Blood and bone marrow changes in malaria

Wickramasinghe, S. N.; Abdalla, Saad

doi:10.1053/beha.1999.0072

Cited by 238 publications

(257 citation statements)

References 77 publications

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“…While platelet-count changes are particularly associated with P. falciparum malaria 9,12,45 , this pathology has also been identified in malaria caused by other species, such as P. vivax 36,46 . Changes in other platelet parameters, such as PT, MPV or PDW, have not been well described in malaria patients.…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have found that patients infected with P. vivax or P. falciparum develop anemia, monocytosis, eosinopenia and lymphopenia 45 . This study found a progressive reduction in hemoglobin levels and white blood cell counts with reduced PCs, which resulted in anemia, monocytopenia, neutropenia and lymphopenia.…”

Section: Discussionmentioning

confidence: 99%

“…Low PCs have been associated with increased parasite load. This association may result from sensitization induced by the parasitized red blood cells in the platelet, with consequent increased platelet sensitivity to adenosine diphosphate (ADP) and higher dense-granule secretion 45,46 . These changes could ultimately promote platelet aggregation on the endothelium, which has been demonstrated in cerebral malaria 27 .…”

Section: Discussionmentioning

confidence: 99%

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Platelet profile is associated with clinical complications in patients with vivax and falciparum malaria in Colombia

Martinez-Salazar

Tobón-Castaño

2014

Rev. Soc. Bras. Med. Trop.

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Introduction: Thrombocytopenia is a common complication in malaria patients. The relationship between abnormal platelet profi le and clinical status in malaria patients is unclear. In low and unstable endemic regions where vivax malaria predominates, the hematologic profi les of malaria patients and their clinical utility are poorly understood. The aim of this study was to characterize the thrombograms of malaria patients from Colombia, where Plasmodium vivax infection is common, and to explore the relationship between thrombograms and clinical status. Methods: Eight hundred sixty-two malaria patients were enrolled, including 533 (61.8%) patients infected with Plasmodium falciparum, 311 (36.1%) patients infected with Plasmodium vivax and 18 (2.1%) patients with mixed infections. Results: The most frequently observed changes were low platelet count (PC) and high platelet distribution width (PDW), which were observed in 65% of patients; thrombocytopenia with <50,000 platelets/µL was identifi ed in 11% of patients. Patients with complications had lower PC and plateletcrit (PT) and higher PDW values. A higher risk of thrombocytopenia was identifi ed in patients with severe anemia, neurologic complications, pulmonary complications, liver dysfunction, renal impairment and severe hypoglycemia. The presence of thrombocytopenia (<150,000 platelets/µL) was associated with a higher probability of liver dysfunction. Conclusions: Young age, longer duration of illness and higher parasitemia are associated with severe thrombocytopenia. Our study showed that thrombocytopenia is related to malaria complications, especially liver dysfunction. High PDW in patients with severe malaria may explain the mechanisms of thrombocytopenia that is common in this group of patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Platelet profile is associated with clinical complications in patients with vivax and falciparum malaria in Colombia

Martinez-Salazar

Tobón-Castaño

2014

Rev. Soc. Bras. Med. Trop.

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“…Severe vitamin A deficiency alone in rats produced a microcytic, hypochromic polycythemia, whereas simultaneous vitamin A and iron deficiencies produced a normocytic, hypochromic anemia (Amine et al, 1970). The anemia of acute malaria is generally a normocytic, normochromic anemia (Wickramasinghe & Abdalla, 2000). Medications that may complicate the interpretation of red cell indices include trimethoprim, a widely used antibiotic that can cause a megaloblastic anemia (Magee et al, 1981), isoniazid and pyrazinamide, tuberculosis medications that can cause a sideroblastic anemia (Sharp et al, 1990), and chloroquine, which may suppress erythropoietin production (El Hassan et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

The anemia of vitamin A deficiency: epidemiology and pathogenesis

Bloem²

2002

Eur J Clin Nutr

300

223

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Objective: To gain insight into vitamin A deficiency as a cause of anemia. Methods: Comprehensive review of the scientific literature. Results: Although vitamin A deficiency is recognized to cause anemia, 'vitamin A deficiency anemia' lacks complete characterization as a distinct clinical entity. Vitamin A appears to be involved in the pathogenesis of anemia through diverse biological mechanisms, such as the enhancement of growth and differentiation of erythrocyte progenitor cells, potentiation of immunity to infection and reduction of the anemia of infection, and mobilization of iron stores from tissues. Epidemiological surveys show that the prevalence of anemia is high in populations affected by vitamin A deficiency in developing countries. Improvement of vitamin A status has generally been shown to reduce anemia, but the actual public health impact on anemia is unclear. Conclusions: Further work is needed to elucidate the biological mechanisms by which vitamin A causes anemia. The inclusion of anemia as an outcome measure in future micronutrient intervention studies should help provide further insight into the anemia of vitamin A deficiency.

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“…I): 52-63, 2011 Malaria affects almost all blood components and is a true haematological infectious disease. Anaemia and thrombocytopenia are the most frequent malaria-associated haematological complications (Wickramasinghe & Abdalla 2000) and have received more attention in the scientific literature due to their associated mortality. On the other hand, thrombocytopenia is less studied, causes negligible mortality and is an isolated phenomenon; there is no report of a single patient in the literature who has died only because of malaria-associated thrombocytopenia.…”

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confidence: 99%

Thrombocytopenia in malaria: who cares?

Lacerda

Mourão

Coelho

et al. 2011

Mem. Inst. Oswaldo Cruz

186

173

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Key words: Plasmodium falciparum -Plasmodium vivax -malaria -thrombocytopenia -plateletsMalaria and thrombocytopenia • Marcus Vinícius Guimarães Lacerda et al. 53Data on the real burden of thrombocytopenia associated with malaria is contradictory in the literature and it is not usually considered when conducting patient selection. Table I shows the major publications estimating the frequency of thrombocytopenia. Most of these data were published in the late 1990s, probably in time with the surge in the availability of affordable automated machines capable of performing full blood counts (FBC). Manual platelet counting is time-consuming and usually needs to be requested by the physician with the routine blood count in most of the endemic areas for malaria. In only three publications is there an adequate randomised enrollment of patients with appropriate sample size calculation to estimate the frequency of bleeding and its association with the respective platelet count (Lacerda 2007, Silva 2009, Kochar et al. 2010. Only one study has ruled out other common causes of thrombocytopenia that are also endemic in the studied area (Lacerda 2007). There is a wide range of thrombocytopenia occurrence in these reports, which may be explained by distinct selection criteria of the enrolled patients. There are also differences in the selection of outpatients or inpatients from tertiary care centres that tend to present with severe thrombocytopenia. Furthermore, clinical manifestations of thrombocytopenia are usually described as case reports and most of these are due to P. vivax (Table II).In 2005, 138 of 684 (20.1%) malarial cases hospitalised in a tertiary care centre in Manaus had thrombocytopenia as the cause of admission, which corresponded to 6.8% of hospitalisations due to all causes in this reference institution (unpublished observations). Hospitalisation, however, does not add any benefit to the patient and because there is no evidence for any intervention, this simply increases public health costs in underdeveloped and under-resourced areas.Pathogenesis of malarial thrombocytopenia -Coagulation disturbances -A study based on 31 American soldiers in Vietnam with chloroquine-resistant falciparum malaria noted the following changes in the acute phase of the disease using the same patients as their own controls during convalescence: decrease in the platelet count and prothrombim activation time, increase in the activated thromboplastin time, and reduction in factors V, VII and VIII with normal fibrinogen (Dennis et al. 1967). This report suggested that thrombocytopenia was simply a consequence of the coagulation disorders presented by these patients, an idea that persisted for many decades in the literature. In another series of 21 patients with falciparum malaria, six had developed disseminated intravascular coagulation (DIC). The authors noted that the patients with more severe thrombocytopenia also had DIC and that there was correlation between platelet count and C3 protein levels. However, the reduction in C3 was pr...

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Blood and bone marrow changes in malaria

Cited by 238 publications

References 77 publications

Platelet profile is associated with clinical complications in patients with vivax and falciparum malaria in Colombia

Platelet profile is associated with clinical complications in patients with vivax and falciparum malaria in Colombia

The anemia of vitamin A deficiency: epidemiology and pathogenesis

Thrombocytopenia in malaria: who cares?

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