Prevalence of thrombocytopenia in HIV‐infected and non‐HIV infected drug users and homosexual men

Mientjes, G. H. C.; Ameijden, E. J. C. Van; Mulder, J.; Hoek, Janet; Coutinho, Roel A.; Borne, A E von dem

doi:10.1111/j.1365-2141.1992.tb06476.x

Cited by 41 publications

(30 citation statements)

References 20 publications

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“…/L, while 6 (3.3%) of intravenous drug users had a count of < 50 × 10 9 /L. 5 These differences may be explained, in part, by the higher incidence of co-infection with hepatitis C and underlying liver disease in HIV-infected intravenous drug users. 6 In a prospective multicenter cohort study of 738 HIVinfected hemophilia patients, the incidence over time of HIV-related conditions was determined in 130 children and 193 adults.…”

Section: Epidemiologymentioning

confidence: 83%

“…22 Severe thrombocytopenia in patients with advanced HIV infection is frequently associated with additional cytopenias. [1][2][3][4][5][6] In a study of 52 HIV-infected intravenous drug users with thrombocytopenia, 4 patients (8%) with advanced HIV infection had a hypocellular bone marrow examination and pancytopenia. 19 HIV-infected drug users were also more likely to have antibodies to both hepatitis B and C and to have abnormal liver function studies.…”

Section: 18mentioning

confidence: 99%

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Viral-Associated Immune Thrombocytopenic Purpura

Liebman

2008

Hematology

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Chronic immune thrombocytopenic purpura (CITP) is a diagnosis of exclusion that occurs either de novo or secondary to other underlying disorders. Chronic infection with human immunodeficiency virus (HIV)andChronic immune thrombocytopenic purpura (CITP) is characterized by accelerated platelet destruction and variably impaired platelet production resulting in thrombocytopenia. CITP has been classified either as a primary autoimmune disorder (idiopathic thrombocytopenic purpura) or as secondary to a number of underlying disorders. Common conditions associated with secondary CITP include lymphoproliferative disorders and other autoimmune collagen vascular diseases. CITP is also associated with certain chronic infections. While the association between human immunodeficiency virus (HIV) infection and immune thrombocytopenia has been well known for over 20 years, recent studies have suggested that infection with Helicobacter pylori or hepatitis C virus (HCV) may be an even more frequent cause of chronic thrombocytopenia.The relationship between these chronic infections and the development of immune-mediated thrombocytopenia represents a largely unexplored paradigm in which the host response to an infectious agent results in a loss of immune self-regulation. The pathophysiology of infection-related ITP involves diverse immunologic pathways as well as nonimmune mechanisms that accelerate platelet destruction and/or decrease platelet production. A diagnosis of CITP associated with these chronic infections must include consideration of other potential causes of thrombocytopenia. For example, thrombocytopenia with HCV infection can also result from the hepatic cirrhosis leading to portal hypertension with splenic platelet sequestration and/or decreased hepatic production of thrombopoietin. However, the relationship between the infectious agent itself and the development of thrombocytopenia is clearly demonstrated by the improvements in platelet counts that follows successful treatment of the underlying infection. Therefore, the diagnostic and therapeutic algorithm for managing infection-related ITP can differ significantly from that of primary, i.e., idiopathic, thrombocytopenic purpura.

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Section: Epidemiologymentioning

confidence: 83%

Section: 18mentioning

confidence: 99%

Viral-Associated Immune Thrombocytopenic Purpura

Liebman

2008

Hematology

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“…For instance, it has been shown that 46% of critically ill medical and surgical patients have a platelet count lower than 150¥10 9 /L, 1 and that the prevalence of thrombocytopenia is 20% in patients with systemic lupus erythematosus, 2 37% in human immunodeficiency virus-positive drug users, 3 18% in patients with chronic active hepatitis B, and 13% in those with chronic hepatitis C. 4 In contrast, almost nothing is known about the prevalence of thrombocytopenia in the general population, although there is a general consensus that a low platelet count is recognized with increasing frequency in apparently healthy subjects, especially due to the measurement of platelet numbers as part of routine blood testing. 5,6 In some of these cases, further clinical investigation reveals that thrombocytopenia is secondary to an occult disease, while in others it is found that the low platelet count is inherited.…”

Section: Introductionmentioning

confidence: 99%

Analysis of 12,517 inhabitants of a Sardinian geographic isolate reveals that predispositions to thrombocytopenia and thrombocytosis are inherited traits

Biino¹,

Balduini²,

Casula³

et al. 2010

Haematologica

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The online version of this article has a Supplementary Appendix. BackgroundThrombocytopenia is a common finding in several diseases but almost nothing is known about the prevalence of thrombocytopenia in the general population. We examined the prevalence of thrombocytopenia and determinants of platelet count in a healthy population with a wide age range. Design and MethodsWe performed a cross-sectional study on 12,517 inhabitants of ten villages (80% of residents) in a secluded area of Sardinia (Ogliastra). Participants underwent a complete blood count evaluation and a structured questionnaire, used to collect epidemiological data. ResultsWe observed a platelet count lower than 150¥10 9 /L in 3.2% (2.8%-3.6%) of females and 4.8% (4.3%-5.4%) of males, with a value of 3.9% (3.6%-4.3%) in the entire population. Thrombocytopenia was mild (platelet count: 100¥10 9 /L -150¥10 9 /L), asymptomatic and not associated with other cytopenias or overt disorders in most cases. Its standardized prevalence was quite different in different villages, with values ranging from 1.5% to 6.8%, and was negatively correlated with the prevalence of a mild form of thrombocytosis, which ranged from 0.9% to 4.5%. Analysis of platelet counts across classes of age revealed that platelet number decreased progressively with aging. As a consequence, thrombocytopenia was nearly absent in young people and its prevalence increased regularly during lifetime. The opposite occurred for thrombocytosis. ConclusionsGiven the high genetic differentiation among Ogliastra villages with "high" and "low" platelet counts and the substantial heritability of this quantitative trait (54%), we concluded that the propensity to present mild and transient thrombocytosis in youth and to acquire mild thrombocytopenia during aging are new genetic traits.

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“…Según algunos estudios, esta trombocitopenia puede ser producida por la combinación de todos Anticuerpos antiplaquetarios en infección viral 1. los mecanismos patogénicos de destrucción plaquetaria expuestos inicialmente (33,34).…”

Section: Virus De La Inmunodeficiencia Humanaunclassified

“…La síntesis de anticuerpos antiplaquetarios en la infección por VIH-1, se ha explicado por medio de dos mecanismos; el primero es la activación policlonal de los linfocitos B por fallas del sistema inmunológico, que lleva a la producción de anticuerpos autorreactivos o autoanticuerpos (35-39), y la segunda explicación es la capacidad del VIH de integrarse a las plaquetas y a precursores megacariocíticos (33,38), que induciría el desarrollo de nuevos antígenos sobre la superficie de las plaquetas debido a la interacción de estructuras virales con estructuras plaquetarias, o modificaría la conformación de las glucoproteínas presentes en su membrana (exposición de antígenos plaquetarios crípticos). En ambos casos, el resultado sería la formación de autoanticuerpos dirigidos contra estos nuevos antígenos, según lo planteado por Ballem et al (38), lo cual conduciría a un secuestro prematuro de las plaquetas mediado por el sistema fagocítico mononuclear y su posterior destrucción (figura 1) (33-35).…”

Section: Virus De La Inmunodeficiencia Humanaunclassified

Papel de los anticuerpos antiplaquetarios en la infección viral: una revisión sistemática de la literatura

et al. 2011

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Introducción. La trombocitopenia es un fenómeno frecuente en las infecciones virales. Uno de los mecanismos propuesto como posible explicación de su desarrollo es la destrucción plaquetaria periférica mediada por anticuerpos antiplaquetarios. Objetivo. Revisar los resultados de los trabajos originales que existen en la literatura sobre infección viral y anticuerpos antiplaquetarios en humanos, y su efecto sobre el recuento total de plaquetas. Materiales y métodos. Se hizo una búsqueda en PubMed empleando la combinación de términos: "viral infection (OR Virus diseases) AND antibody antiplatelet (OR thrombocytopenia); y antibody antiplatelet AND HIV (OR Measles, OR Dengue, OR Chickenpox OR varicella, OR Epstein Barr, OR Mumps, OR Rubella". Se obtuvieron 218 referencias, de las cuales, 65 correspondían al objetivo de la revisión. Resultados. En la búsqueda se encontró que la trombocitopenia mediada por anticuerpos antiplaquetarios se ha documentado en infecciones virales por VIH, sarampión, dengue, varicelazóster, Epstein-Barr, parotiditis y rubéola. La presencia de anticuerpos antiplaquetarios en infecciones virales por VIH, virus de Epstein-Barr y dengue, se ha asociado con la presencia de la trombocitopenia y con la gravedad de la enfermedad. Conclusiones. Aunque la aparición de anticuerpos antiplaquetarios no se considera el único mecanismo que explica la trombocitopenia desarrollada en las infecciones virales mencionadas, de acuerdo con la literatura científica disponible, su presencia se asocia con la gravedad de la trombocitopenia y con potenciales implicaciones clínicas en los pacientes.Palabras clave: virosis, anticuerpos, plaquetas, trombocitopenia, humanos. Roll of antibodies antiplatelets in viral infection: a systematic review of literatureIntroduction. Thrombocytopenia is a frequent phenomenon in viral infections. Peripheral platelet destruction mediated by anti-platelet antibodies has been one of the proposed causal mechanisms. Objective. Results were collected and analyzed from published studies on associations of human viral infections on anti-platelet antibodies and total platelet counts. Materials and methods. A PubMed search was conducted using the following terms: Viral infection (OR Virus diseases) AND antiplatelet antibody (OR thrombocytopenia) AND HIV (OR measles OR dengue OR chickenpox OR varicella OR Epistein Barr OR mumps OR rubella). Two hundred eighteen reference hits were obtained, 65 of which were relevant to this review. Results. Antiplatelet antibody-mediated thrombocytopenia has been documented in cases of HIV, measles, dengue, chickenpox, Epstein-Barr, mumps and rubella. Moreover, the presence of these antibodies has been associated with severity the disease and thrombocytopenia in viral infections. Conclusions. Although the presence of antiplatelet antibodies was not the only mechanism for explaining the thrombocytopenia developed in these viral infections, their presence was associated with severity of thrombocytopenia and with the clinical presentation of these patients.

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Prevalence of thrombocytopenia in HIV‐infected and non‐HIV infected drug users and homosexual men

Cited by 41 publications

References 20 publications

Viral-Associated Immune Thrombocytopenic Purpura

Viral-Associated Immune Thrombocytopenic Purpura

Analysis of 12,517 inhabitants of a Sardinian geographic isolate reveals that predispositions to thrombocytopenia and thrombocytosis are inherited traits

Papel de los anticuerpos antiplaquetarios en la infección viral: una revisión sistemática de la literatura

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