RESUMO

Introducción: Las parasitosis intestinales y la anemia son un problema de salud pública mundial. Estos parásitos tienen tropismo hacia el intestino delgado, afectan la absorción de micronutrientes durante la eritropoyesis, produciendo la aparición de un síndrome anémico por un recuento bajo de glóbulos rojos y déficit de hemoglobina. Objetivo: Establecer la asociación de la infección por parásitos intestinales y síndrome anémico en niños en edad escolar. Materiales y métodos: Búsq ueda sistemática de literatura publicada entre 2010-2021 sobre asociación entre infección por parásitos intestinales y síndrome anémico en escolares. Resultados: Se identificó 1151 publicaciones, al aplicar los criterios de inclusión y exclusión, se redujeron a 33, encontrándose 9 agentes asociados a anemia, siendo A. lumbricoides (27,27%), A. duodenalis y T. trichiura los helmintos más prevalentes, y G. duodenalis (6,06%) el protozoario más común. El 39,39% de los estudios incluyó ambos agentes. África (21), Asia (6), Sudamérica (5) y Centroamérica (1) tienen la mayoría de publicaciones. Se observa asociación significativa entre infección parasitaria y la anemia IC=95%. Conclusión: La evidencia demuestra alta prevalencia de anemias carenciales de tipo ferropénica y megaloblástica, con asociación significativa entre un mayor porcentaje de infecciones por helmintos y síndrome anémico, en comparación con infecciones por protozoos.

Introduction: Intestinal parasitic infections and anemia are a global public health problem. These parasites have a tropism for the small intestine, which affects the micronutrients absorption during erythropoiesis and causes an anemic syndrome due to a low red blood cell count and hemoglobin deficiency. Objective: To establish the association of intestinal parasite infection and anemic syndrome in schoolchildren. Materials and methods: Systematic search of literature published between 2010 and 2021 about the association between intestinal parasitic infections and anemic syndrome in schoolchildren. Results: 1151 publications were identified, which were reduced to 33 when the inclusion and exclusion criteria were applied. There were 9 parasites, and the helminths commonly associated with anemia were A. lumbricoides (27.27%), A. duodenalis y T. trichiura, whereas G. duodenalis (6.06%) was the most frequent protozoan. The regions with most publications were Africa (21), Asia (6), South America (5), and Central America (1). There was a significant association between parasitic infection and anemia (CI=95%). Conclusion: High prevalence of deficiency anemia, such as iron deficiency and megaloblastic anemia, was observed. Also, there was a significant association between a higher percentage of helminth infections and anemic syndrome compared to infections caused by protozoans.

Introdução: Parasitas intestinais e anemia constituem um problema global de saúde pública. Esses parasitas têm tropismo para o intestino delgado, afetam a absorção de micronutrientes durante a eritropoiese, produzindo o aparecimento de uma síndrome anêmica devido à baixa contagem de glóbulos vermelhos e à deficiência de hemoglobina. Objetivo: Estabelecer a associação entre infecção por parasitas intestinais e síndrome anêmica em crianças em idade escolar. Materiais e métodos: Pesquisa sistemática da literatura publicada entre 2010-2021 sobre a associação entre infecção por parasitas intestinais e síndrome anêmica em escolares. Resultados: foram identificadas 1.151 publicações, ao aplicar os critérios de inclusão e exclusão, foram reduzidos para 33, encontrando 9 agentes associados à anemia, sendo A. lumbricoides (27,27%), A. duodenalis e T. trichiura os helmintos mais prevalentes e G. duodenalis (6,06%) o protozoário mais comum. 39,39% dos estudos incluíram ambos os agentes. África (21), Ásia (6), América do Sul (5) e América Central (1) têm o maior número de publicações. Observa-se associação significativa entre infecção parasitária e anemia IC=95%. Conclusão: As evidências mostram alta prevalência de anemias ferroprivas e megaloblásticas, com associação significativa entre maior percentual de infecções helmínticas e síndrome anêmica, em comparação com infecções por protozoários.

Assuntos

Assuntos

RESUMO

Introduction: Megaloblastic anemias secondary to Vitamin B12 deficiency are a group of pathologies produced by defective nuclear DNA synthesis. Objective: To describe the maturation alterations found in hematopoietic precursors of the bone marrow in a series of patients with megaloblastic anemia. Methods: Were included patients attended at the Regional Hospital of Concepción with bone marrow samples sent for the study of cytopenia by flow cytometry whose final diagnosis was megaloblastic anemia. The immunophenotype was performed with CD45, CD34, CD117, HLA-DR, markers of neutrophil (CD13, CD11b, CD10, CD16) and/or erythroblast (CD105, CD71, CD36) maturation. Results: From the flow cytometry laboratory database, 8 patients with megaloblastic anemia were identified, and myelodysplastic syndromes (n=9) and normal or reactive bone marrow (n=10) were used as controls. 44% were men, with a median age of 58 years. Megaloblastic anemia was associated with a higher proportion of size and complexity of erythroid and myeloid progenitors compared to lymphocytes compared to controls. The total percentage of erythroblasts and the proportion of CD34+ myeloid cells associated with erythroid lineage was higher in megaloblastic anemia, associated with a maturation arrest in the CD105+ precursor stage (69% vs 19% and 23%, p<0.001). The heterogeneity of CD36 and CD71 in megaloblastic anemia was similar to myelodysplastic syndromes. Conclusions: Megaloblastic anemia produces a heterogeneous involvement of hematopoiesis, characterized by a greater size and cellular complexity of precursors of the neutrophil and erythroid series and a maturation arrest of the erythroblasts.

Introducción: Anemias megaloblásticas secundarias a la deficiencia de vitamina B12 son patologías producidas por una síntesis defectuosa del ADN nuclear. Objetivo: Describir las alteraciones madurativas encontradas en precursores hematopoyéticos de la médula ósea de una serie de pacientes con anemia megaloblástica. Métodos: Se incluyeron pacientes atendidos en el Hospital Regional de Concepción con muestras de médula ósea enviadas para estudio de citopenias por citometría de flujo cuyo diagnóstico fue anemia megaloblástica. El inmunofenotipo se realizó con CD45, CD34, CD117, HLA-DR, marcadores de maduración de serie de neutrófilo (CD13, CD11b, CD10, CD16) y/o eritroblasto (CD105, CD71, CD36). Resultados: Se identificaron 8 pacientes con anemia megaloblástica y como controles se utilizaron síndromes mielodisplásicos (n=9) y médula ósea normal o reactiva (n=10). El 44% eran hombres, con una mediana de edad de 58 años. La anemia megaloblástica se asoció con una mayor proporción de tamaño y complejidad de progenitores eritroides y mieloides con respecto de los linfocitos en comparación a los controles. El porcentaje total de eritroblastos y la proporción de células mieloides CD34+ comprometidas con el linaje eritroide fue mayor en anemia megaloblástica, asociado a una parada madurativa en la etapa de precursor CD105+ (69% vs 19% y 23%, p <0.001). La heterogeneidad de CD36 y CD71 en anemia megaloblástica fue similar a los síndromes mielodisplásicos. Conclusiones: la anemia megaloblástica produce una afectación heterogénea de la hematopoyesis, caracterizada por un mayor tamaño y complejidad celulares de precursores de la serie neutrófilo y eritroide y una detención madurativa de los eritroblastos.

Assuntos

RESUMO

El folato es un miembro del grupo de la vitamina B y está relacionado con enfermedades crónicas como anemia megaloblástica, enfermedad cardiovascular, cáncer, disfunción cognitiva y riesgo de defectos del tubo neural. La proteína 5,10-metilentetrahidrofolato reductasa (MTHFR) juega un papel clave en el metabolismo del folato mediante la síntesis de nucleótidos y reacciones de metilación. El gen MTHFR se encuentra en el cromosoma 1 (1p36.3), y se han descrito dos alelos comunes, el alelo C677T (termolábil) y el alelo A1298C.El objetivo de este estudio es evaluar la distribución de los polimorfismos genéticos en MTHFR C677T y A1298C en la población venezolana. METODOS: estudio de tipo transversal, descriptivo, experimental y correlacional Las muestras de sangre se colectaron en 314 donantes no emparentados y sanos de la población. Los polimorfismos de un solo nucleótido(SNP) MTHFR 677C>T y 1298A>C se analizaron mediante polimorfismo de longitud de fragmento de restricción de reacción en cadena de polimerasa (PCR-RFLP). El desequilibrio de ligamiento (LD) entre pares de SNP se calculó mediante la prueba X. usando Prism 5 (GraphPad software, Inc). RESULTADOS: Encontramos mayor frecuencia genotípica de heterocigotos para el polimorfismo MTHFR C677T en la población general venezolana, con excepción del grupo caucásico. El polimorfismo MTHFR A1298C en el 70%de la población de estudio es homocigoto de tipo salvaje, encontrándose una baja frecuencia de homocigoto mutado. CONCLUSIONES: Se encontraron diferencias significativas entre grupos étnicos, destacando la importancia del genotipado racial de estos polimorfismos en la población venezolana(AU)

Folate is a member of the vitamin B and it has also been indicated that may be related to chronic diseases such as megaloblastic anemia, cardiovascular disease, cognitive dysfunction and risk of neural tube. Methylenetetrahydro folatereductase (MTHFR) is a key enzyme of folate pathway by nucleotide synthesis and methylation reactions. Several polymorphisms were reported in MTHFR gene but C677Tand A1298 polymorphism are most studied and these have been reported to be risk factor for several diseases/disorders. The present study was designed to determine the frequency of MTHFR polymorphisms in Venezuelan healthy population. METHODS: The blood samples were collected from 314 unrelated and healthy donors from population. Both the MTHFR 677C>T and 1298A>C single nucleotide polymorphisms (SNPs) were analyzed by Polymerase chainreaction-restriction fragment length polymorphism (PCR-RFLP). Linkage disequilibrium (LD) between pair of SNPs was calculated through the .. test using Prism 5 (GraphPad sftoware, Inc). RESULTS: We find higher genotypic frequency of heterozygotes for the MTHFR C677T polymorphism in the Venezuelan general population, with the exception of the Caucasian group. MTHFR A1298C polymorphism in 70%of the study population is homozygous wild type, finding alow frequency of homozygous mutated. CONCLUSIONS: Significant differences between ethnic groups were found,highlighting the importance of racial genotyping of these polymorphisms in the Venezuelan population(AU)

Assuntos

RESUMO

Introducción: La anemia megalobástica es un trastorno madurativo de los precursores eritroides y mieloides causado por déficit de vitamina B12, ácido fólico, o ambos. Es poco común en la infancia y su prevalencia se desconoce por ser una enfermedad poco frecuente. Objetivo: Describir diferentes formas de presentación de la anemia megaloblástica en el lactante. Presentación de casos: Se presentan dos casos de lactantes, en el caso 1 la madre tuvo una alimentación precaria durante el embarazo y la lactancia, prolongó la lactancia materna exclusiva más de 6 meses. La paciente comenzó a perder las habilidades ganadas en el desarrollo psicomotor y presentó trastornos neurológicos graves, por lo que se consideró que se trataba de una enfermedad progresiva del sistema nervioso central. En el caso 2, en el que se prolongó la lactancia materna exclusiva, apareció trombocitopenia, por lo que se sospechó una enfermedad hematológica maligna. Resultados: En ambos casos después de realizar diversas pruebas para descartar enfermedades neurológicas (caso 1) y enfermedades hematológicas (caso 2) se diagnosticó anemia megaloblástica por déficit de vitamina B12 por disminución en la ingesta y una reserva limítrofe en la madre que lacta. En ambos casos los síntomas desaparecieron con el tratamiento vitamínico sustitutivo. Conclusiones: En el lactante la anemia megaloblástica se puede presentar de diferentes formas clínicas a pesar de tener la misma causa, un déficit en la ingesta y una reserva escasa de la madre durante el embarazo y lactancia(AU)

Introduction: Megaloblastic anemia is a maturing disorder of the erythroid and myeloid precursors caused by deficiency of vitamin B12, folic acid, or both. It is uncommon in childhood and its prevalence is unknown because it is a rare disease. Objective: To describe different forms of presentation of megaloblastic anemia in infants. Presentation of cases: Two cases of infants are presented, in case 1 the mother had a precarious diet during pregnancy and lactation, and prolonged exclusive breastfeeding more than 6 months. The patient began to lose the skills gained in psychomotor development and presented severe neurological disorders, so it was considered that it was a progressive disease of the central nervous system. In case 2, in which exclusive breastfeeding was prolonged, thrombocytopenia appeared, so a malignant hematological disease was suspected. Results: In both cases, after performing various tests to rule out neurological diseases (case 1) and hematological diseases (case 2), megaloblastic anemia was diagnosed due to vitamin B12 deficiency due to a decrease in intake and a borderline reserve in the breastfeeding mother. In both cases the symptoms disappeared with vitamin replacement therapy. Conclusions: In the infant, megaloblastic anemia can occur in different clinical ways despite having the same cause, a deficit in intake and a low reserve of the mother during pregnancy and lactation(AU)

Assuntos

Assuntos

RESUMO

INTRODUCTION: In infants, vitamin B12 deficiency is mainly due to nutritional deficiencies related to maternal deficit. Most cases of maternal deficiencies are associated with vegetarian diets. Pernicious anemia is an au toimmune disease that affects the absorption of this vitamin. Although it is less common than nutri tional deficiency, is also an important cause of maternal deficiency. OBJECTIVE: to report a case of an infant with vitB12 deficiency, secondary to pernicious anemia in his mother, and to review the most important aspects of this disease in childhood. CLINICAL CASE: Nine months-old male infant, without pathological perinatal history, exclusively breastfed, with persistent rejection of solid food from 6 months of age. One month before hospitalization, he progressively presented hyporesponsiveness, with fluctuating state of alertness, regression of motor development milestones, and vomiting. The blood count showed macrocytic anemia and neutropenia. Vitamin B12 deficiency was confirmed in the patient. He received treatment with intramuscular vitamin B12 with good clinical and laboratory response. Maternal B12 deficiency was confirmed as the cause of the infant's deficiency. Since the mother reported no dietary restrictions, anti-intrinsic factor and anti-parietal cell antibodies were measured, leading to the diagnosis of pernicious anemia. CONCLUSIONS: Early recognition is essential to prevent the development of potentially irreversible neurological damage. Maternal pernicious ane mia should be considered in children with megaloblastic anemia, especially in those whose mothers do not follow vegetarian diets.

Assuntos

Assuntos

RESUMO

Cada vez más los pacientes diagnosticados con anemia son referidos al gastroenterólogo para su evaluación. La necesidad de realizar un adecuado planteo clínico y una correcta interpretación de las pruebas de diagnóstico ha motivado la revisión de este tema. Varios trastornos gastroenterológicos, con frecuencia, conducen a anemia como resultado de pérdidas sanguíneas, inflamación, malabsorción o a consecuencia de las terapias farmacológicas. En algunas patologías como la cirrosis, EII o neoplasias las causas son a menudo multifactoriales. Esta revisión, pretende proporcionar un enfoque útil para la práctica clínica. Para ello se ha revisado la información actualizada acerca de la patogénesis, diagnóstico y tratamiento de la anemia vinculada a patologías digestivas y se han confeccionados cuadros y algoritmos para facilitar su comprensión.

More and more patients diagnosed with anemia are referred to the gastroenterologist for evaluation. The need to carry out an adequate clinical approach and a correct interpretation of diagnostic tests has motivated this review. Several digestive diseases frequently lead to anemia because of blood loss, inflammation, malabsorption, or drug therapies. In some of them such as cirrhosis, IBD or neoplasms, the etiology is multifactorial. This review is intended to provide a useful approach to clinical practice. To this aim, updated information on the pathogenesis, diagnosis, and treatment of anemia related to digestive diseases has been reviewed, and tables and algorithms have been built to favor its understanding.

Cada vez mais pacientes diagnosticados com anemia são encaminhados ao gastroenterologista para avaliação. A necessidade de realizar uma abordagem clínica adequada e uma interpretação correta dos testes de diagnóstico motivou a revisão deste tema. Vários distúrbios gastroenterológicos freqüentemente levam à anemia como resultado de perda de sangue, inflamação, má absorção ou pelas próprias terapias farmacológicas. Em algumas patologias como cirrose, DII ou neoplasias, as causas costumam ser multifatoriais. Esta revisão visa fornecer uma abordagem útil à prática clínica. Para esse fim, foram revisadas informações atualizadas sobre a patogênese, o diagnóstico e o tratamento da anemia associada à patologia digestiva e foram elaboradas tabelas e algoritmos para facilitar seu entendimento.

Assuntos

Assuntos