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[Subclinical micronutrients deficiencies related to metabolic syndrome].
Jiménez Ortega, AI, Martínez García, RM, Velasco Rodríguez-Belvis, M, Ruiz Herrero, J, Salas González, MªD, Ortega, RM
Nutricion hospitalaria. 2018;(Spec No6):60-63
Abstract
Metabolic syndrome is the name given to a set of risk factors that increases the risk of cardiovascular disease and other health problems, such as diabetes and stroke. There are different cut-off points to establish the definition of metabolic syndrome according to various international organizations, although in all definitions are considered four main data related to: 1) obesity; 2) alteration of glucose metabolism; 3) alteration of lipid metabolism; and 4) hypertension. Strategies for the treatment of the metabolic syndrome include changes in lifestyle (diet and physical activity), along with pharmacological treatment in certain cases. There is little evidence of the effect of different micronutrients in this syndrome, although there are many investigations in this line.
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2.
Mineral metabolism and cardiovascular disease in CKD.
Fujii, H, Joki, N
Clinical and experimental nephrology. 2017;(Suppl 1):53-63
Abstract
The mineral bone disorder of CKD, called Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), has a major role in the etiology and progression of cardiovascular disease in CKD patients. Since the main emphasis in CKD-MBD is on three categories (bone abnormalities, laboratory abnormalities, and vascular calcifications), we have routinely accepted ectopic cardiovascular calcifications as a central risk factor in the pathophysiology of CKD-MBD for cardiac events. However, recent compelling evidence suggests that some CKD-MBD-specific factors other than vascular calcification might contribute to the onset of cardiovascular disease. Most notable is fibroblast growth factor-23 (FGF23), which is thought to be independently associated with cardiac remodeling. Slow progression of cardiac disorders, such as vascular calcification and cardiac remodeling, characterizes cardiac disease due to CKD-MBD. In contrast, fatal arrhythmia may be induced when QT prolongation occurs with CKD-MBD treatment, such as with lower Ca dialysate or the use of calcimimetics. Sudden onset of fatal cardiac events, such as heart failure and sudden cardiac death, due to fatal arrhythmia would be another distinctive phenomenon of CKD-MBD. This may be defined as CKD-MBD-specific cardiac complex syndrome.
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3.
Mineral metabolism abnormalities and vitamin D receptor activation in cardiorenal syndromes.
Ronco, C, Cozzolino, M
Heart failure reviews. 2012;(2):211-20
Abstract
Over the last decade, it has become increasingly clear that the cardiovascular and renal systems are interdependent. Primary disorders of either system have been shown to disturb the other system. As a result, a class of cardiorenal syndromes (CRS) has been identified wherein a vicious cycle is established as an acute/chronic dysfunction of either the kidney or the heart exacerbates the loss of function in the other organ. Progressive loss of kidney function observed in patients with CRS (mostly types 2 and 4) leads to reduced production of calcitriol (active vitamin D) and an imbalance in calcium and phosphorus levels, which are correlated with increased rates of cardiovascular events and mortality. In addition, hypocalcemia can lead to prolonged and excessive secretion of parathyroid hormone (PTH), eventually leading to development of secondary hyperparathyroidism. Therefore, based on this important mechanism of organ damage, one of the major goals of therapy for patients with CRS is to restore regulatory control of PTH. Although administration of calcitriol increases serum calcium levels and reduces PTH levels, it is also associated with elevated serum levels of calcium-phosphorus product. Therefore, compounds that selectively activate vitamin D receptors, potentially reducing calcium × phosphate toxicity, are likely to enhance cardiorenal protection and provide significant clinical benefit.
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4.
Chronic kidney disease-mineral-bone disorder: a new paradigm.
Moe, SM, Drüeke, T, Lameire, N, Eknoyan, G
Advances in chronic kidney disease. 2007;(1):3-12
Abstract
Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and an important cause of morbidity, decreased quality of life, and extraskeletal calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified on the basis of bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) recently sponsored a Controversies Conference to evaluate this definition. The recommendations were that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD and (2) the term CKD-mineral and bone disorder (CKD-MBD) be used to describe the broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is manifested by an abnormality of any one or a combination of the following: laboratory-abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; bone-changes in bone turnover, mineralization, volume, linear growth, or strength; and calcification-vascular or other soft-tissue calcification. The pathogenesis and clinical manifestations of these components of CKD-MBD are described in detail in this issue of Advances in Chronic Kidney Disease.
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5.
Mineralization of the basal ganglia: implications for neuropsychiatry, pathology and neuroimaging.
Casanova, MF, Araque, JM
Psychiatry research. 2003;(1):59-87
Abstract
This article examines the evidence for and against the existence of basal ganglia mineralization as a defined clinico-pathological entity. In reviewing the literature on basal ganglia mineralization, this article emphasizes evidence derived from different neuroimaging modalities, genetics, metabolic studies, postmortem series and their possible neuropsychiatric correlates. Relevant articles were collected through Medline and Index Medicus searches. Researchers have encountered multiple difficulties in accepting basal ganglia mineralization as a distinct entity. This syndrome lacks set clinical criteria or a unique etiology; not surprisingly, numerous articles have applied varied definitions. Because many of the reported cases have not been examined postmortem, both the extent and nature of their mineralization remains uncertain. Furthermore, researchers have considered small foci of basal ganglia mineralization a normal phenomenon of aging. However, when brain deposits are extensive, they are associated with a set of age-dependent, progressive clinical symptoms. They include cognitive impairment, extrapyramidal symptoms and psychosis. Most cases are related to abnormalities of calcium metabolism, but rare familial cases of idiopathic origin have been reported. Overabundant mineralization of the brain is judged pathological based on its amount, distribution and accompanying clinical symptoms. Although its relation with calcium dysregulation is well known, modern studies have emphasized abnormalities of iron and dopamine metabolism. The authors suggest that these metabolic abnormalities may link basal ganglia mineralization to psychotic symptomatology.
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6.
Dietary minerals and modification of cardiovascular risk factors.
Vaskonen, T
The Journal of nutritional biochemistry. 2003;(9):492-506
Abstract
High serum cholesterol, hypertension and obesity are major risk factors for cardiovascular diseases, and together with insulin resistance form a deadly disorder referred to as the metabolic syndrome. All the aspects of this syndrome are strongly related to dietary and lifestyle factors; therefore, it would be reasonable to look for dietary approaches to their modification. Mineral nutrients, such as calcium, potassium and magnesium, lower blood pressure, and especially calcium has beneficial effects also on serum lipids. Recent evidence suggests that increased intake of calcium may help in weight control as well. This review summarizes previous literature on the effects and use of dietary minerals on serum lipids, blood pressure and obesity, with specific focus on the effects of calcium. Calcium and magnesium as divalent cations can form insoluble soaps with fatty acids in the intestine and thus prevent the absorption of part of the dietary fat. Decreased absorption of saturated fat leads to reduction in serum cholesterol level via decreased production of VLDL and increased intake of LDL in the liver. Dietary calcium may also bind bile acids, which increases the conversion of cholesterol to bile acids in the liver. Furthermore, calcium appears to enhance the cholesterol-lowering effect of plant sterols. Thus, dietary combination of the mineral nutrients and plant sterols provides a promising novel approach to the modification of cardiovascular risk factors.
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7.
Effects of propofol containing EDTA on mineral metabolism in medical ICU patients with pulmonary dysfunction.
Abraham, E, Papadakos, PJ, Tharratt, RS, Hall, JB, Williams, GJ
Intensive care medicine. 2000;:S422-32
Abstract
OBJECTIVE To determine whether the addition of disodium edetate (EDTA) to propofol significantly alters mineral metabolism, adverse events, and outcome in critically ill medical patients with acute pulmonary dysfunction. DESIGN Multicentre, double-randomised, double-blind, comparative trial. SETTING Medical intensive care units of 5 health centres. PATIENTS A total of 85 haemodynamically stable men and women aged 18-81 years who had pulmonary dysfunction or adult respiratory distress syndrome as a primary diagnosis or complication and who were expected to require at least 48 hours of sedation and mechanical ventilation. INTERVENTIONS Patients were randomised to receive propofol with or without EDTA and then to 1 of 2 sedation levels: light (Modified Ramsay Sedation Scale [MRSS] score of 2 to 3) or deep (MRSS score of 4 to 5). Propofol was administered by continuous infusion at an initial rate of 5 microg/kg per min and titrated as needed. MEASUREMENTS AND RESULTS Approximately 63 % of patients had a high severity of illness as indicated by an Acute Physiology and Chronic Health Evaluation II score > or = 19. As expected, these patients had a higher mortality rate but did not require a higher dose of propofol or propofol with EDTA. Extensive evaluation of cation homeostasis showed that ionised calcium and magnesium concentrations remained remarkably stable during treatment. Total calcium concentration was low as a result of hypoalbuminemia. Parathyroid hormone (PTH) concentration was elevated in both study groups at baseline, on day 4, and at the end of sedation. There were no significant differences in electrolyte levels and no progression to renal dysfunction. There were also no significant differences in haemodynamic or adverse-event profiles. Treatment-related adverse events occurred in 5 patients in each group; 4 of these (in 3 patients receiving propofol and 1 patient receiving propofol with EDTA) were considered serious. Because a large percentage of patients experienced a change in sedation level, no analyses were performed using sedation level. CONCLUSIONS The addition of EDTA to propofol does not alter calcium and magnesium homeostasis in critically ill patients with acute pulmonary dysfunction. The reason for the elevation in PTH concentrations in such patients is not known.