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problems, but also consequences that might last in offspring throughout life. Many epidemiological studies have disclosed that small for gestational age (SGA) is associated with an increased risk of insulin resistance in adult life. We reported that intracellular magnesium of cord blood platelets is lower in SGA groups than that in appropriate for gestational age groups, suggesting that intrauterine magnesium deficiency may result in SGA. Taken together, intrauterine magnesium deficiency in the fetus may lead to or at least program insulin resistance after birth. In this review, we propose that intrauterine magnesium deficiency may induce metabolic syndrome in later life. We discuss the potential contribution of aberrant magnesium regulation to SGA and to the pathogenesis of metabolic syndrome.

 

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Bae YJ, et al.

Biol Trace Elem Res; 2011 June:141(1-3):224-31.

 

Manganese (Mn) is an essential element for normal human development and bodily functions. In this study, the researchers examined whether Mn supplementation can alter the serum lipid parameters and liver function in Ca-deficient ovariectomized (OVX) rats. Sixty female Sprague-Dawley rats (6 weeks) were divided into five groups and bred for 12 weeks: sham-operated control group (Sham), OVX Ca deficiency group (OLCa) with Ca-deficient diet (0.1% Ca modified AIN-93N diet), OVX Ca deficiency and Mn supplementation group (OLCaMn), OVX with adequate Ca group (OACa; 0.5% Ca AIN-93N diet), and OVX with adequate Ca and Mn supplementation group (OACaMn). A low Ca diet increased the liver weight and serum levels of GOT, GPT, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol in OVX rats. Mn supplementation decreased these parameters in Ca-deficient OVX rat. The results of the study suggest Mn supplementation results in reductions of the blood cholesterol levels, which show an increase due to Ca deficiency in OVX rats.

 

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Jaiser SR, et al.

J Neurol: 2010 Jun;257(6):869-81.

 

Acquired copper deficiency has been regarded as a cause of anemia and neutropenia for over half a century. Copper deficiency myelopathy (CDM) was only described within the last decade, and represents a treatable cause of non-compressive myelopathy which closely mimics subacute combined degeneration due to vitamin B12 deficiency. Here, 55 case reports from the literature are reviewed regarding their demographics, aetiology, haematological and biochemical parameters, spinal imaging, treatment and outcome. The pathophysiology of disorders of copper metabolism is discussed. CDM most frequently presented in the fifth and sixth decades and was more common in women (F:M = 3.6:1). Risk factors included previous upper gastrointestinal surgery, zinc overload and malabsorption syndromes, all of which impair copper absorption in the upper gastrointestinal tract. No aetiology was established in 20% of cases. High zinc levels were detected in some cases not considered to have primary zinc overload, and in this situation the contribution of zinc to the copper deficiency state remained unclear. Cytopenias were found in 78%, particularly anemia, and a myelodysplastic syndrome may have been falsely diagnosed in the past. Spinal MRI was abnormal in 47% and usually showed high T2 signal in the posterior cervical and thoracic cord. In a clinically compatible case, CDM may be suggested by the presence of one or more risk factors and/or cytopenias. Low serum copper and caeruloplasmin levels confirmed the diagnosis and, in contrast to Wilson's disease, urinary copper levels were typically low. Treatment comprised copper supplementation and modification of any risk factors, and led to haematological normalization and neurological improvement or stabilization. Since any neurological recovery was partial and case numbers of CDM will continue to rise with the growing use of bariatric gastrointestinal surgery, clinical vigilance will remain the key to minimizing neurological sequelae.