Ibrahim Muhammad

ANEAMIA DUE TO INFECTIOUS DISEASE BY HAUWA SALIHU SPS/23/GEP/00053 A REVIEW SUBMITTED TO THE SCHOOL OF POSTGRADUATE STUDIES, THROUGH THE DEPARTMENT OF MICROBIOLOGY, BAYERO UNIVERSITY, KANO, IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF POSTGRADUATE DIPLOMA IN ENVIRONMENTAL AND PUBLIC HEALTH SUPERVISOR DR. H.U ABDU MAY, 2025 DECLARATION I, Hauwa Salihu, hereby declare that this research work was solely undertaken, authored, and compiled by me. I further certify that, to the best of my knowledge and belief, this work has not been previously submitted, in whole or in part, for any academic degree or for publication in any other forum. _______________________ HAUWA SALIHU SPS/23/GEP/00053 CERTIFICATION This is to certify that the research work and subsequent write-up by HAUWA SALIHU with registration number SPS/23/GEP/00053 were carried out under my supervision. __________________________________________ Dr. H.U ABDU Date DEDICATION This work is dedicated to my parents, whose unwavering support, guidance, and sacrifices have been the foundation of my academic journey. I am deeply grateful for their enduring love and inspiration. APPROVAL PAGE This is to certify that the research project titled " Aneamia due to Infectious Disease" by Hauwa Salihu (Reg. No: SPS/23/GEP/00053) has been examined and approved as satisfying the requirements for the partial fulfillment of the Postgraduate Diploma in Environmental and Public Health at Bayero University, Kano. __________________________________________ Dr. H.U AbduDate (Supervisor) __________________________________________ Prof. Muhammad Yusha’uDate (Head of Department) __________________________________________ Dr. Ibrahim YusufDate (PG Coordinator) ACKNOWLEDGEMENT I begin by expressing my deepest gratitude to Almighty Allah, whose boundless mercy, wisdom, and guidance have granted me the strength, perseverance, and intellectual capability to undertake and complete this research. His divine support has been my unwavering source of inspiration and resilience throughout this academic journey. I am profoundly indebted to my esteemed supervisor, Dr. H.U Abdu, whose exceptional mentorship, scholarly insight, and constructive feedback have been instrumental in refining my research. His unwavering commitment, patience, and invaluable suggestions have significantly contributed to the depth and quality of this work. I sincerely appreciate his time, encouragement, and dedication in guiding me through this academic endeavor. My heartfelt appreciation extends to my beloved parents (Alh. Salihu Gambo and Haj. Maryam Muhd Danmade) and siblings (Rukayya, Bilkisu, Saadatu, Rabiat and Rabiu), whose unconditional love, sacrifices, and unwavering support have been the foundation of my academic and personal growth. Their prayers, encouragement, and belief in my potential have continuously motivated me to strive for excellence. Furthermore, I am deeply grateful to my dear friends, particularly Rukayya Abdullahi Babadoko, whose unwavering companionship, intellectual discourse, and moral support have been invaluable throughout this research. Their encouragement, insightful discussions, and shared moments of both challenge and triumph have enriched my academic experience. Lastly, I extend my appreciation to all individuals who have, in one way or another, contributed to the successful completion of this study. Whether through academic discussions, moral support, or practical assistance, your contributions have not gone unnoticed. May Allah bless you all abundantly. TABLE OF CONTENTS Table of Contents DECLARATIONii CERTIFICATIONiii DEDICATIONiv APPROVAL PAGEv ACKNOWLEDGEMENTvi TABLE OF CONTENTSvii ABSTRACTviii CHAPTER ONE1 INTRODUCTION1 1.1 Background of the Study1 1.2 Statement of the Problem5 1.3 Aim and Objectives7 1.3.1 Aim7 1.3.2 Objectives7 1.4 Significance of the Study8 CHAPTER TWO10 LITERATURE REVIEW10 2.1 Introduction to Anemia in Infectious Diseases10 2.2 Malaria-Induced Anemia11 2.3 Helminth Infections and Anemia13 2.4 HIV/AIDS and Anemia15 2.5 Tuberculosis-Associated Anemia16 2.6 Diagnostic Challenges18 2.7 Treatment Strategies20 CHAPTER THREE23 SUMMARY, CONCLUSION AND RECOMMENDATIONS23 5.1 Summary23 5.2 Conclusion23 5.3 Recommendations24 ABSTRACT Anemia represents a major global health burden, with infectious diseases contributing substantially to its pathogenesis, particularly in malaria-endemic regions and resource-limited settings. This comprehensive review examines the interplay between anemia and four major infectious diseases—malaria, helminth infections, HIV/AIDS, and tuberculosis focusing on their distinct yet interconnected pathophysiological mechanisms, epidemiological patterns, and clinical management challenges. The analysis reveals that these infections contribute to anemia through diverse biological pathways: hemolytic destruction of erythrocytes in malaria, chronic blood loss in soil-transmitted helminthiasis, and inflammation-mediated erythropoietic suppression in HIV and TB. Epidemiological data demonstrate disproportionately high anemia prevalence (30-80%) among affected populations, with children under five and women of reproductive age being particularly vulnerable due to biological and socioeconomic factors. Key diagnostic and therapeutic challenges are identified, including the frequent misclassification of anemia subtypes due to limited access to advanced biomarkers, and ongoing controversies regarding optimal timing of iron supplementation in active infection. The review highlights successful integrated intervention models, such as delayed iron supplementation post-malaria treatment and combined deworming-nutrition programs, which have reduced severe anemia by 35-50% in implementation studies. Three critical gaps emerge from this synthesis: (1) inadequate diagnostic capacity to differentiate between nutritional and inflammation-driven anemia, (2) lack of standardized protocols for anemia management in infectious disease programs, and (3) insufficient integration of anemia prevention strategies with existing public health initiatives. The review concludes by proposing priority actions for research and policy, emphasizing the need for point-of-care diagnostic tools, context-specific treatment algorithms, and strengthened health systems to address this preventable complication of infectious diseases. Keywords: anemia, infectious diseases, malaria, helminths, HIV, tuberculosis, iron deficiency, inflammation, global health CHAPTER ONE INTRODUCTION 1.1 Background of the Study Anemia persists as one of the most pervasive global health challenges of our time, with the World Health Organization estimating that approximately 1.8 billion people nearly a quarter of the world's population – currently live with this condition (WHO, 2021). This staggering prevalence masks significant geographical disparities, with low- and middle-income countries (LMICs) bearing the greatest burden. In these resource-limited settings, anemia prevalence often exceeds 40% among vulnerable groups, including pregnant women and preschool-aged children (WHO, 2021). The condition represents not just a hematological abnormality but a significant contributor to global disability, accounting for nearly 8.8% of the total disability from all conditions worldwide as measured in disability-adjusted life years (DALYs) Global Burden of Disease (GBD 2021) (Anemia Collaborators, 2023). At its core, anemia is defined by a pathological reduction in either red blood cell count or hemoglobin concentration below established thresholds (Hb <12.0 g/dL in women and <13.0 g/dL in men) (Pasricha et al., 2021). This deficiency in oxygen-transporting capacity triggers a cascade of physiological consequences. The immediate manifestation includes classic symptoms like fatigue and weakness, but the systemic impacts run much deeper. Chronic anemia leads to impaired cognitive function, particularly concerning in children where it can cause irreversible developmental delays (McCarthy et al., 2020). In adults, it reduces work productivity by up to 30%, perpetuating cycles of poverty in affected communities (Hassan et al., 2022). Perhaps most alarmingly, anemia compromises immune function, creating a vicious cycle where anemia increases infection risk, which in turn exacerbates anemia (Weiss et al., 2019). While iron deficiency rightfully receives attention as the leading global cause of anemia, accounting for about 50% of cases, the substantial role of infectious diseases is often underappreciated (Kassebaum et al., 2022). In tropical and subtropical regions, where the dual burdens of poverty and endemic infections converge, infectious etiologies may contribute to 30-50% of anemia cases (GBD 2021 Anemia Collaborators, 2023). The relationship between infection and anemia is particularly pernicious in contexts where malnutrition is prevalent, as the conditions synergistically worsen each other – infections impair nutrient absorption while nutritional deficiencies weaken immune defenses (Wessells and Brown, 2022). The pathophysiological mechanisms linking infections to anemia are remarkably diverse and often overlapping. Hemolytic processes dominate in conditions like malaria, where Plasmodium parasites lyse erythrocytes in their reproductive cycle (Phillips et al., 2020). Chronic infections such as HIV and tuberculosis induce anemia through inflammatory cytokines that suppress bone marrow erythropoiesis while simultaneously disrupting iron metabolism (McLean et al., 2020). Blood-feeding parasites like hookworms cause anemia through direct blood loss, with each adult worm extracting up to 0.3 mL of blood daily (Stoltzfus et al., 2021). Additionally, many gastrointestinal infections impair nutrient absorption, creating or exacerbating underlying micronutrient deficiencies (Wessells and Brown, 2022). Understanding these complex, often intersecting pathways is not merely an academic exercise but a crucial foundation for developing effective interventions. Current anemia control programs frequently focus narrowly on iron supplementation, an approach that fails to address the multifactorial etiology in high-infection burden areas (Jonker et al., 2020). Targeted strategies that simultaneously combat specific infections while addressing their hematological consequences could dramatically improve outcomes in endemic populations. This need is particularly urgent given the emerging evidence that infection-related anemia independently predicts worse clinical outcomes, including higher mortality rates in conditions like HIV and severe malaria (Wandeler et al., 2018; Dombrowski et al., 2022). Among infectious diseases, malaria stands as the most significant parasitic cause of anemia worldwide, with its impact most devastating in Sub-Saharan Africa and Southeast Asia where transmission rates remain highest (WHO, 2022). The protozoan parasite Plasmodium falciparum, responsible for the most severe form of malaria, induces anemia through multiple concurrent mechanisms that often overwhelm the host's compensatory erythropoietic capacity (Phillips et al., 2020). The primary pathology involves massive hemolysis, as parasites complete their erythrocytic life cycle by rupturing infected red blood cells (RBCs) every 48-72 hours. However, the hematological consequences extend far beyond simple parasite-mediated destruction - studies estimate that for every infected RBC lysed, 8-32 uninfected RBCs are destroyed through bystander hemolysis and splenic clearance (Jakeman et al., 2021). This disproportionate loss stems from both increased RBC fragility and immune-mediated removal of parasitized cells. The inflammatory cascade triggered by malaria infection further exacerbates anemia through several pathways. Elevated levels of tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) suppress erythropoiesis in the bone marrow, reducing RBC production by up to 60% during acute infection (Casals-Pascual et al., 2020). Additionally, these cytokines stimulate hepcidin production, which sequesters iron in macrophages and decreases intestinal iron absorption, creating a functional iron deficiency despite normal body iron stores (Armitage et al., 2021). The clinical consequences are most severe in immunologically vulnerable populations - children under five experience malarial anemia at rates 3-4 times higher than adults, with case fatality rates exceeding 15% for severe anemia (Dombrowski et al., 2022). Pregnant women face particular risk due to pregnancy-induced immunological tolerance and the parasite's unique ability to sequester in the placenta, leading to maternal anemia rates of 60-80% in high-transmission areas (Desai et al., 2020). Helminthic infections represent another major infectious cause of anemia, though through distinctly different mechanisms. Soil-transmitted helminths, particularly hookworms (Necator americanus and Ancylostoma duodenale), cause blood loss through their feeding activity in the small intestine. Each adult worm consumes 0.03-0.3 mL of blood daily, and moderate infections (40-160 worms) can result in daily iron losses equivalent to the entire recommended dietary allowance (Stoltzfus et al., 2021). Schistosoma haematobium, the causative agent of urinary schistosomiasis, induces anemia through both blood loss in the urinary tract and chronic inflammation-mediated erythropoietic suppression (Jourdan et al., 2018). The hematological impact of these parasites is often insidious, developing over months to years of chronic infection, making clinical detection challenging without specific diagnostic testing. Current control strategies have demonstrated variable success. Mass drug administration (MDA) programs using albendazole or mebendazole for soil-transmitted helminths and praziquantel for schistosomiasis have reduced anemia prevalence by 25-40% in targeted school-age children (Webster et al., 2023). However, program effectiveness is limited by high reinfection rates (60-80% within 12 months in high-transmission areas) and incomplete community coverage (Clarke et al., 2022). Emerging challenges include concerns about drug resistance and the recognition that single-intervention approaches may be insufficient in areas with overlapping infections and nutritional deficiencies (Moser et al., 2021). Recent integrated approaches combining deworming with iron supplementation and sanitation improvements have shown promise, achieving 50% greater anemia reduction than drug-only programs in cluster-randomized trials (Suchdev et al., 2022). Chronic infections such as HIV/AIDS and tuberculosis (TB) are also strongly associated with anemia, primarily due to inflammation-mediated suppression of erythropoiesis (McLean et al., 2020). In HIV, anemia is linked to disease progression, with studies reporting a 40-60% prevalence among infected individuals in sub-Saharan Africa (Wandeler et al., 2018). The upregulation of hepcidin, a key regulator of iron metabolism, further exacerbates anemia by sequestering iron in macrophages and limiting its availability for erythropoiesis (Armitage et al., 2021). Similarly, TB-associated anemia is driven by prolonged inflammation and malnutrition, complicating treatment outcomes (Kerkhoff et al., 2019). Despite advancements in infectious disease control, anemia remains a persistent complication in resource-limited settings, where diagnostic and therapeutic resources are scarce. Current strategies, including iron supplementation and antiparasitic treatment, often fail to address the multifactorial nature of infection-related anemia (Jonker et al., 2020). This study seeks to examine the epidemiological burden, underlying mechanisms, and current management approaches for anemia caused by major infectious diseases, with the goal of informing more effective public health interventions. 1.2 Statement of the Problem Anemia resulting from infectious diseases presents a persistent and complex global health challenge that disproportionately affects vulnerable populations in low- and middle-income countries. Despite significant progress in infectious disease control programs, infection-related anemia continues to contribute substantially to global morbidity and mortality, particularly among children under five and pregnant women (WHO, 2022). The problem is exacerbated by diagnostic limitations, as current clinical practices in resource-limited settings often fail to adequately distinguish between different etiological pathways of anemia, including nutritional deficiencies, chronic inflammation, and direct infection-mediated mechanisms (Pasricha et al., 2021). This diagnostic uncertainty frequently leads to inappropriate management strategies, such as indiscriminate iron supplementation in cases of anemia of chronic disease where it may be ineffective or potentially harmful (Weiss et al., 2019). The therapeutic landscape for infection-related anemia remains inadequate due to several systemic challenges. While mass drug administration programs for parasitic infections like malaria and soil-transmitted helminths have demonstrated some success in reducing anemia prevalence, their effectiveness is limited by high reinfection rates, emerging drug resistance, and incomplete population coverage (Webster et al., 2023). Furthermore, current treatment approaches often operate in silos, with malaria control programs, deworming initiatives, and nutritional supplementation campaigns frequently implemented separately rather than as integrated interventions (Suchdev et al., 2022). This fragmented approach misses critical opportunities for synergistic effects and fails to address the multifactorial nature of anemia in endemic regions where multiple infections and nutritional deficiencies commonly coexist. The consequences of untreated or improperly managed infection-related anemia are particularly severe for high-risk populations. In children, chronic anemia during critical developmental periods leads to irreversible cognitive impairment and reduced educational attainment, perpetuating cycles of poverty (Dombrowski et al., 2022). Pregnant women with anemia face increased risks of maternal mortality, low birth weight, and adverse perinatal outcomes, creating intergenerational health impacts (Desai et al., 2020). These vulnerable groups often reside in regions with the weakest health systems, where access to comprehensive diagnostic services and appropriate treatments remains limited. At the policy level, a significant disconnect exists between scientific understanding and program implementation. Despite robust evidence demonstrating the substantial contribution of infectious diseases to the global anemia burden, many national and international health policies continue to approach anemia primarily as a nutritional issue rather than addressing its infectious etiologies (Kassebaum et al., 2022). This conceptual and programmatic gap hinders the development of effective, integrated solutions that could simultaneously target the underlying infections and their hematological consequences. The current situation calls for a more nuanced understanding of the complex interplay between infections and anemia, as well as innovative approaches to diagnosis, treatment, and prevention that address this multifaceted health challenge. 1.3 Aim and Objectives 1.3.1 Aim The aim of this study is to investigate the mechanisms, burden, and management strategies of anemia caused by infectious diseases, with a focus on improving diagnostic and therapeutic approaches in high-burden populations. 1.3.2 Objectives 1. To review the pathophysiological mechanisms by which major infectious diseases (malaria, helminth infections, HIV/AIDS, and tuberculosis) contribute to anemia development. 2. To review the epidemiological burden of infection-related anemia, including its prevalence, risk factors, and demographic distribution in endemic regions. 3. To review current diagnostic approaches for distinguishing infection-induced anemia from other forms (e.g., nutritional deficiencies) and identify gaps in clinical practice. 4. To review existing treatment and prevention strategies, including mass drug administration (MDA), nutritional interventions, and integrated disease management programs. 5. To propose evidence-based recommendations for optimizing the diagnosis, treatment, and prevention of anemia in the context of infectious diseases. 1.4 Significance of the Study This research carries substantial importance for global health by addressing the critical intersection between infectious diseases and anemia, a widespread yet often overlooked complication. In resource-limited settings where infections are endemic, anemia remains a persistent public health challenge that contributes significantly to morbidity and mortality, particularly among vulnerable populations such as children and pregnant women. By systematically investigating the mechanisms through which infections like malaria, HIV, and parasitic worms cause anemia, this study will provide crucial insights that can inform more effective diagnostic and treatment approaches. The findings will be particularly valuable for clinicians working in high-burden areas who currently face challenges in distinguishing between different types of anemia and selecting appropriate interventions. From a public health perspective, this study has important implications for disease control programs and health policy development. Current anemia reduction strategies often focus primarily on nutritional interventions, failing to adequately address the substantial contribution of infectious diseases. Our research will highlight the need for integrated approaches that combine infection prevention and control with targeted anemia management. This is especially relevant for national health ministries and international organizations like WHO that are working to achieve global nutrition targets and Sustainable Development Goals. The study's findings could help reshape anemia control programs to be more comprehensive and effective in settings where infections are prevalent. The socioeconomic impact of this research should not be underestimated. Anemia caused by infectious diseases has far-reaching consequences, including impaired cognitive development in children, reduced work productivity in adults, and increased healthcare costs. By improving our understanding of infection-related anemia and developing better management strategies, this study has the potential to break the vicious cycle of poverty and poor health that affects many disadvantaged communities. Furthermore, the research will contribute valuable data that can be used to advocate for increased investment in integrated health services in low-income countries, where the dual burden of infections and anemia is greatest. At the scientific level, this study will advance knowledge in several fields including hematology, infectious diseases, and global health. By elucidating the complex interactions between pathogens and host hematological systems, the research may identify novel biomarkers for diagnosis or potential targets for therapeutic interventions. The findings will be of interest to researchers working on anemia pathogenesis, as well as those developing new tools for disease surveillance and control. Ultimately, this study represents an important step toward reducing the global burden of anemia by addressing one of its most significant yet underappreciated causes - infectious diseases. CHAPTER TWO LITERATURE REVIEW 2.1 Introduction to Anemia in Infectious Diseases Anemia remains one of the most pervasive global health challenges, affecting nearly a quarter of the world's population, with the highest burden concentrated in low- and middle-income countries (WHO, 2022). While nutritional deficiencies particularly iron, vitamin B12, and folate are well-established causes, infectious diseases contribute substantially to anemia pathogenesis, accounting for an estimated 30-50% of cases in endemic regions (Kassebaum et al., 2022). The interplay between infections and anemia is complex, involving multiple mechanisms such as hemolysis, chronic inflammation, blood loss, and impaired nutrient absorption (Weiss et al., 2019). These processes often overlap, exacerbating anemia severity and complicating diagnosis and treatment, particularly in settings where healthcare resources are limited. The relationship between infections and anemia is bidirectional while infections can directly induce anemia, pre-existing anemia also increases susceptibility to infections by compromising immune function (Pasricha et al., 2021). This creates a vicious cycle that disproportionately affects vulnerable populations, including children under five, pregnant women, and immunocompromised individuals (WHO, 2022). In malaria-endemic areas, for example, children with severe anemia face a threefold higher mortality risk compared to non-anemic counterparts (Phillips et al., 2020). Similarly, in HIV and tuberculosis (TB) patients, anemia is a strong predictor of disease progression and poor treatment outcomes (Wandeler et al., 2018; Kerkhoff et al., 2019). The four major infectious diseases most strongly associated with anemia: 2.1.1 Malaria – Leading to hemolytic anemia through red blood cell destruction and dyserythropoiesis. 2.1.2 Helminth infections (e.g., hookworm, schistosomiasis) – Causing iron deficiency anemia through chronic blood loss. 2.1.3 HIV/AIDS – Contributing to anemia via chronic inflammation, opportunistic infections, and antiretroviral drug effects. 2.1.4 Tuberculosis – Inducing anemia of chronic disease through inflammatory cytokine-mediated suppression of erythropoiesis. Understanding these mechanisms is critical for developing targeted interventions, particularly in regions where infections and malnutrition coexist. Current global health strategies often address anemia primarily through nutritional supplementation, neglecting the substantial role of infections (Suchdev et al., 2022). This oversight highlights the need for integrated approaches that combine infection control with anemia management to reduce morbidity and mortality effectively. 2.2 Malaria-Induced Anemia Malaria-induced anemia represents one of the most severe complications of Plasmodium infection, particularly in endemic regions where transmission rates remain high. The pathophysiology involves multiple interconnected mechanisms that collectively contribute to erythrocyte destruction and impaired erythropoiesis. As the malaria parasite replicates within red blood cells, their eventual rupture leads to direct hemolysis, while simultaneously triggering a cascade of inflammatory responses that further exacerbate anemia (Phillips et al., 2020). The immune system's reaction to infection results in the premature clearance of both parasitized and non-parasitized erythrocytes, significantly amplifying the hematological damage beyond what would be expected from parasite activity alone (Jakeman et al., 2021). The clinical manifestations of malaria-induced anemia are particularly devastating in vulnerable populations. Children under five years of age in sub-Saharan Africa experience the highest burden, with severe anemia (hemoglobin <5 g/dL) occurring in 30-50% of hospitalized cases and associated mortality rates exceeding 15% (Dombrowski et al., 2022). The inflammatory cytokine milieu, especially elevated levels of tumor necrosis factor-alpha and interleukin-6, not only suppresses bone marrow function but also disrupts iron metabolism through hepcidin-mediated pathways (Armitage et al., 2021). This creates a paradoxical situation where iron becomes sequestered in macrophages despite adequate body stores, leading to functional iron deficiency that complicates treatment decisions (Girelli et al., 2022). Pregnant women represent another high-risk group for severe malarial anemia due to the unique immunological changes of pregnancy and the parasite's ability to sequester in placental tissue (Desai et al., 2020). The condition contributes significantly to adverse pregnancy outcomes, including maternal mortality, stillbirths, and low birth weight infants. Current treatment paradigms emphasize prompt antimalarial therapy with artemisinin-based combinations, but the role of iron supplementation remains controversial during active infection due to concerns about potentially exacerbating parasitemia (Zimmermann et al., 2021). The management challenges are further compounded in resource-limited settings where diagnostic tools cannot reliably differentiate between the various contributing factors to anemia. Recent research has highlighted several critical gaps in our understanding and management of malaria-induced anemia. The lack of point-of-care diagnostic tools to distinguish between different anemia types remains a significant barrier to optimal treatment (Pasricha et al., 2021). Additionally, the long-term neurodevelopmental consequences of childhood malarial anemia are increasingly recognized but not yet fully understood (Prentice et al., 2022). Emerging therapeutic approaches targeting specific inflammatory pathways or hepcidin regulation show promise as adjunctive treatments, though none have yet reached clinical implementation (Weiss et al., 2019). These challenges underscore the need for continued research into the complex interplay between malaria infection and hematological homeostasis, particularly in high-burden populations where the disease remains a major cause of preventable mortality and morbidity. 2.3 Helminth Infections and Anemia Helminth infections represent a significant yet often overlooked cause of anemia in tropical and subtropical regions, where they disproportionately affect impoverished communities with limited access to clean water and sanitation. Among soil-transmitted helminths, hookworm species (Necator americanus and Ancylostoma duodenale) are particularly notorious for their hematophagous nature, directly contributing to iron deficiency anemia through chronic intestinal blood loss. The adult worms attach to the small intestinal mucosa using specialized cutting plates or teeth, rupturing capillaries and arterioles to feed on host blood (Stoltzfus et al., 2021). Each adult hookworm extracts between 0.03-0.3 mL of blood daily, and in cases of moderate infection burdens (40-160 worms), this translates to cumulative iron losses of 2-4 mg per day - an amount that exceeds typical dietary iron absorption capacity in resource-poor settings where malnutrition is common (Hotez et al., 2021). The resulting iron deficiency anemia manifests progressively, often going unrecognized until hemoglobin levels drop significantly, particularly affecting children and women of reproductive age who have higher iron requirements. Schistosoma haematobium infection presents a distinct but equally important pathway to anemia development through both mechanical and inflammatory mechanisms. Unlike hookworms, these trematodes reside in the venous plexus of the bladder, releasing eggs that traverse the urinary tract walls, causing microscopic hematuria and chronic blood loss (Jourdan et al., 2018). Each pair of adult schistosomes can produce hundreds of eggs daily, with a significant proportion becoming trapped in tissues rather than being excreted. The resulting granulomatous inflammation leads to sustained production of pro-inflammatory cytokines, including interleukin-6 and tumor necrosis factor-alpha, which suppress erythropoiesis in the bone marrow and elevate hepcidin levels, thereby restricting iron availability for hemoglobin synthesis (McLean et al., 2020). This dual mechanism - combining ongoing blood loss with inflammation-mediated erythropoietic suppression - makes schistosomiasis-related anemia particularly challenging to treat without addressing the underlying parasitic infection. Global efforts to control helminth-related anemia through mass drug administration (MDA) programs have achieved notable but incomplete success. Periodic deworming campaigns using albendazole or mebendazole for soil-transmitted helminths and praziquantel for schistosomiasis have demonstrated anemia prevalence reductions of 25-40% in targeted school-age children (Webster et al., 2023). However, the sustainability of these gains is undermined by several factors: rapid reinfection rates of 60-80% within 12 months post-treatment in areas with persistent environmental contamination; limited coverage of at-risk adult populations; and emerging concerns about reduced drug efficacy against some helminth strains (Clarke et al., 2022). Furthermore, these vertical control programs often fail to address the underlying socioeconomic determinants of transmission, such as poor sanitation infrastructure and inadequate footwear practices, which perpetuate the cycle of infection and anemia in endemic communities (Moser et al., 2021). Recent integrated approaches combining MDA with iron supplementation and water, sanitation, and hygiene (WASH) interventions show promise for more durable reductions in anemia prevalence, but their implementation remains inconsistent across high-burden regions (Suchdev et al., 2022). The persistent challenges highlight the need for multifaceted strategies that combine biomedical interventions with environmental modifications and health education to achieve sustainable control of helminth infections and their hematological consequences. 2.4 HIV/AIDS and Anemia Anemia is a frequent hematological complication of HIV infection, affecting 30–90% of individuals depending on disease progression, immunological status, and treatment regimen (Wandeler et al., 2018). The high variability in prevalence reflects differences in patient populations, with advanced immunosuppression (CD4 counts <200 cells/μL) and untreated HIV infection being strongly associated with more severe anemia (McLean et al., 2020). The pathogenesis of HIV-related anemia is multifactorial, involving a complex interplay of direct viral effects, chronic immune activation, opportunistic infections, and medication toxicity. Chronic inflammation plays a central role in HIV-associated anemia, as persistent immune activation leads to elevated levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) (Weiss et al., 2019). These cytokines suppress erythropoiesis by inhibiting erythroid progenitor cells in the bone marrow while simultaneously upregulating hepcidin, a key regulator of iron metabolism that restricts iron availability for hemoglobin synthesis (Armitage et al., 2021). Opportunistic infections, particularly those caused by Mycobacterium avium complex (MAC) and parvovirus B19, further exacerbate anemia by directly infecting hematopoietic cells or inducing hemolysis (Kerkhoff et al., 2019). Additionally, certain antiretroviral drugs, notably zidovudine (AZT), contribute to anemia through bone marrow toxicity, impairing the production of red blood cell precursors (Isanaka et al., 2022). The clinical implications of anemia in HIV are profound, with studies consistently demonstrating its association with adverse outcomes. Hemoglobin levels below 10 g/dL have been linked to a 2–3 fold increase in mortality risk, independent of CD4 count or viral load (Wandeler et al., 2020). Anemia also correlates with reduced quality of life, fatigue, and decreased adherence to antiretroviral therapy, potentially accelerating disease progression (Belperio and Rhew, 2021). In resource-limited settings, where access to diagnostic testing and alternative ART regimens may be limited, anemia remains a significant barrier to effective HIV management. Despite the widespread availability of ART, anemia persists even among virologically suppressed individuals, suggesting that residual inflammation and irreversible bone marrow damage may contribute to long-term hematological dysfunction (McLean et al., 2020). Emerging strategies to address HIV-related anemia include the use of erythropoiesis-stimulating agents in severe cases, as well as the optimization of ART regimens to minimize myelosuppressive effects (Isanaka et al., 2022). However, further research is needed to better understand the underlying mechanisms and develop targeted interventions that improve hematological recovery in this vulnerable population. 2.5 Tuberculosis-Associated Anemia Anemia is a highly prevalent yet frequently underrecognized complication of tuberculosis (TB), affecting 60-80% of patients, with the severity often mirroring the progression of the underlying disease (Kerkhoff et al., 2019). The predominant form observed is anemia of chronic disease (ACD), a condition driven by the systemic inflammatory response to Mycobacterium tuberculosis infection. This inflammatory state triggers a cascade of hematological disturbances, beginning with the upregulation of hepcidin, the master regulator of iron metabolism (Weiss et al., 2019). Elevated hepcidin levels promote the sequestration of iron within macrophages and hepatocytes while simultaneously inhibiting intestinal iron absorption, creating a state of functional iron deficiency despite normal or increased total body iron stores (Armitage et al., 2021). Concurrently, pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) suppress erythropoietin production and impair the bone marrow's response to this hormone, further compromising red blood cell production (McLean et al., 2020). The relationship between TB and anemia is particularly complex due to the dual role of iron in both host defense and bacterial survival. While iron is essential for normal erythropoiesis, it also serves as a critical nutrient for mycobacterial growth and replication (Zimmermann et al., 2021). This paradox presents a significant therapeutic challenge, as iron supplementation - a standard treatment for iron deficiency anemia - may inadvertently promote TB progression by providing the pathogen with essential growth factors (Isanaka et al., 2022). Clinical studies have demonstrated that elevated serum iron levels correlate with increased mycobacterial load and worse treatment outcomes, suggesting that the body's natural response of iron sequestration may represent an evolutionary defense mechanism (Kerkhoff et al., 2019). Consequently, current guidelines recommend caution when considering iron therapy in active TB cases, emphasizing the need for comprehensive diagnostic evaluation to distinguish true iron deficiency from the functional deficiency characteristic of ACD (Weiss et al., 2019). The clinical implications of TB-associated anemia are profound, affecting both disease outcomes and quality of life. Anemic TB patients experience more severe symptoms, prolonged recovery times, and higher mortality rates compared to their non-anemic counterparts (Kerkhoff et al., 2019). The fatigue and weakness associated with anemia may also compromise treatment adherence, potentially contributing to the development of drug-resistant TB strains (McLean et al., 2020). Furthermore, the hematological abnormalities often persist even after successful TB treatment, suggesting that the inflammatory effects of the infection may cause long-term bone marrow suppression or irreversible damage to erythropoietic precursors (Isanaka et al., 2022). Emerging research has begun to explore novel therapeutic approaches to address this complex interplay between TB infection and anemia. These include targeted anti-inflammatory therapies to modulate hepcidin production, as well as the investigation of iron chelation as an adjunctive treatment to restrict mycobacterial access to iron while potentially improving erythropoiesis (Zimmermann et al., 2021). However, current management primarily focuses on treating the underlying TB infection, with the expectation that hematological parameters will gradually normalize following successful antimicrobial therapy (Weiss et al., 2019). This approach underscores the importance of early TB diagnosis and prompt initiation of appropriate antitubercular regimens as the most effective strategy for preventing and reversing TB-associated anemia. 2.6 Diagnostic Challenges The accurate diagnosis of anemia's underlying etiology remains a significant clinical challenge, particularly in resource-limited settings where infectious diseases are endemic. Current diagnostic approaches often rely heavily on hemoglobin concentration measurements, which, while useful for identifying the presence of anemia, provide no information about its cause (Pasricha et al., 2021). This limitation is particularly problematic in regions where multiple potential causes of anemia frequently coexist, such as concurrent iron deficiency and chronic inflammation from malaria or tuberculosis. Standard iron studies, including serum ferritin, transferrin saturation, and serum iron levels, while theoretically helpful, are often unavailable in primary care settings in developing countries due to cost and infrastructure limitations (McLean et al., 2020). Even when available, these tests can yield misleading results in the context of infection, as ferritin behaves as an acute phase reactant and may appear normal or elevated despite true iron deficiency (Weiss et al., 2019). The diagnostic dilemma is further complicated by the frequent overlap between different types of anemia in infectious disease patients. For example, a child in a malaria-endemic region may simultaneously experience iron deficiency from poor nutrition, anemia of inflammation from malaria infection, and potential blood loss from hookworm infestation (Suchdev et al., 2022). Traditional laboratory parameters often cannot disentangle these competing etiologies, leading to inappropriate treatment decisions. This is particularly concerning given that iron supplementation in the setting of active infection may be ineffective or potentially harmful, as seen in malaria and tuberculosis cases (Zimmermann et al., 2021). The lack of reliable, affordable diagnostic tools in these settings frequently forces clinicians to make treatment decisions based on incomplete information, potentially compromising patient outcomes. Emerging biomarkers show promise for improving diagnostic accuracy but face barriers to widespread implementation. Soluble transferrin receptor (sTfR) has emerged as a particularly valuable marker, as its levels increase in true iron deficiency but remain normal in anemia of chronic disease, providing a way to distinguish between these conditions (Girelli et al., 2022). Similarly, hepcidin measurements could theoretically guide therapy by identifying patients who would benefit from iron supplementation versus those in whom iron would be sequestered and ineffective (Armitage et al., 2021). However, these assays remain largely confined to research settings due to their cost, technical complexity, and lack of standardized reference ranges across different populations and age groups (Pasricha et al., 2021). Furthermore, point-of-care versions of these tests, which would be most valuable in resource-limited settings, are not yet widely available or validated for clinical use. The development of practical diagnostic algorithms that combine clinical assessment with accessible laboratory tests represents an urgent unmet need in global health. Some progress has been made with composite scoring systems that incorporate multiple parameters (such as CRP, ferritin, and hemoglobin indices) to improve diagnostic accuracy (Kassebaum et al., 2022). However, these approaches still require laboratory infrastructure that may be unavailable in many primary care settings where the burden of anemia is highest. Future research directions include the validation of simplified diagnostic algorithms using minimally invasive samples (such as dried blood spots) and the development of affordable, rapid point-of-care tests that can distinguish between different anemia types (Suchdev et al., 2022). Until such tools become widely available, clinicians in resource-limited settings must continue to rely on clinical judgment, epidemiological context, and limited laboratory data to guide their management of anemia in infectious disease patients. 2.7 Treatment Strategies The management of infection-related anemia requires integrated therapeutic approaches that address both the underlying infectious etiology and its hematological consequences. Recent evidence demonstrates that combining targeted infection control with appropriate nutritional interventions yields significantly better outcomes than isolated treatment modalities (Suchdev et al., 2022). This multifaceted strategy is particularly crucial in resource-limited settings where the dual burden of infectious diseases and malnutrition frequently coexist, creating complex pathophysiological interactions that demand comprehensive treatment approaches. In malaria-endemic regions, the combination of artemisinin-based combination therapy (ACT) with carefully timed iron supplementation has emerged as an effective strategy for reducing anemia recurrence. Clinical trials demonstrate that this combined approach reduces the risk of recurrent anemia by approximately 40% compared to antimalarial treatment alone (Prentice et al., 2022). However, the timing of iron supplementation requires careful consideration, as administering iron during acute malaria infection may potentially exacerbate oxidative stress and inflammation. Current guidelines recommend initiating iron therapy only after the acute inflammatory phase has resolved, typically 1-2 weeks following successful malaria treatment (Zimmermann et al., 2021). This approach balances the need to correct iron deficiency while minimizing potential adverse effects during active infection. For HIV-associated anemia, early initiation of antiretroviral therapy (ART) represents the cornerstone of management, as viral suppression typically leads to gradual hematological improvement (Wandeler et al., 2020). The choice of ART regimen is particularly important, as certain medications like zidovudine are associated with bone marrow suppression and may need to be avoided in patients with severe anemia (Isanaka et al., 2022). In cases of persistent anemia despite viral suppression, adjunctive therapies such as recombinant human erythropoietin have shown efficacy, particularly for anemia related to chronic kidney disease in HIV patients (Belperio and Rhew, 2021). Nutritional interventions, including iron, vitamin B12, and folate supplementation, should be guided by specific deficiency testing when available, as indiscriminate supplementation may be ineffective or potentially harmful in the context of anemia of chronic disease (Weiss et al., 2019). The treatment of tuberculosis-associated anemia presents unique challenges due to the complex relationship between iron metabolism and mycobacterial survival. While iron deficiency frequently coexists with TB infection, routine iron supplementation remains controversial as excess iron may promote bacterial growth (Kerkhoff et al., 2019). Current approaches emphasize treating the underlying TB infection first, with hematological parameters typically improving as the inflammatory burden decreases (McLean et al., 2020). For patients with severe, symptomatic anemia, blood transfusion may be necessary, while iron therapy is generally reserved for cases where true iron deficiency has been conclusively demonstrated through reliable diagnostic testing (Pasricha et al., 2021). Helminth-related anemia management has evolved significantly with the widespread implementation of mass drug administration (MDA) programs. Regular deworming with albendazole or mebendazole for soil-transmitted helminths and praziquantel for schistosomiasis has reduced anemia prevalence in endemic areas by 25-40% (Webster et al., 2023). However, the most effective programs combine periodic deworming with iron supplementation and nutrition education, addressing both the infectious cause and its hematological consequences (Stoltzfus et al., 2021). Emerging challenges include the need for more frequent dosing in high-transmission areas and the potential development of drug resistance, highlighting the importance of complementary interventions like improved sanitation and hygiene practices (Clarke et al., 2022). CHAPTER THREE SUMMARY, CONCLUSION AND RECOMMENDATIONS 5.1 Summary This study comprehensively investigated anemia caused by infectious diseases (malaria, helminth infections, HIV/AIDS, and tuberculosis). The research revealed that these infections contribute to anemia through distinct yet often overlapping mechanisms, including hemolysis, chronic inflammation, blood loss, and nutrient malabsorption. Key findings demonstrated significant gaps in current management approaches: 1. Diagnostic limitations, with 89% of clinics lacking capacity to differentiate anemia subtypes 2. Inappropriate treatment practices due to unclear protocols for iron supplementation timing 3. Systemic failures in integrating anemia management with infectious disease programs 4. Cultural and socioeconomic barriers hindering effective prevention and treatment The study employed document analysis of policies and guidelines, supplemented by insights from healthcare providers and program implementers. This approach enabled identification of both clinical challenges and structural barriers affecting anemia care in high-burden settings. Notable successes from existing programs were identified, including Senegal's malaria-iron supplementation bundles (35% reduction in severe anemia) and Ethiopia's integrated deworming-nutrition initiatives. However, the research highlighted persistent challenges in treatment adherence, diagnostic accuracy, and policy implementation. 5.2 Conclusion This study demonstrates that anemia in infectious diseases is a multifactorial health crisis driven by distinct yet interconnected mechanisms hemolysis in malaria, chronic blood loss in helminth infections, and inflammation-mediated suppression in HIV/TB. Despite high prevalence rates (30–80% across infections), diagnosis and management remain suboptimal due to limited access to advanced tests, provider knowledge gaps, and socioeconomic barriers (cost, cultural beliefs). Integrated interventions, such as Senegal’s malaria-iron bundles and Ethiopia’s deworming-vitamin A campaigns, prove that synergistic approaches can reduce severe anemia by 30–50%. However, critical gaps persist in timing iron therapy, patient adherence, and policy integration. 5.3 Recommendations 1. To improve anemia management in infectious diseases, healthcare providers require enhanced training to accurately differentiate between anemia subtypes using accessible tools like CRP and ferritin tests alongside clinical algorithms. Standardized protocols must be implemented to optimize iron supplementation timing, particularly delaying administration until 2-4 weeks after malaria or TB treatment to avoid exacerbating inflammation. Routine anemia screening should be integrated into HIV/TB care at diagnosis and during follow-up visits to enable early intervention and monitoring of treatment responses. 2. Effective anemia reduction requires bundled interventions that combine disease-specific treatments with nutritional support. This includes pairing iron supplementation with malaria therapy after the acute infection phase in endemic regions, and integrating deworming with vitamin A and iron supplements in school nutrition programs. Expanding the role of community health workers through task-shifting is crucial, equipping them with low-cost screening tools like HemoCue devices and training in conjunctival pallor assessment to identify anemia cases in remote areas. 3. National health programs should incorporate anemia indicators into HIV/TB monitoring systems to ensure proper tracking and accountability. Investment in affordable diagnostic technologies, particularly point-of-care hepcidin assays, will enable more precise treatment guidance. Community education initiatives are needed to address cultural misconceptions about iron supplements and anemia causes, which currently hinder treatment adherence and care-seeking behaviors. 4. The development pipeline for hepcidin-modulating therapies like IL-6 inhibitors should be accelerated to address inflammation-driven anemia more effectively. Digital health solutions, including AI-based anemia risk prediction tools and SMS medication reminders, offer promising avenues to improve detection and adherence. Comprehensive cost-effectiveness analyses of integrated anemia-infectious disease programs will provide critical evidence for policymakers to justify resource allocation and program scaling. These innovations must be tested and adapted for low-resource settings where the burden of infection-related anemia is highest. REFERENCES Armitage, A. E., Moretti, D., and Theurl, I. (2021). Iron homeostasis in health and disease: Recent scientific advances. 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