Sickle Cell Anemia And Malaria Pdf

sickle cell anemia and malaria pdf

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Normally, RBCs are shaped like discs, which gives them the flexibility to travel through even the smallest blood vessels. However, with this disease, the RBCs have an abnormal crescent shape resembling a sickle. This makes them sticky and rigid and prone to getting trapped in small vessels, which blocks blood from reaching different parts of the body.

Sickle cell disease SCD is a group of blood disorders typically inherited from a person's parents.

Sickle Cell Anaemia and Malaria

Julie Makani, Albert N. Komba, Sharon E. Williams; Malaria in patients with sickle cell anemia: burden, risk factors, and outcome at the outpatient clinic and during hospitalization. Blood ; 2 : — Approximately children are born with sickle cell anemia SCA in Africa annually, yet few survive beyond childhood.

Falciparum malaria is considered a significant cause of this mortality. We conducted a 5-year prospective surveillance study for malaria parasitemia, clinical malaria, and severe malarial anemia SMA in Dar-es-Salaam, Tanzania, between and We recorded 10 visits to the outpatient clinic among patients with SCA and visits among patients without SCA.

Furthermore, patients with SCA had higher rates of malaria during hospitalization than at clinic, the ORs being 4. Although malaria was rare among patients with SCA, parasitemia during hospitalization was associated with both severe anemia and death.

Effective treatment for malaria during severe illness episodes and further studies to determine the role chemoprophylaxis are required. Recently, there have been 3 important developments in the fields of malaria and SCA that prompted us to review the role of malaria in SCA. In this study we followed a cohort of patients with SCA in Tanzania between and and investigated the burden of malaria by documenting malaria events both at the outpatient clinic and during hospitalization.

This is the largest and most densely populated region in Tanzania, with a population of 2. All patients with SCA were provided information about SCA, malaria, and the study both verbally and with printed leaflets in the local language, Kiswahili. Advice was given about the general management of SCA and procedures for seeking care in the event of acute illness events such as fever, pain, or symptomatic anemia.

Each patient was then invited to join the study. Patients who agreed either signed a consent form or provided a thumbprint if they could not write, in accordance with the Declaration of Helsinki. For children, consent was requested from the parent or guardian. After informed consent, detailed histories and examinations were recorded onto standardized proformas. Investigations included a full blood count, biochemical analysis, and detection of malaria parasitemia.

Because patients with SCA are generally perceived to be at risk of malaria mortality, any parasitemia, irrespective of density or absence of symptoms, was treated following recommended protocols: chloroquine, sulfadoxine pyrimethamine, or artemether lumefantrine for uncomplicated malaria and quinine for severe malaria.

During episodes of acute illness, patients were encouraged to contact either a study physician or their nearest health facility, following the referral procedures through the public health care system.

The decision to admit patients with SCA rested with the attending clinician in the hospital casualty department, following criteria set by MNH. Clinical and laboratory data were collected at admission. Additional investigations were performed as clinically indicated. Patients suspected to have SCA who had not been recruited into the cohort were also identified during hospitalization and recruited into the study. Reticulocytes were counted following standard methods with new methylene blue staining.

Biochemical tests were performed with the use of a chemistry analyzer Roche Cobas Mira or Abbott Architect. All persons were investigated for malaria at all visits.

P falciparum densities were assessed by counting the number of asexual-stage parasites per white blood cells WBCs and expressed as parasites per microliter whole blood. For patients with SCA we used All data were checked for consistency before double entry onto a database written in MySQLv5. Patients entered the SCA cohort on the day they were first seen at the hospital, whether at the OPD clinic or during hospitalization.

Persons with SCA and without SCA who were seen in the casualty department but were not hospitalized were not included in the study. Incidence rates for malaria events were calculated for the whole study period, combining events at OPD clinic and during hospitalization. The rates were calculated by the ratio of relevant malaria events divided by the number of person-years of exposure PYOs and were presented as the number of events per PYOs.

The age-specific incidence of malaria was calculated by analyzing the frequency of events in each person, excluding episodes that were clustered within a person. The analysis period was from March 24, , to March 23, The OPD clinic data were derived from 10 visits among patients with SCA median age, 11 years; range, 4 months to 47 years and visits from among persons without SCA median age, Control data were collected from patients without SCA aged 6 months to 10 years who were admitted between and The prevalence of malaria in the various subject groups is summarized in Figure 1.

Flow of persons and visits in the study with prevalence of malaria parasitemia. Clinic refers to events at outpatient clinic visits; admissions refer to events during hospitalization. Number of visits refers to all visits; n is number of persons. Malaria refers to malaria parasitemia. The number after malaria is the number of episodes of malaria parasitemia, figures in parentheses is the prevalence per visit not per person. The overall prevalence of malaria parasitemia at the OPD clinic was 88 of 0.

Further, the prevalence was significantly lower both in subjects with HbAS 0. The events in patients with SCA both at the outpatient clinic and during hospitalization are shown in Table 1. The prevalence of parasitemia, malaria, and SMA were all higher during hospitalization than at the outpatient clinic. Among patients with SCA visiting the OPD clinic, subjects were only clinically ill with either fever or severe anemia associated with parasitemia on 14 0.

Six patients 0. During hospitalization, 11 1. OR indicates the odds ratio for events for hospitalized patients versus the outpatient clinic. The OPD clinic was used as baseline. The features associated with parasitemia in patients with SCA are summarized in Table 2. During OPD clinic visits, factors that were significantly associated with parasitemia on univariate analysis included fever, higher oxygen saturation, spleen and liver enlargement, high WBC count and mean corpuscular volume, and low Hb.

On multivariate analysis, high WBC count was the only feature that remained significantly associated OR, 3. Factors associated with malaria parasitemia in individuals with sickle cell anemia at the outpatient clinic and during hospitalization. The following values were the The denominators denote available data. The presenting symptoms in patients with SCA during hospitalization occurred with the following frequencies: pain was reported in of Parasitemia was detected in 21 admissions 3.

The factors associated with malaria parasitemia during hospitalization on univariate analysis are summarized in Table 2. At admission, patients with SCA with parasitemia were older, had lower Hb concentrations, and had higher mean corpuscular volumes, reticulocyte counts, and plasma aspartate transaminase AST concentrations than patients without parasitemia. The risk of death during hospitalization was higher in patients with parasitemia OR, 4. The factors that were independently associated with parasitemia were severe anemia OR, 3.

Multivariate analysis of factors associated with malaria parasitemia at OPD clinic and during hospitalization in patients with SCA. During the 5 years of study, we recorded PYO. The incidence rate of parasitemia was 2. Malaria events stratified into 2 age bands older and younger than 5 years , excluding events clustered in persons, is shown in Table 4.

Compared with persons older than 5 years, children younger than 5 years had a lower prevalence of parasitemia OR, 0. Age-specific incidence of malaria parasitemia, clinical malaria, and severe malarial anemia in patients with sickle cell anemia.

This is the first detailed report to have focused on the importance of malaria as a cause of morbidity and mortality in patients living with SCA. Conversely, there is more compelling evidence to suggest that patients with SCA are protected from malaria, both in terms of a lower prevalence of malaria infection and a lower parasite density.

Ethical concerns about conducting an observational study of subjects with SCA, generally considered to be at risk of malaria, in a group who were essentially not on effective chemoprophylaxis, was countered because the malaria prevalence in Dar-es-Salaam is generally low 0. The most striking finding in our study was the lower prevalence of malaria parasitemia in patients with SCA than in patients without SCA, both at the outpatient clinic and during hospitalization.

A degree of malaria resistance in patients with SCA seems plausible, given that protection is unequivocal in heterozygotes HbAS. The incidence of malaria parasitemia in our study was 2. The incidence of parasitemia in children younger than 5 years was lower than in children older than 5 years, a finding that may be due to protection of younger children by ITNs, provided free in Tanzania to children of this age group.

The spectrum of malarial disease includes asymptomatic infection, febrile episodes, and severe illness anemia and cerebral complications. However, in this study more patients had SMA 1. We found that malaria events occurred at higher rates in patients with SCA during hospitalization than at the outpatient clinic. This suggests that, although patients with SCA are at lower risk of malaria than persons without SCA, protection is not complete, and malaria is an important factor that needs to be considered during hospitalization.

We acknowledge that this finding may simply reflect the fact that patients with malaria are more likely to have severe illness and to be hospitalized.

However, the aim of the study was not to determine whether malaria was the cause of hospitalization but to look for an association between malaria parasitemia and clinical events, including during hospitalization.

Parasitemia was significantly associated with mortality during hospitalization 9. Therefore, the consequences of malaria in SCA appear to be severe during acute illness, as previously suggested by Molineaux et al. Our study has several limitations. First, the overall prevalence of malaria parasitemia at the OPD clinic was only 0.

The second limitation is that, because this study was conducted in a referral hospital, it was open to several potential biases relating to the treatment-seeking behavior of patients with SCA and the perception of their health care providers. There is a possibility that some events may have been missed as a result of treatment at casualty, other health care facilities, or at home. Furthermore, although we did not change protocols of referral and management in the hospital, SCA is known to have a high risk of mortality, and, because patients were both part of a cohort study and were encouraged to present early in the event of an intercurrent illness, this may have introduced a bias toward higher rates of presentation and hospitalization in patients with SCA.

A stronger study design might have included a prospective cohort study that reported careful monitoring of SCA and control subjects that used well-defined criteria for medical consultation, diagnosis of asymptomatic malarial parasitemia and acute malaria infection. Nevertheless, at the outset of our study, we did not make any assumptions about malaria and did not alter the current practice of referral and hospitalization to observe the actual practice in the community.

Given existing attitudes to malaria in patients with SCA, it would have been difficult to design a comparative cohort study of this sort without close monitoring of effective antimalarial chemoprophylaxis. In summary, in our study, conducted in an area of low but perennial malarial transmission; we found that malaria was less common in subjects with SCA than in subjects without SCA both at the outpatient clinic and during hospitalization.

This raises the question of whether, and under what circumstances, malaria prophylaxis is required in patients with SCA.

Malaria and Sickle Cell Anemia

Sickle cell anaemia is a major chapter within haemolytic anaemias; at the same time, its epidemiology is a remarkable signature of the past and present world distribution of Plasmodium falciparum malaria. In this brief review, in keeping with the theme of this journal, we focus on the close and complex relationship betweeen this blood disease and this infectious disease. On one hand, heterozygotes for the sickle gene AS are relatively protected against the danger of dying of malaria, as now firmly established through a number of clinical field studies from different parts of Africa. In addition, experimental work is consistent with a plausibile mechanism: namely, that in AS heterozygotes P falciparum -infected red cells sickle preferentially and are then removed by macrophages. On the other hand, patients who are homozygous for the sickle gene and therefore suffer from sickle cell anaemia SCA are highly susceptible to the lethal effects of malaria. The simplest explanation of this fact is that malaria makes the anaemia of SCA more severe; in addition, in SCA there is often hyposplenism, which reduces clearance of parasites. From the point of view of public health it is important that in malaria-endemic countries patients with SCA, and particularly children, be protected from malaria by appropriate prophylaxis.

Julie Makani, Albert N. Komba, Sharon E. Williams; Malaria in patients with sickle cell anemia: burden, risk factors, and outcome at the outpatient clinic and during hospitalization. Blood ; 2 : — Approximately children are born with sickle cell anemia SCA in Africa annually, yet few survive beyond childhood.


In addition, experimental work is consistent with a plausibile mechanism: namely, that in AS heterozygotes P falciparum-infected red cells sickle.


Sickle cell disease

Dynamic Modeling of Diseases and Pests pp Cite as. Malaria is one of the most severe human diseases, causing more than — million cases today 1 , leading to an estimated 2. Children ages one to four are most vulnerable to malaria due to their immature immune systems. Malaria is caused by a parasite transmitted to humans or animals by the Anopheles mosquito. The human parasite, Plasmodium falciparum , digests the hemoglobin found in red blood cells RBCs and breaks down the adhesive properties of the cells.

Malaria resistance by the sickle cell trait genotype HbAS has served as the prime example of genetic selection for over half a century. Nevertheless, the mechanism of this resistance remains the subject of considerable debate. While it probably involves innate factors such as the reduced ability of Plasmodium falciparum parasites to grow and multiply in HbAS erythrocytes, recent observations suggest that it might also involve the accelerated acquisition of malaria-specific immunity.

Sickle cell anaemia is a major chapter within haemolytic anaemias; at the same time, its epidemiology is a remarkable signature of the past and present world distribution of Plasmodium falciparum malaria. In this brief review, in keeping with the theme of this journal, we focus on the close and complex relationship betweeen this blood disease and this infectious disease. On one hand, heterozygotes for the sickle gene AS are relatively protected against the danger of dying of malaria, as now firmly established through a number of clinical field studies from different parts of Africa.

Sickle Cell Anemia

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SICKLE CELL ANAEMIA AND MALARIA

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