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Introducción: Blastocystis spp., se ha identificado como un patógeno emergente causante de diarrea en hombre y en animales. Objetivo: Realizar una revisión sobre las principales características de este parásito y su rol patogénico. Metodología: Se realizó una revisión bibliográfica sobre ciclo de vida, subtipos, epidemiología, y sus posibles factores de virulencia Estas revisiones fueron extraídas de bases de datos como PUBMED, SCIENCE DIRECT, SCIELO, EBSCO y HINARI. Resultados: Blastocystis spp., es de interés por su alta prevalencia en diferentes grupos poblacionales, constante en los estudios epidemiológicos de las parasitosis humanas. Se ha evidenciado en pacientes asintomáticos y en otros con síntomas gastrointestinales, lo que depende del subtipo presente en el portador, sin embargo, esta divergencia se presta para problemas de interpretación. Conclusiones: A pesar de los estudios epidemiológicos, terapéuticos e inmunológicos que se han realizado aún no se tiene claro su ciclo de vida completo, factores de virulencia y patogenicidad.

Introduction: Blastocystis spp., has been identified as an emerging pathogen causing diarrhea in humans and animals. Objective: To conduct a review of the main features of this parasite and its pathogenic role. Methodology: A literature review on the major characteristics of Blastocystis spp., life cycle, subtypes, epidemiology and potential virulence factors was performed Reviews and research articles were extracted from databases such as PUBMED, SCIENCE DIRECT, SCIELO, HINARI and EBSCO. Results: Blastocystis spp. is of interest because of its high prevalence in different population groups, being constant in epidemiological studies of human parasitosis. It has been shown in asymptomatic patients with gastrointestinal symptoms in others, depending on the subtype present in the carrier. However, this difference is due to problems of interpretation. Conclusions: Although epidemiological, therapeutic and immunological studies have been conducted yet, it is not clear its entire life cycle, virulence factors and pathogenicity.

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BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is a result of fetomaternal incompatibility. Platelet destruction is caused by a maternal antibody directed against a fetal platelet antigen inherited from the father and lacking on the mother's platelets. The incidence and features of transplacental alloimmunization depend on the frequency of expression of platelet specific antigens; which are highly variable among different populations. AIM: To determine the prevalence and characteristics of transplacental alloimmunization in a large group of pregnant women in Chile. MATERIAL AND METHODS: We studied 3,041 samples obtained during the third trimester of gestation. In all samples, anti platelet antibodies were screened by ELISA with platelet membranes fixed to a microtiter plate. Positive samples were further studied for antigenic specificity with the monoclonal antibody specific immobilization of platelet antigens (MAIPA) test. RESULTS: Anti platelet antibodies were found in 261 samples (8.5%). The MAIPA test identified 6 samples with antibodies directed against major platelet membrane glycoproteins, 2 anti GPIb, 2 anti GPIIb/IIIa and 2 anti GPIa/IIa. In four cases, anti HLA antibodies coexisted. Two cases corresponded to well defined platelet antigen systems: one anti HPA-1a and one anti HPA-5b. No clinical evidence of thrombocytopenia of the newborn was detected in all these cases with anti GP antibodies. CONCLUSIONS: A prevalence of platelet specific antibodies of 0.2% with only one anti HPA-1a was detected. These findings are in contrast with those of other populations but in accordance with the low frequency of the HPA-1 b/b phenotype in the Chilean population. The very low incidence of platelet specific antibodies and the lack of association with clinical thrombocytopenia in the newborn, do not support the recommendation of routine antenatal screening to all women in Chile.

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BACKGROUND: Refractoriness continues to be a major complication of platelet transfusion therapy in patients with multiple transfusions. Despite most cases are secondary to non-immune causes, the most serious is that associated to alloimmunization. The incidence and consequences of HLA and non-HLA (platelet specific) antibodies are unknown in our country. AIM: To prospectively determine the frequency and characteristics of post transfusion alloimmunization and the incidence of platelet specific antibodies. PATIENTS AND METHODS: Forty one adults and 24 children with a recently diagnosed malignancy and undergoing chemotherapy that required multiple transfusions were studied. Screening for antiplatelet antibodies (platelet membrane ELISA) was performed before the first transfusion, every four weeks or whenever the 1 hour corrected count increment for platelet transfusions was lower than 5000. Platelet specific antibodies were identified with a monoclonal antibody-specific immobilization of platelet antigens (MAIPA), with anti-GPIb, GPIIb/IIIa, GPIa/Iia and anti-HLA class I. RESULTS: Adult patients received an average of 10.2 +/- 5.5 units of red blood cells and 58.6 +/- 35.4 units of platelets. Children received 4.8 +/- 3.7 units of red blood cells and 9.6 +/- 6.7 units of platelets. HLA antibodies appeared in 7 of 41 adult patients (17%), platelet specific alloantibodies were found in two patients (one anti GP Ia/IIa and one anti GP Ib). Platelet refractoriness appeared in three alloimmunized patients. No child had detectable serum antibodies during follow up. CONCLUSIONS: Platelet transfusion refractoriness of immune origin occurs infrequently in our population and the presence of platelet antibodies does not mean that it will appear. The use of leukocyte depleted blood components to prevent refractoriness cannot be justified at this time.

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