Prevalence of Malnutrition and Anaemia in Children ≤ 5 Years of Age in Some Conflict Hit Areas of Meme Division of the South West Region of Cameroon

Malnutrition refers to the deficiency, imbalances, or excesses in a person’s intake of energy or nutrients [1]. Khan defines anaemia as below level of Haemoglobin in red blood shown by a lower number of functioning red blood cells [2]. The crisis in the North West and South West Regions of Cameroon has led to several negative effects on children’s living conditions. There has been an increase in malnutrition and anaemia in the South West Region and Kumba in particular. The main objective of this study was “to examine the prevalence of malnutrition and anaemia in children ≤ 5 years of age in some conflict-hit areas of Meme Division”. A descriptive cross-sectional study was conducted in 2023 from March to June. We recruited 200 children ≤ 5 years into the study from three hospitals. The regional hospital annex in Kumba, Presbyterian General Hospital Kumba and the Ntam Hospital in Kumba. Socio-demographic factors were assessed using questionnaire, nutritional status was assessed by the use anthropometric measurements and an auto haematology analyser was used to determine anaemia. The overall prevalence of malnutrition in the study area was 40.5%. The prevalence of malnutrition varied significantly (P < 0.001) with the study sites. The overall prevalence of anaemia in the study area was 70.5%. The prevalence of anaemia was not significantly associated with the study sites. The prevalence of Malnutrition and Anaemia in children ≤ 5 years of age is very high in the Kumba municipalities. This could be attributed to the ongoing crisis which has caused a lot of social migrations from rural areas to Urban areas which are safer.

Effect of ginsenoside Rg1 on hematopoietic stem cells in treating aplastic anemia in mice via MAPK pathway

BACKGROUND Aplastic anemia(AA)presents a significant clinical challenge as a life-threatening condition due to failure to produce essential blood cells,with the current the-rapeutic options being notably limited.AIM To assess the therapeutic potential of ginsenoside Rg1 on AA,specifically its protective effects,while elucidating the mechanism at play.METHODS We employed a model of myelosuppression induced by cyclophosphamide(CTX)in C57 mice,followed by administration of ginsenoside Rg1 over 13 d.The invest-igation included examining the bone marrow,thymus and spleen for pathological changes via hematoxylin-eosin staining.Moreover,orbital blood of mice was collected for blood routine examinations.Flow cytometry was employed to identify the impact of ginsenoside Rg1 on cell apoptosis and cycle in the bone marrow of AA mice.Additionally,the study further evaluated cytokine levels with enzyme-linked immunosorbent assay and analyzed the expression of key proteins in the MAPK signaling pathway via western blot.RESULTS Administration of CTX led to significant damage to the bone marrow’s structural integrity and a reduction in hematopoietic cells,establishing a model of AA.Ginsenoside Rg1 successfully reversed hematopoietic dysfunction in AA mice.In comparison to the AA group,ginsenoside Rg1 provided relief by reducing the induction of cell apoptosis and inflammation factors caused by CTX.Furthermore,it helped alleviate the blockade in the cell cycle.Treatment with ginsenoside Rg1 significantly alleviated myelosuppression in mice by inhibiting the MAPK signaling pathway.CONCLUSION This study suggested that ginsenoside Rg1 addresses AA by alleviating myelosuppression,primarily through modulating the MAPK signaling pathway,which paves the way for a novel therapeutic strategy in treating AA,highlighting the potential of ginsenoside Rg1 as a beneficial intervention.

Late Onset Combined Immune Deficiency (LOCID) Revealed by a Haemolytic Anaemia in a Child: A Case Report

Variable Common Immune Deficiency (VCID) is a very heterogeneous condition both clinically and immunologically. It is a group of molecular abnormalities responsible for a defect in antibody production leading to hypogammaglobulinemia often associated with autoimmune and/or lymphoproliferative manifestations. Late Onset Combined Immune Deficiency (LOCID) is a type of Variable Common Immune Deficiency (VCID) defined by a defect in antibody production (IgG and IgA ± IgM type), profound CD4 T-cell lymphopenia and frequent opportunistic infections. LOCID has been considered as a distinct entity from VCID due to its particular clinical and immunological profile.

Bowel inflammatory presentations on computed tomography in adult patients with severe aplastic anemia during flared inflammatory episodes

BACKGROUND Patients with severe aplastic anemia(SAA)frequently present with inflammatory episodes,and during flared inflammatory episodes,hematopoietic function is further exacerbated.The gastrointestinal tract is the most common site for infectious and inflammatory diseases,and its structural and functional features confer on it the most potent capacity to affect hematopoietic and immune functions.Computed tomography(CT)is a readily accessible approach to provide highly useful information in detecting morphological changes and guiding further work-ups.AIM To explore CT imaging presentations of gut inflammatory damage in adult SAA patients during inflammatory episodes.METHODS We retrospectively evaluated the abdominal CT imaging presentations of 17hospitalized adult patients with SAA in search of the inflammatory niche when they presented with systemic inflammatory stress and exacerbated hematopoietic function.In this descriptive manuscript,the characteristic images that suggested the presence of gastrointestinal inflammatory damage and related imaging presentations of individual patients were enumerated,analyzed and described.RESULTS All eligible patients with SAA had CT imaging abnormalities that suggested the presence of an impaired intestinal barrier and increased epithelial permeability.The inflammatory damages were concurrently present in the small intestine,the ileocecal region and the large intestines.Some readily identified imaging signs,such as bowel wall thickening with mural stratification(“water holo sign”,“fat holo sign”,intramural gas and subserosal pneumatosis)and mesenteric fat proliferation(fat stranding and“creeping fat sign”),fibrotic bowel wall thickening,“balloon sign”,rugged colonic configuration,heterogeneity in the bowel wall texture,and adhered and clustered small bowel loop(including various patterns of“abdominal cocoon”),occurred at a high incidence,which suggested that the damaged gastrointestinal tract is a common inflammatory niche responsible for the systemic inflammatory stresses and the exacerbated hematopoietic failure in patients with SAA.Particularly,the“fat holo sign”was present in 7 patients,a rugged colonic configuration was present in 10 patients,the adhesive bowel loop was present in 15 patients,and extraintestinal manifestations suggestive of tuberculosis infections were present in 5 patients.According to the imaging features,a suggestive diagnosis of Crohn’s disease was made in 5patients,ulcerative colitis in 1 patient,chronic periappendiceal abscess in 1 patient,and tuberculosis infection in 5 patients.Other patients were diagnosed with chronic enteroclolitis with acutely aggravated inflammatory damage.CONCLUSION Patients with SAA had CT imaging patterns that suggested the presence of active chronic inflammatory conditions and aggravated inflammatory damage during flared inflammatory episodes.

Flared inflammatory episode transforms advanced myelodysplastic syndrome into aplastic pancytopenia:A case report and literature review

BACKGROUND Myelodysplastic syndrome(MDS)is a hematological neoplasm,and an increase in myeloblasts is representative of leukemic hematopoiesis in advanced MDS.Lowrisk MDS usually exhibits deranged autoimmunity resembling that of aplastic anemia(AA),whereas advanced MDS is characterized by a phenotype of immune exhaustion.MDS can be normo/hyperplastic or hypoplastic.Generally,bone marrow cellularity and myeloblasts increase with disease progression.Transformation from advanced MDS to AA-like syndrome with leukemic cell regression has not previously been reported.CASE SUMMARY A middle-aged Chinese woman had a 4-year history of leukocytopenia.Six months prior to admission,the patient developed gradually worsening fatigue and performance status.The leukocytopenia further progressed.She was diagnosed with MDS with excess blasts-2 based on increased bone marrow cellularity and an increased percentage of myeloblasts on marrow and blood smears,an increased percentage of cluster of differentiation(CD)34+CD33+progenitors in immunotyping analysis,a normal karyotype in cytogenetic analysis,and the identification of somatic mutations in CBL,KMT2D and NF1 in molecular analysis.Initially,neutropenia was the predominant hematological abnormality,with mild anemia and thrombocytosis,and the degree of fatigue was far more severe than the degree of anemia.In the following months,the patient experienced several febrile episodes.Intravenous antibiotic treatments were able to control the febrile episodes,but the elevated inflammatory indices persisted.The hematological parameters dramatically fluctuated with the waxing and waning of the inflammatory episodes.With recurrent flares of the inflammatory condition,agranulocytosis and severe anemia developed,with mild thrombocytopenia.During the patient’s hospitalization,computed tomography(CT)scans revealed the presence of extensive inflammatory lesions involving the lungs,mediastinum,pleura,gastrointestinal tract,peritoneum and urinary tract,with imaging features suggestive of the reactivation of disseminated tuberculosis.Reevaluation of the bone marrow smears revealed that the cellularity became hypoplastic,and the leukemic cells regressed,suggesting that both normal and leukemic hematopoiesis had been heavily suppressed.Immunological analysis of the bone marrow samples revealed a decreased percentage of CD34+cells and an immunological signature resembling that of severe AA(SAA),confirming the regression of the leukemic cells by autoimmune-mediated attacks.The patient demonstrated resistance to multiple drugs,including antituberculotics,recombinant human granulocyte colony-stimulating factor,broad-spectrum antibiotics,voriconazole,ganciclovir,immune suppressants,eltrombopag and intravenous immunoglobulin,which further worsened the hematological injury and patient’s performance status.The patient eventually died of overwhelming infection and multidrug resistance.CONCLUSION Advanced MDS can transform to aplastic cytopenia with leukemic cell regression and an immunological signature of SAA during inflammatory flare-ups.

Leukemic transformation during anti-tuberculosis treatment in aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome:A case report and review of literature

BACKGROUND Accumulating evidence demonstrates that autoimmune hematopoietic failure and myeloid neoplasms have an intrinsic relationship with regard to clonal hematopoiesis and disease evolution.In approximately 10%-15%of patients with severe aplastic anemia(SAA),the disease phenotype is transformed into myeloid neoplasms following antithymocyte globulin plus cyclosporine-based immunosuppressive therapy.In some of these patients,myeloid neoplasms appear during or shortly after immunosuppressive therapy.Leukemic transformation in SAA patients during anti-tuberculosis treatment has not been reported.CASE SUMMARY A middle-aged Chinese female had a 6-year history of non-SAA and a 2-year history of paroxysmal nocturnal hemoglobinuria(PNH).With aggravation of systemic inflammatory symptoms,severe pancytopenia developed,and her hemoglobinuria disappeared.Laboratory findings in cytological,immunological and cytogenetic analyses of bone marrow samples met the diagnostic criteria for“SAA.”Definitive diagnosis of disseminated tuberculosis was made in the search for infectious niches.Remarkable improvement in hematological parameters was achieved within 1 mo of anti-tuberculosis treatment,and complete hematological remission was achieved within 4 mo of treatment.Frustratingly,the hematological response lasted for only 3 mo,and pancytopenia reemerged.At this time,cytological findings(increased bone marrow cellularity and an increased percentage of myeloblasts that accounted for 16.0%of all nucleated hematopoietic cells),immunological findings(increased percentage of cluster of differentiation 34+cells that accounted for 12.28%of all nucleated hematopoietic cells)and molecular biological findings(identification of somatic mutations in nucleophosmin-1 and casitas B-lineage lymphoma genes)revealed that“SAA”had transformed into acute myeloid leukemia with mutated nucleophosmin-1.The transformation process suggested that the leukemic clones were preexistent but were suppressed in the PNH and SAA stages,as development of symptomatic myeloid neoplasm through acquisition and accumulation of novel oncogenic mutations is unlikely in an interval of only 7 mo.Aggravation of inflammatory stressors due to disseminated tuberculosis likely contributed to the repression of normal and leukemic hematopoiesis,and the relief of inflammatory stressors due to anti-tuberculosis treatment contributed to penetration of neoplastic hematopoiesis.The concealed leukemic clones in the SAA and PNH stages raise the possibility of an inflammatory stress-fueled antileukemic mechanism.CONCLUSION Aggravated inflammatory stressors can repress normal and leukemic hematopoiesis,and relieved inflammatory stressors can facilitate penetration of neoplastic hematopoiesis.

Distortion product otoacoustic emissions in newborn babies with and without late-term maternal iron deficiency anaemia

Background:Studies on animals have demonstrated that maternal iron deficiency anaemia(IDA)could result in decreased cochlear sensory hair cells and reduced amplitudes of distortion-product otoacoustic emissions(DPOAEs)of young guinea pigs.Thus,it is essential to study the functioning of cochlear hair cells using DPOAEs in human newborn babies with maternal IDA.The current study explores maternal IDA’s effect on DPOAEs in newborn babies.Method:A total of 110 newborn babies with gestational age≥34 weeks were considered and a‘betweensubjects’design was used.The participants were divided into 3 groups-“Normal”(61 babies without maternal IDA),“Mild”(28 babies with mild maternal IDA)and“Moderate”(21 babies with moderate maternal IDA).The cord blood was collected and the DPOAEs were recorded for each baby for a range of frequencies(1 k 8 kHz)and a range of intensities(7040 dB SPL in 10 dB steps).Results:The analysis of both DP-gram and DP input-output(I/O)function showed that there was no significant difference(p>0.05)across the normal,mild,and moderate groups in the overall presence of DPOAEs as well as the amplitude across frequencies or intensities(7040 dB SPL).Also,the overall correlation of RBC indices with DPOAE amplitude across frequencies as well as the slope of the I/O function showed no relationship.Conclusion:The current study concludes that there is no effect of late-term maternal IDA on the DPOAEs of newborn babies.

Hematopoietic stem cell transplantation of aplastic anemia by relative with mutations and normal telomere length: A case report

BACKGROUND Immunosuppressive therapy and matched sibling donor hematopoietic stem cell transplantation(MSD-HSCT)are the preferred treatments for aplastic anemia(AA).CASE SUMMARY In this report,we describe a 43-year-old male patient with severe AA who carried BRIP1(also known as FANCJ),TINF2,and TCIRG1 mutations.Screening of the family pedigree revealed the same TINF2 mutation in his mother and older brother,with his older brother also carrying the BRIP1 variant and demonstrating normal telomere length and hematopoietic function.The patient was successfully treated with oral cyclosporine A,eltrombopag,and acetylcysteine,achieving remission 4 years after receiving MSD-HSCT from his older brother.CONCLUSION This case provides a valuable clinical reference for individuals with suspected pathogenic gene mutations,normal telomere length,and hematopoietic function,highlighting them as potential donors for patients with AA.

Factors Associated with Haemolytic Anaemia in the Internal Medicine Department of the Douala General Hospital in Cameroon

Introduction: Haemolytic anaemia (HA) is defined as a decrease in haemoglobin (Hb) levels below baseline due to excessive and premature destruction of red blood cells (RBCs) in the periphery resulting in a shortened life span of less than 120 days. Haemolysis can be corpuscular or extra-corpuscular. The aim of our study was to investigate the factors associated with it for optimal management of patients hospitalised in internal medicine at the Douala General Hospital (DGH). Methodology: We conducted an analytical cross-sectional study, including all patients admitted to the internal medicine department of the DGH from 11 February to 20 May 2022, and excluding patients with non-compliant samples. The search for haemolytic anaemia was carried out by means of blood count, reticulocyte count, blood smear, unconjugated bilirubin, lactate dehydrogenase and direct Coombs test. Sociodemographic, clinical and biological parameters were collected and analysed. Correlation was defined for a p value 0.05. Results: This study included 147 patients, 50.34% of whom were men, for a sex ratio of 1.01. The mean age was 52 ± 17.9 years. The most represented age group was 56 - 70 years (n = 49;33%) with extremes from 15 to 90 years. We counted 29.3% cases of haemolytic anaemia (HA) and 13.9% cases of autoimmune haemolytic anaemia (AIHA). Haemolytic anaemia (HA) was present in 54.14% of men for a sex ratio of 1.38;the most represented age group was 40 - 55 years, 37.2%. HA was associated with jaundice (OR: 3.74, CI: [1.70 - 8.22], p = 0.001), HIV - AIDS (OR: 2.72, CI: [0.98 - 7.53], p = 0.05), thrombocytopaenia (OR: 3.53, CI: [1.58 - 7.89], p = 0.02). LDH was elevated (OR: 2.86, CI: [1.30 - 6.26], p = 0.00) as well as elevated reticulocyte count (OR: 3.84, CI: [1.75 - 8.44], p = 0.01). Unconjugated bilirubin was elevated in all these patients. In multivariate analysis, factors associated with HA were a history of HIV/AIDS, jaundice, thrombocytopaenia and elevated reticulocyte count. Conclusion: Hemolytic anaemia is common in internal medicine and is significantly associated with thrombocytopenia, HIV/AIDS infection and jaundice.

Use of iron in perinatal anaemia:Indications for women’s health care policies and procedure

This paper reviews management of obstetric anaemia and the role of intravenous iron for the treatment of obstetric anaemia.Red blood cell transfusions are routinely used for haemoglobin restoration in anaemic women.The decision for red blood cell transfusion is made on a combination of haemoglobin level and clinical status,and it is suggested that transfusions are not necessary in those who are well compensated or when alternative therapy is available.To reduce the risk,intravenous iron infusion is proposed as a bloodless therapeutic approach.There are a variety of iron preparations.Intravenous iron infusion can reduce the requirement for blood transfusion in hemodynamically stable women with perinatal anaemia,especially in resource-scarce settings.It a cost-effective bloodless approach for the treatment of anaemia than can enhance patient outcomes.According to the literature,when haemoglobin is greater than 90 g/L,blood transfusion is not often required.In perinatal women with anaemia,the decision whether to administer blood or iron is based on patient preferences,haemoglobin levels,clinical symptoms,past and present medical conditions and the clinician’s judgement.Nevertheless,due to the lack of rigid criteria for blood transfusions in the majority of clinical settings,it is considered the default treatment for anaemia in perinatal women.

Tuberculosis-induced aplastic crisis and atypical lymphocyte expansion in advanced myelodysplastic syndrome:A case report and review of literature

BACKGROUND Myelodysplastic syndrome(MDS)is caused by malignant proliferation and ineffective hematopoiesis.Oncogenic somatic mutations and increased apoptosis,necroptosis and pyroptosis lead to the accumulation of earlier hematopoietic progenitors and impaired productivity of mature blood cells.An increased percentage of myeloblasts and the presence of unfavorable somatic mutations are signs of leukemic hematopoiesis and indicators of entrance into an advanced stage.Bone marrow cellularity and myeloblasts usually increase with disease progression.However,aplastic crisis occasionally occurs in advanced MDS.CASE SUMMARY A 72-year-old male patient was definitively diagnosed with MDS with excess blasts-1(MDS-EB-1)based on an increase in the percentages of myeloblasts and cluster of differentiation(CD)34+hematopoietic progenitors and the identification of myeloid neoplasm-associated somatic mutations in bone marrow samples.The patient was treated with hypomethylation therapy and was able to maintain a steady disease state for 2 years.In the treatment process,the advanced MDS patient experienced an episode of progressive pancytopenia and bone marrow aplasia.During the aplastic crisis,the bone marrow was infiltrated with sparsely distributed atypical lymphocytes.Surprisingly,the leukemic cells disappeared.Immunological analysis revealed that the atypical lymphocytes expressed a high frequency of CD3,CD5,CD8,CD16,CD56 and CD57,suggesting the activation of autoimmune cytotoxic T-lymphocytes and natural killer(NK)/NKT cells that suppressed both normal and leukemic hematopoiesis.Elevated serum levels of inflammatory cytokines,including interleukin(IL)-6,interferon-gamma(IFN-γ)and tumor necrosis factor-alpha(TNF-α),confirmed the deranged type I immune responses.This morphological and immunological signature led to the diagnosis of severe aplastic anemia secondary to large granule lymphocyte leukemia.Disseminated tuberculosis was suspected upon radiological examinations in the search for an inflammatory niche.Antituberculosis treatment led to reversion of the aplastic crisis,disappearance of the atypical lymphocytes,increased marrow cellularity and 2 mo of hematological remission,providing strong evidence that disseminated tuberculosis was responsible for the development of the aplastic crisis,the regression of leukemic cells and the activation of CD56+atypical lymphocytes.Reinstitution of hypomethylation therapy in the following 19 mo allowed the patient to maintain a steady disease state.However,the patient transformed the disease phenotype into acute myeloid leukemia and eventually died of disease progression and an overwhelming infectious episode.CONCLUSION Disseminated tuberculosis can induce CD56+lymphocyte infiltration in the bone marrow and in turn suppress both normal and leukemic hematopoiesis,resulting in the development of aplastic crisis and leukemic cell regression.

Construction of gene/protein interaction networks and enrichment pathway analysis for paroxysmal nocturnal hemoglobinuria and aplastic anemia

Background:To develop a protein-protein interaction network of Paroxysmal nocturnal hemoglobinuria(PNH)and Aplastic anemia(AA)based on genetic genes and to predict pathways underlying the molecular complexes in the network.Methods:In this research,the PNH and AA-related genes were screened through Online Mendelian Inheritance in Man(OMIM).The plugins and Cytoscape were used to search literature and build a protein-protein interaction network.Results:The protein-protein interaction network contains two molecular complexes that are five higher than the correlation integral values.The target genes of this study were obtained:CD59,STAT3,TERC,TNF,AKT1,C5AR1,EPO,IL6,IL10 and so on.We also found that many factors regulate biological behaviors:neutrophils,macrophages,vascular endothelial growth factor,immunoglobulin,interleukin,cytokine receptor,interleukin-6 receptor,tumor necrosis factor,and so on.This research provides a bioinformatics foundation for further explaining the mechanism of common development of both.Conclusion:This indicates that the PNH and AA is a complex process regulated by many cellular pathways and multiple genes.

Screening of aplastic anaemia-related genes in bone marrow CD4^+ T cells by suppressive subtractive hybridization

Background CD4^＋ T cells play a crucial role in the pathogenesis of aplastic anaemia. However, the mechanisms of over-proliferation, activation, infiltration of bone marrow and damage to haematopoietic ceils of CD4^＋ T cells in aplastic anaemia are unclear. Therefore, we screened differentially expressed genes of bone marrow CD4^＋ T cells of aplastic anaemia patients and normal donors by suppressive subtractive hybridization to investigate the pathogenesis of aplastic anaemia. Methods The bone marrow mononuclear cells of a first visit aplastic anaemia patient and a healthy donor of the same age and sex were isolated using lymphocyte separating medium by density gradient centrifugation. With the patients as ＂tester＂ and donor as ＂driver＂, their CD4^＋T cells were separated with magnetic bead sorting and a cDNA library established by suppressive subtractive hybridization. Then 15 of the resulting subtracted cDNA clones were randomly selected for DNA sequencing and homological analysis. With semiquantitative RT-PCR, bone marrow samples from 20 patients with aplastic anaemia and 20 healthy donors assessed the expression levels of differentially expressed genes from SSH library. Results PCR detected 89 clones in the library containing an inserted fragment of 100 bp to 700 bp. Among 15 sequenced clones, 12 were known genes including 3 repeated genes. Compared with normal donors, there were 9/12 genes over-expressed in bone marrow CD4^＋T cells of patients with aplastic anaemia. The effects of these genes included protein synthesis, biology oxidation, signal transduction, proliferative regulation and cell migration. Not all these genes had been reported in the mechanisms of haematopoietic damage mediated by CD4^＋ T cells in aplastic anaemia. Conclusions Screening and cloning genes, which regulate functions of CD4^＋ T cells, are helpful in elucidating the mechanisms of over proliferation, activation, infiltrating bone marrow and damaging haematopoietic cells of CD4^＋ T cells in aplasUc anaemia.

Hepatitis- associated aplastic anaemia:clinical characteristics and immunosuppressive therapy outcomes

Objective To analyze the clinical characteristics and to evaluate immunosuppressive therapy(IST)response and survival in hepatitis-associated aplastic anemia(HAAA).Methods We retrospectively analyzed clinical characteristics,IST response,long-term survival and clonal evolution in 41 HAAA patients,and

Helicobacter pylori infection as a cause of iron deficiency anaemia of unknown origin

AIM: To assess the aetiological role of Helicobacter pylori (H. pylori) infection in adult patients with ironrefractory or iron-dependent anaemia of previously unknown origin. METHODS: Consecutive patients with chronic irondeficient anaemia (IDA) with H. pylori infection and a negative standard work-up were prospectively evaluated. All of them had either iron refractoriness or iron dependency. Response to H. pylori eradication was assessed at 6 and 12 mo from follow-up. H. pylori infection was considered to be the cause of the anaemia when a complete anaemia resolution without iron supplements was observed after eradication. RESULTS: H. pylori was eradicated in 88 of the 89 patients. In the non-eradicated patient the four eradicating regimens failed. There were violations of protocol in 4 patients, for whom it was not possible to ascertain the cause of the anaemia. Thus, 84 H. pylori eradicated patients (10 men; 74 women) were available to assess the effect of eradication on IDA. H. pylori infection was considered to be the aetiology of IDA in 32 patients (38.1%; 95%CI: 28.4%-48.8%). This was more frequent in men/postmenopausal women than in premenopausal women (75% vs 23.3%; P < 0.0001) with an OR of 9.8 (95%CI: 3.3-29.6). In these patients, anaemia resolution occurred in the first follow-up visit at 6 mo, and no anaemia or iron deficiency relapse was observed after a mean follow-up of 21 ± 2 mo. CONCLUSION: Gastric H. pylori infection is a frequent cause of iron-refractory or iron-dependent anaemia of previously unknown origin in adult patients.

The effects of co-infection with human parvovirus B19 and Plasmodium falciparum on type and degree of anaemia in Ghanaian children

Objective:To determin the extent to which parvovirus B19(B19V)and co-infection of B19V and malaria contribute to risk of anaemia in children.Methods:B19V DNA and malaria parasites were screened for 234 children at the PMI,Children's Hospital in Accra.The role of B19V and coinfection with B19V and malaria in anaemia was evaluated by analysing full blood cell counts,malaria and B19V DNA results from these children.Results:The prevalence of B19V,malaria and co-infection with B19V and malaria was 4.7%,41.9%and 2.6%,respectively.Malaria posed a greater risk in the development of mild anaemia compared to severe anaemia(OR=5.28 vrs3.15)whereas B19V posed a higher risk in the development of severe anaemia compared to mild anaemia(OR=4.07 vrs 1.00)from a non-anaemic child.Persons with co-infection with B19V and malaria had 2.23 times the risk(95%CI=0.40-12.54)of developing severe anaemia should they already have a mild anaemia.The degree of anaemia was about three times affected by coinfection(Pillai's trace=0.551,P=0.001)as was affected by malaria alone(Pillai's trace=0.185,P=0.001).B19V alone did not significantly affect the development of anaemia in a non-anaemic child.Microcytic anaemia was associated with B19V and co-infection with B19V and malaria more than normocytic normochromic anaemia.Conclusions:B19V was associated with malaria in cases of severe anaemia.The association posed a significant risk for exacerbation of anaemia in mild anaemic children.B19V and co-infection with B19V and malaria may be associated with microcytic anaemia rather than normocytic normochromic anaemia as seen in cases of B19V infection among persons with red cell abnormalities.

Clinical Observation on Treatment of Chronic Aplastic Anemia by Shengxuening (生血宁) and Cyclosporin A

Objective： To explore the therapy to further elevate the efficacy of the treatment of chronic aplastic anemia （CAA）. Methods： Forty-five patients with CCA were assigned into two groups, the 26 patients in the treated group were treated by Shengxuening （ 生血宁, a Chinese herbal preparation） and cyclosporin A （CsA）, and the 19 patients in the control group were treated with androgen alone, with the therapeutic course lasting for over 3 months. Changes of peripheral blood picture, and the colony productivity of burst forming unit-erythroid （BFU-E）, colony forming unit-erythroid （CFU-E） and colony forming unit-granulocyte macrophage （CFU-GM） in bone marrow were observed before and after 3 months treatment. The amount of erythrocyte and platelet infusion, frequency of infection, condition of hemorrhage and relevant death were also observed. The follow-up study was conducted for over half a year. Results： The total effective rate in the treated group was 84.6 %, which was significantly higher than that in the control group （52.6 %, P〈0.05）. Levels of hemoglobin, reticulocyte, neutrophil and platelet increased after treatment in the treated group, as compared with those before treatment, with significant difference （ P〈0.05）, and the colony productivity of BFU-E, CFU-E and CFU-GM in bone marrow also got significantly increased （ P〈0.01 ）, and showed significant difference from those in the control group （P〈0.05）. Conclusion： Shengxuening-assisting CsA therapy is an effective measure for treatment of CAA.

Proliferation and Apoptosis of Bone Marrow CD4^+ T Cells in Patients with Aplastic Anemia and Impacts of the Secreted Cytokines on Hematopoietic Stem Cells from Umbilical Cord Blood

Recent studies indicate that immune-associated aplastic anemia(AA)resembles such autoimmune diseases as insulin-dependent diabetes and chronic autoimmune thyroiditis that belong to organ-specific autoimmune diseases.Many independent investigation groups have successfully isolated the pathopoiesis-associated T cell clone causing hematopoiesis failure with a CD4 phenotype from peripheral blood and bone marrow(BM)in AA patients.In the current study,BM CD4+ T cells were isolated from AA patients and healthy con...

Role of Stem Cell Factor and Its Receptor in the Pathogenesis of Pediatric Aplastic Anemia

In order to investigate the levels of stem cell factor (SCF) and its receptor c-kit protein and mRNA in pediatric aplastic anemia (AA) and their relevance to the pathogenesis, immunocytochemical and in situ hybridization were utilized to detect the expression of SCF and its receptor c-kit gene protein and mRNA, respectively in 59 children with AA and 51 normal controls. The relationship between SCF and c-kit and the pathogenesis of AA was analyzed subsequently. The results showed that the positive rate of SCF protein and mRNA expression in children with AA was significantly lower than that in healthy controls (P<0.05). However, there was no significant difference in the positive rate of c-kit protein and mRNA expression between children with AA and control group (P>0.05). It was concluded that the expression of SCF is significantly decreased in children with AA, which may be closely associated with the pathogenesis of the AA. c-kit may be unrelated to the development of pediatric AA. Therefore, AA in children may have abnormalities at SCF/c-kit signal transduction levels.

Yin and Yang of mesenchymal stem cells and aplastic anemia

Acquired aplastic anemia(AA) is a bone marrow failure syndrome characterized by peripheral cytopenias and bone marrow hypoplasia. It is ultimately fatal without treatment, most commonly from infection or hemorrhage. Current treatments focus on suppressing immune-mediated destruction of bone marrow stem cells or replacing hematopoietic stem cells(HSCs) by transplantation. Our incomplete understanding of the pathogenesis of AA has limited development of targeted treatment options. Mesenchymal stem cells(MSCs) play a vital role in HSC proliferation; they also modulate immune responses and maintain an environment supportive of hematopoiesis. Some of the observed clinical manifestations of AA can be explained by mesenchymal dysfunction. MSC infusions have been shown to be safe and may offer new approaches for the treatment of this disorder. Indeed, infusions of MSCs may help suppress auto-reactive, T-cell mediated HSC destruction and help restore an environment that supports hematopoiesis. Small pilot studies using MSCs as monotherapy or as adjuncts to HSC transplantation have been attempted as treatments for AA. Here we review the current understanding of the pathogenesis of AA and the function of MSCs, and suggest that MSCs should be a target for further research and clinical trials in this disorder.