Browsing by Subject "Anemia"
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- ItemOpen AccessAnaemia in acute HIV-1 subtype C infection(Public Library of Science, 2008) Mlisana, Koleka; Auld, Sara C; Grobler, Anneke; Loggerenberg, Francois van; Williamson, Carolyn; Iriogbe, Itua; Sobieszczyk, Magdalena E; Karim, Salim S Abdool; Team, for the CAPRISA Acute Infection StudyBACKGROUND: The high prevalence of anaemia and the increased morbidity and mortality associated with anaemia during AIDS has been well described yet there has been little information about anaemia and changes in haemoglobin levels during acute and early HIV-1 infection. METHODS: HIV-negative women (n = 245) were enrolled into an observational cohort as part of the Centre for the AIDS Programme of Research in South Africa (CAPRISA) Acute Infection Study. Acute infection was diagnosed following a positive HIV RNA PCR in the absence of antibodies, or detection of HIV-1 antibodies within 3 months of a previously negative antibody test. Haemotologic parameters were assessed before infection and at regular intervals in the first twelve months of HIV infection. RESULTS: Fifty-seven participants with acute HIV infection were identified at a median of 14.5 days post-infection (range 10-81) and were enrolled in the CAPRISA Acute Infection cohort at a median of 41 days post-infection (range 15-104). Mean haemoglobin prior to HIV-1 infection was 12.7 g/dL, with a mean decline of 0.46 g/dL following infection. The prevalence of anaemia increased from 25.0% prior to HIV-1 infection to 52.6% at 3 months post-infection, 61.1% at 6 months post-infection, and 51.4% at 12 months post-infection. CONCLUSIONS: Haematologic derangements and anaemia with a trend towards iron deficiency are common with acute HIV-1 subtype C infection in this small cohort. The negative impact of anaemia concurrent with established HIV infection upon morbidity and mortality has been well documented but the prognostic potential and long-term effects of anaemia during acute HIV-1 infection remain unknown.
- ItemOpen AccessAnaemia, haemoglobin level and cause-specific mortality in people with and without diabetes(Public Library of Science, 2012) Kengne, Andre Pascal; Czernichow, Sébastien; Hamer, Mark; Batty, G David; Stamatakis, EmmanuelBACKGROUND: Both anaemia and cardiovascular disease (CVD) are common in people with diabetes. While individually both characteristics are known to raise mortality risk, their combined influence has yet to be quantified. In this pooling project, we examined the combined impact of baseline haemoglobin levels and existing CVD on all-cause and CVD mortality in people with diabetes. We draw comparison of these effects with those apparent in diabetes-free individuals. Methods/Principal FINDINGS: A combined analyses of 7 UK population-based cohorts resulted in 26,480 study members. There were 946 participants with physician-diagnosed diabetes, 2227 with anaemia [haemoglobin<13 g/dl (men) or <12 (women)], 2592 with existing CVD (stroke, ischaemic heart disease), and 21,396 with none of the conditions. Across diabetes and anaemia subgroups, and using diabetes-free, non-anaemic participants as the referent group, the adjusted hazard ratios (HR) were 1.46 (95% CI: 1.30-1.63) for anaemia, 1.67 (1.45-1.92) for diabetes, and 2.10 (1.55-2.85) for diabetes and anaemia combined. Across combined diabetes, anaemia and CVD subgroups, and compared with non-anaemic, diabetes-free and CVD-free participants, HR (95% CI) for all-cause mortality were 1.49 (1.32-1.69) anaemia, 1.60 (1.46-1.76) for existing CVD, and 1.66 (1.39-1.97) for diabetes alone. Equivalents were 2.13 (1.48-3.07) for anaemia and diabetes, 2.68 (2.14-3.36) for diabetes and existing CVD, and 3.25 (1.88-5.62) for the three combined. Patterns were similar for CVD mortality. Conclusions/Significance Individually, anaemia and CVD confer similar mortality risks in people with diabetes, and are excessively fatal in combination. Screening for anaemia would identify vulnerable diabetic patients whose outcomes can potentially be improved.
- ItemOpen AccessAnemia in type 2 diabetic patients and correlation with kidney function in a tertiary care sub-Saharan African hospital: a cross-sectional study(2016) Feteh, Vitalis F; Choukem, Simeon-Pierre; Kengne, André Pascal; Nebongo, Daniel N; Ngowe-Ngowe, MarcelinBackgroundAnemia is common in diabetic patients and increases morbidity and mortality, but its burden has been less well characterized in sub-Saharan Africans. We determined the prevalence of anemia and investigated the related factors, with a particular focus on the role of declining renal function, in type 2 diabetic patients attending a tertiary health care institution in Cameroon.MethodsHemoglobin (Hb) levels were measured in a consecutive sample of patients with type 2 diabetes, who reported for annual review at the outpatient section of the Douala General Hospital in 2013. Patients were classified as anemic according to the World Health Organisation criteria (Hb < 12g/dl for females and Hb < 13g/dl for males). Estimated glomerular filtration rate (eGFR) was calculated using the abbreviated Modification of Diet in Renal Disease Study Group formula. Determinants of Hb concentration and anemia were investigated using multivariable logistic regressions.ResultsA total of 636 patients were examined including 263 (prevalence rate 41.4%) who had anemia. The prevalence of anemia increased significantly with deteriorating kidney function, although up to 31.9% of patients with normal kidney function had anemia. Compared with their non-anemic counterparts, anemic diabetic patients were older, had longer duration of diabetes, lower eGFR, higher prevalence of proteinuria and diabetic retinopathy (all p < 0.05). In multivariable logistic regressions, eGFR (p = 0.001) and presence of retinopathy (p = 0.023) were the independent determinants of prevalent anemia.ConclusionsThe prevalence of anemia is high in type 2 diabetic patients attending referral institutions in Cameroon, including among those without chronic kidney disease. Routine screening for anemia in all diabetic patients may aid early identification and correction as appropriate.
- ItemOpen AccessNK-, NKT-and CD8-derived IFNγ drives myeloid cell activation and erythrophagocytosis, resulting in Trypanosomosis-associated acute anemia(Public Library of Science, 2015) Cnops, Jennifer; Trez, Carl De; Stijlemans, Benoit; Keirsse, Jiri; Kauffmann, Florence; Barkhuizen, Mark; Keeton, Roanne; Boon, Louis; Brombacher, Frank; Magez, StefanAfrican trypanosomes are the causative agents of Human African Trypanosomosis (HAT/Sleeping Sickness) and Animal African Trypanosomosis (AAT/Nagana). A common hallmark of African trypanosome infections is inflammation. In murine trypanosomosis, the onset of inflammation occurs rapidly after infection and is manifested by an influx of myeloid cells in both liver and spleen, accompanied by a burst of serum pro-inflammatory cytokines. Within 48 hours after reaching peak parasitemia, acute anemia develops and the percentage of red blood cells drops by 50%. Using a newly developed in vivo erythrophagocytosis assay, we recently demonstrated that activated cells of the myeloid phagocytic system display enhanced erythrophagocytosis causing acute anemia. Here, we aimed to elucidate the mechanism and immune pathway behind this phenomenon in a murine model for trypanosomosis. Results indicate that IFNγ plays a crucial role in the recruitment and activation of erythrophagocytic myeloid cells, as mice lacking the IFNγ receptor were partially protected against trypanosomosis-associated inflammation and acute anemia. NK and NKT cells were the earliest source of IFNγ during T. b. brucei infection. Later in infection, CD8+ and to a lesser extent CD4+ T cells become the main IFNγ producers. Cell depletion and transfer experiments indicated that during infection the absence of NK, NKT and CD8+ T cells, but not CD4+ T cells, resulted in a reduced anemic phenotype similar to trypanosome infected IFNγR-/- mice. Collectively, this study shows that NK, NKT and CD8+ T cell-derived IFNγ is a critical mediator in trypanosomosis-associated pathology, driving enhanced erythrophagocytosis by myeloid phagocytic cells and the induction of acute inflammation-associated anemia.
- ItemOpen AccessThe role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice(Public Library of Science, 2008) Magez, Stefan; Schwegmann, Anita; Atkinson, Robert; Claes, Filip; Drennan, Michael; De Baetselier, Patrick; Brombacher, FrankAuthor Summary African trypanosomiasis is a disease caused by different species of extracellular flagellated protozoan trypanosome parasites. Trypanosomes have developed a mechanism of regular antigenic variation of their variant-specific surface glycoprotein (VSG) coat which allows chronic infection. Replacement of this coat occurs at rapid regular time intervals, allowing the parasite to escape from an effective host antibody responses. So far, primary T-cell independent antibody responses have been described to constitute the main host defense mechanism, relying largely on IgM antibody induction. Using genetically engineered B lymphocyte- or IgM-deficient mouse strains, we show that lack of B-cells or IgM did not prevent infection-associated anemia. More importantly, we show that in the absence of IgM, parasitemia was controlled almost as well as in wild-type mice, with only slightly increased mortality. In addition, we show in vivo that antigenic variation is not affected by the lack of IgM.