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1.
Rev. peru. med. exp. salud publica ; 32(2): 326-334, abr.-jun. 2015. ilus
Article in Spanish | LILACS, LIPECS, INS-PERU | ID: lil-753289

ABSTRACT

La enfermedad mineral ósea (EMO) es un término amplio que incluye a las alteraciones séricas del calcio, fósforo, vitamina D, paratohormona, anormalidades en el crecimiento, mineralización ósea y/o a las calcificaciones extraesqueléticas que acompañan al paciente con enfermedad renal crónica (ERC). Está presente en casi la totalidad de pacientes en diálisis y con el trasplante renal puede no siempre mejorar. Se han identificado nuevos factores y hormonas; como klotho y factor de crecimiento de fibroblastos-23 (FGF-23) que interactúan con la vitamina D y con la paratohormona en el manejo renal del calcio y fósforo. Ciertos reportes indican que son marcadores precoces del desarrollo de EMO, incluso cuando la función renal está levemente disminuida y los niveles de paratohormona son normales. La EMO ha sido asociada con mayor mortalidad, principalmente por su vinculación con la calcificación vascular. Este proceso conlleva a un incremento de eventos cardiovasculares que constituyen la principal causa de morbimortalidad en pacientes con ERC, sobre todo aquellos que se encuentran en diálisis, independientemente de la modalidad que los pacientes sigan. La forma de presentación de la EMO puede ser de alto o bajo recambio. Aunque no está completamente definido qué es lo que determina que se exprese una en particular, se ha encontrado que la enfermedad de bajo recambio se relaciona con malnutrición, uso inadecuado de calcitriol y diálisis ineficiente. El conocimiento de la EMO es relevante por su asociación con las complicaciones mencionadas y porque constituye un parámetro para evaluar la terapia instalada.


Mineral Bone Disorder (MBD) is a broad term that includes abnormal serum calcium, phosphorus, vitamin D, parathyroid hormone, growth abnormalities, bone mineralization and/or extraskeletal calcifications in patients with chronic kidney disease (CKD ). It is present in almost all patients on dialysis and may not always improve with a kidney transplant. New factors and hormones have been identified, such as Klotho and fibroblast growth factor-23 (FGF-23) that interact with vitamin D and the parathyroid hormone in the renal management of calcium and phosphorus. Some reports indicate that they are early markers of the development of MBD, even when kidney function is slightly decreased and parathyroid hormone levels are normal. MBD has been associated with higher mortality, mainly because of its link with vascular calcification. This process leads to an increase in cardiovascular events which are the leading cause of morbidity and mortality in CKD patients, especially those who are on dialysis, regardless of the modality that the patients follow. The presentation of the BMD can be of high or low turnover. Although it is not completely defined what determines that a particular form of presentation is expressed, it has been found that the low turnover disease is related to malnutrition, inappropriate use of calcitriol and inefficient dialysis. Knowledge of BMD is relevant for its association with the complications mentioned above and because it constitutes a parameter for assessing the instituted therapy.


Subject(s)
Humans , Vitamin B Deficiency , Parathyroid Hormone , Renal Insufficiency, Chronic , Calcium Metabolism Disorders
2.
Journal of the Korean Balance Society ; : 77-80, 2014.
Article in Korean | WPRIM | ID: wpr-761166

ABSTRACT

Bilateral vestibulopathy (BV) is a clinical entity with impaired function of bilateral peripheral vestibular system, which is characterized by movement-induced vertigo, oscillopsia and gait unsteadiness. Among various etiologies of BV, alcohol and vitamin B deficiency has rarely been reported. We experienced a case of BV with vitamin B deficiency in a 24-year-old man who was previously exposed to alcohol. He had osillopsia and gait unsteadiness as a primary symptom, and was treated successfully with vestibular rehabilitation and vitamin supplement. Bithermal caloric test, rotatory chair test and head impulse test showed the result compatible with BV.


Subject(s)
Humans , Young Adult , Alcoholism , Alcohols , Avitaminosis , Caloric Tests , Gait , Head Impulse Test , Rehabilitation , Vertigo , Vitamin B Deficiency , Vitamins
3.
Rev. panam. salud pública ; 31(1): 68-73, ene. 2012. tab
Article in Spanish | LILACS | ID: lil-618470

ABSTRACT

OBJETIVO: Comparar el origen de la anemia nutricional según las variables sociodemográficas y analizar su asociación con la deficiencia en la ingesta de nutrientes hematopoyéticos. MÉTODOS: Se utilizó la base de datos de la Encuesta Nacional de la Situación Nutricional de Colombia, 2005. Los datos se obtuvieron por muestreo complejo representativo de la población y se procesaron con el programa SPSS, v.15. Se seleccionaron mujeres en edad fértil con anemia y se clasificaron en dos grupos según la ferritina sérica. Se determinó la ingesta usual de nutrientes hematopoyéticos y el riesgo de deficiencia. Se compararon las proporciones de los tipos de anemia según las variables sociodemográficas utilizando la prueba F de Rao-Scott de segundo orden (P < 0,05). Se analizó la asociación entre el origen de la anemia y la clasificación del nutriente mediante la razón de posibilidades (odds ratio, OR). RESULTADOS: Muestra: 595 mujeres. Predominó la anemia no ferropénica (67,2 por ciento), sin diferencia estadística por variables sociodemográficas, excepto en la región Pacífica (anemia ferropénica, 52,1 por ciento). La prevalencia de la deficiencia en la ingesta usual de nutrientes hematopoyéticos fue alta. No se encontró asociación significativa entre el déficit de consumo y el origen de la anemia. CONCLUSIONES: La anemia no ferropénica fue más frecuente, sin diferencia según los indicadores sociodemográficos excepto en la región Pacífica. Todas las mujeres presentaron alto riesgo de deficiencia en la ingesta usual de nutrientes hematopoyéticos, pero no se observó una asociación estadísticamente significativa entre la deficiencia y el origen de la anemia nutricional. Se justifica implementar programas orientados a mejorar el aporte de nutrientes y continuar la búsqueda de otras causas de la anemia nutricional diferentes a la deficiencia de hierro.


OBJECTIVES: Compare the nutritional origin of anemia by sociodemographic variables and analyze its association with deficient hematopoietic nutrient intake. METHODS: The database of Colombia's 2005 National Survey of Nutritional Status was used. The data were obtained through complex representative sampling of the population and processed using SPSS v.15. Anemic women of childbearing age were selected and divided into two groups according to serum ferritin levels. Their customary hematopoietic nutrient intake and risk of deficiency were determined. The proportions of anemia types were compared by sociodemographic variables using the F-distribution, the Rao-Scott second order correction (P < 0.05). The association between the origin of the anemia and classification of the nutrient was analyzed using the odds ratio (OR). RESULTS: Sample: 595 women. Non-hypoferric anemia (67.2 percent) predominated, with no statistical difference by sociodemographic variable, except in the Pacific region (hypoferric anemia, 52.1 percent). The prevalence of deficiency in the customary intake of hematopoietic nutrients was high. There was no significant association between the deficit in consumption and the origin of the anemia. CONCLUSIONS: Non-hypoferric anemia was most common, with no difference by sociodemographic indicators except in the Pacific region. All the women were at high risk of deficiency in their customary hematopoietic nutrient intake, but a statistically significant association between the deficiency and the origin of the nutritional anemia was not observed. Programs to improve nutrient intake and a continued search for causes of nutritional anemia other than iron deficiency are justified.


Subject(s)
Adolescent , Adult , Female , Humans , Middle Aged , Young Adult , Anemia/epidemiology , Diet , Malnutrition/complications , Anemia, Iron-Deficiency/epidemiology , Anemia, Iron-Deficiency/etiology , Anemia/blood , Anemia/classification , Anemia/etiology , Avitaminosis/complications , Avitaminosis/epidemiology , C-Reactive Protein/analysis , Colombia/epidemiology , Diet Records , Ferritins/blood , Hemoglobins/analysis , Iron, Dietary , Nutritive Value , Socioeconomic Factors
4.
Arq. bras. endocrinol. metab ; 53(5): 540-549, jul. 2009.
Article in Portuguese | LILACS | ID: lil-525416

ABSTRACT

A hiper-homocisteinemia, quando considerada como fator causal de doenças vasculares, tem suscitado muitas discussões. Estudos caso-controle, retrospectivos e prospectivos têm identificado relação entre concentrações plasmáticas elevadas de homocisteína e doenças vasculares. Na presente revisão, objetivou-se compreender melhor a inter-relação entre as concentrações plasmáticas de homocisteína e doenças vasculares, além do envolvimento de fatores de risco clássicos para a doença: os genéticos, como as mutações em genes que codificam as enzimas envolvidas no metabolismo da homocisteína, e os nutricionais, como a deficiência de vitaminas do complexo B. Foram consultadas as publicações das principais bases de dados em saúde, no período de 1962 a 2009. O mecanismo pelo qual a hiper-homocisteinemia atua como fator de risco para doenças vasculares ainda não está totalmente esclarecido; entretanto, sugere-se o envolvimento da disfunção endotelial e da peroxidação lipídica. O tratamento da hiper-homocisteinemia fundamenta-se na suplementação alimentar e medicamentosa, com ácido fólico e vitaminas B6 e B12.


Hyperhomocysteinemia, when considered as a causal factor of vascular diseases, has been subject of much discussion. Case-control, retrospective and prospective studies have identified a relationship between high plasma concentrations of homocysteine and vascular disease. The aim of the present review was to better understand the interrelation between plasma concentrations of homocysteine and vascular diseases, as well as the involvement of classical risk factors for the disease: genetic factors, such as mutations in the genes that codify the enzymes involved in the metabolism of homocysteine, and nutritional factors, such as complex B vitamin deficiency. The publications of the main databases in health were consulted for the period 1962 to 2009. The mechanism by which hyperhomocysteinemia acts as a risk factor for vascular diseases still has not been fully clarified, but involvement of endothelial dysfunction and lipid peroxidation is suggested. The treatment of hyperhomocysteinemia is based on food supplements and medication, with folic acid and vitamins B6 and B12.


Subject(s)
Humans , Cardiovascular Diseases/etiology , Homocysteine/blood , Hyperhomocysteinemia/complications , Biomarkers/blood , Cardiovascular Diseases/blood , Folic Acid/therapeutic use , Homocysteine/genetics , Hyperhomocysteinemia/drug therapy , Hyperhomocysteinemia/genetics , Risk Factors , /therapeutic use , /therapeutic use , Vitamin B Deficiency/complications , Vitamins/therapeutic use
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