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Objectives: Growth differentiation factor 15 (GDF-15) levels increase due to systemic inflammation and chronic disease burden. Since these biological processes are pathogenic factors of malnutrition, we examined the prospective association between GDF-15 serum levels and subsequent malnutrition in older adults. Methods: We used data from 723 women and 735 men aged ≥65 years [mean age (SD): 71.3 (4.18) years] participating in the Seniors-ENRICA-2 cohort, who were followed-up for 2.2 years. Malnutrition was assessed with the Mini Nutritional Assessment-Short form (MNA-SF), where a 12–14 score indicates normal nutritional status, an 8–11 score indicates at risk of malnutrition, and a 0–7 score malnutrition. Associations of GDF-15 and malnutrition were analyzed, separately in women and men, using linear and logistic regression and adjusted for the main potential confounders. Results: The mean (SD) MNA-SF score at baseline was 13.2 (1.34) for women and 13.5 (1.13) for men. Incident malnutrition (combined endpoint “at risk of malnutrition or malnutrition”) over 2.2 years was identified in 55 (9.7%) of women and 38 (5.4%) of men. In women, GDF-15 was linearly associated with a decrease in the MNA-SF score; mean differences (95% confidence interval) in the MNA-SF score were −0.07 (−0.13; −0.01) points per 25% increase in GDF-15, and −0.49 (−0.83; −0.16) for the highest versus lowest quartile of GDF-15. Also in women, GDF-15 was linearly associated with a higher malnutrition incidence, with odds ratio (95% confidence interval) of 1.24 (1.06; 1.46) per 25% increment in GDF-15 and of 3.05 (1.21; 7.65) for the highest versus lowest quartile of GDF-15. Results were similar after excluding subjects with cardiovascular disease and diabetes. No association of GDF-15 with changes in MNA score or malnutrition incidence was found in men. Conclusion: Higher serum GDF-15 concentrations are associated with worsening nutritional status in older women. Further studies should elucidate the reasons for the sex differences in this association and explore the therapeutic potential of modifying GDF-15 to prevent malnutrition.

Cardiovascular diseases (CVD) continue to be the main cause of death in our country. Adequate control of lipid metabolism disorders is a key challenge in cardiovascular prevention that is far from being achieved in real clinical practice. There is a great heterogeneity in the reports of lipid metabolism from Spanish clinical laboratories, which may contribute to its poor control. For this reason, a working group of the main scientific societies involved in the care of patients at vascular risk, has prepared this document with a consensus proposal on the determination of the basic lipid profile in cardiovascular prevention, recommendations for its realization and unification of criteria to incorporate the lipid control goals appropriate to the vascular risk of the patients in the laboratory reports. Resumen: Las enfermedades cardiovasculares (ECV) siguen siendo la principal causa de muerte en nuestro pais. El control adecuado de las alteraciones del metabolismo lipidico es un reto clave en prevencion cardiovascular que esta lejos de alcanzarse en la practica clinica real. Existe una gran heterogeneidad en los informes del metabolismo lipidico de los laboratorios clinicos españoles, lo que puede contribuir al mal control del mismo. Por ello, un grupo de trabajo de las principales sociedades cientificas implicadas en la atencion de los pacientes de riesgo vascular hemos elaborado este documento con una propuesta basica de consenso sobre la determinacion del perfil lipidico basico en prevencion cardiovascular, recomendaciones para su realizacion y unificacion de criterios para incorporar los objetivos de control lipidico adecuados al riesgo vascular de los pacientes en los informes de laboratorio.

Resumen: Las enfermedades cardiovasculares (ECV) siguen siendo la principal causa de muerte en nuestro país. El control adecuado de las alteraciones del metabolismo lipídico es un reto clave en prevención cardiovascular que está lejos de alcanzarse en la práctica clínica real. Existe una gran heterogeneidad en los informes del metabolismo lipídico de los laboratorios clínicos españoles, lo que puede contribuir al mal control del mismo. Por ello, un grupo de trabajo de las principales sociedades científicas implicadas en la atención de los pacientes de riesgo vascular hemos elaborado este documento con una propuesta básica de consenso sobre la determinación del perfil lipídico básico en prevención cardiovascular, recomendaciones para su realización y unificación de criterios para incorporar los objetivos de control lipídico adecuados al riesgo vascular de los pacientes en los informes de laboratorio. Abstract: Cardiovascular diseases (CVD) continue to be the main cause of death in our country. Adequate control of lipid metabolism disorders is a key challenge in cardiovascular prevention that is far from being achieved in real clinical practice. There is a great heterogeneity in the reports of lipid metabolism from Spanish clinical laboratories, which may contribute to its poor control. For this reason, a working group of the main scientific societies involved in the care of patients at vascular risk, has prepared this document with a consensus proposal on the determination of the basic lipid profile in cardiovascular prevention, recommendations for its realization and unification of criteria to incorporate the lipid control goals appropriate to the vascular risk of the patients in the laboratory reports.

Abstract Background High-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) are biomarkers of myocardial infarction and heart failure, respectively, and indicate cardiovascular risk. Since low physical activity (PA) and sedentary behavior (SB) are also associated with higher cardiovascular risk, and this association could be a consequence of higher levels of cardiac biomarkers, we examined the association of device-measured movement behaviors with hs-cTnT and NT-proBNP in older men and women without major cardiovascular disease (CVD). Methods We used data from 1939 older adults from the Seniors-ENRICA-2 study. Accelerometers were used to assess time spent in sleep, SB, light PA (LPA), and moderate-to-vigorous PA (MVPA). Linear regression models were fitted separately in eight strata defined by sex, by median total PA time, and by the presence of subclinical cardiac damage according to cardiac biomarkers levels. Results In the less active men with subclinical cardiac damage, spending 30 min/day more of MVPA was associated with a mean percentage difference (MPD) (95% confidence interval) in hs-cTnT of − 13.1 (− 18.3, − 7.5); MPDs in NT-proBNP per 30 min/day increment were 5.8 (2.7, 8.9) for SB, − 19.3 (− 25.4, − 12.7) for LPA and − 23.1 (− 30.7, − 14.6) for MVPA. In women with subclinical cardiac damage who were less physically active, 30 min/day more of SB, LPA and MVPA were associated with MPDs in hs-cTnT of 2.1 (0.7, 3.6), − 5.1 (− 8.3, − 1.7) and − 17.5 (− 22.9, − 11.7), respectively, whereas in those more active, LPA and MVPA were associated with MPDs of 4.1 (1.2, 7.2) and − 5.4 (− 8.7, − 2.0), respectively. No associations were found with NT-proBNP in women. Conclusions The relationship between movement behaviors and cardiac biomarkers in older adults without major CVD depends on sex, subclinical cardiac damage and PA level. More PA and less SB were generally related to lower cardiac biomarkers levels among less active individuals with subclinical cardiac damage, with greater benefits for hs-cTnT in women than men and no benefits for NT-proBNP in women.

Background: Chronic use of Angiotensin-converting enzyme (ACE) inhibitors (ACEi) and aldosterone-receptor blockers (ARB) is not associated with worse outcomes in patients with COVID-19. However, evidence on the impact of their discontinuation during hospital admission is scarce. Our aim was to determine whether withdrawal of ACEi, ARB and mineralocorticoid receptor antagonists (MRA) is associated with all-cause mortality in a real-life large cohort of patients with SARS-CoV-2 infection. Methods: Observational cohort study from a large referral center from 1 March 2020 to 20 April 2020. Withdrawal of renin-angiotensin-aldosterone system inhibitors was defined as the absence of any received dose during hospital admission in patients receiving chronic treatment. Prescriptions during admission were confirmed by data from the central pharmacy computerized system. Results: A total of 2042 patients (mean age 68.4±17.6, 57.1% male) with confirmed COVID-19 were included. During a median follow-up of 57 (21-55) days, 583 (28.6%) died. Prior to hospital admission 468 (22.9%), 343 (16.8%) and 83 (4.1%) patients were receiving ACEi, ARB and MRA respectively. During the study period, 216 (46.2%), 193 (56.3%) and 41 (49.4%) were withdrawn from the corresponding drug. After adjusting for age, cardiovascular risk factors, baseline comorbidities and in-hospital COVID-19 dedicated treatment, withdrawal of ACE inhibitors (hazard ration [HR] 1.48 [95% confidence interval –CI– 1.16-1.89]) and MRA (HR 2.01 [95% CI 1.30-3.10]) were shown to be independent predictors of all-cause mortality. No independent relationship between ARB withdrawal and mortality was observed. Conclusion: ACEi and MRA withdrawal were associated with higher mortality. Strong consideration should be given to not discontinuing these medications during hospital admission. Resumo: Introdução: O uso crónico de inibidores da ECA (IECA) e de antagonistas dos recetores de aldosterona (ARA) não está associado a resultados piores em doentes com Covid-19. No entanto, a evidência relativa ao impacto da sua retirada durante a admissão hospitalar é escassa. O nosso objetivo foi determinar se a retirada do IECA, ARA e antagonistas dos recetores dos mineralocorticóides (ARM) está associada à mortalidade por todas as causas numa grande coorte real de doentes com infeção por SRA-CoV-2. Métodos: Estudo coorte observacional a partir de um grande centro de referência de 1 de março de 2020 a 20 de abril de 2020. A retirada dos inibidores do sistema RAAS foi definida como a ausência de qualquer dose recebida durante a admissão hospitalar em doentes que recebem tratamento prolongado. As prescrições durante a admissão foram confirmadas por dados do sistema informático da farmácia central. Resultados: Um total de 2042 doentes (idade média de 68,4 ±17,6, 57,1% do sexo masculino) com COVID-19 confirmado foram incluídos. Durante um acompanhamento médio de 57 (21-55) dias, 583 (28,6%) morreram. Conclusão: A retirada do IECA e do ARM foi associada a uma mortalidade mais elevada. Deve ser dada grande atenção para não interromper estes medicamentos durante a admissão hospitalar.

Abstract Background Growth differentiation factor 15 (GDF‐15) is a biomarker for chronic disease burden that might explain the health effects of sedentary behaviours (SBs) and physical activity (PA). We examined associations of device‐measured sleep, SB and PA, and time reallocations among them, with GDF‐15 in older adults. Methods We used data from 2245 older adults participating in the Seniors‐ENRICA‐2 study. Wrist‐worn accelerometers were employed to ascertain total time in sleep, SB, light PA (LPA) and moderate‐to vigorous PA (MVPA). Associations between these activities and serum GDF‐15 levels were analysed using linear regression, including isotemporal substitution models for time reallocations among activities, and adjusted for potential confounders. Analyses were conducted separately in two groups (less active and more active individuals) according to the median total PA time. Results In the less active participants, 30 min/day more of MVPA were related to lower levels of GDF‐15 when replacing sleep (fully adjusted mean percentage differences [95% confidence interval] in GDF‐15 of −9.2% [−13.2, −5.0]), SB (−9.8% [−13.6, −5.8]) and LPA (−5.8% [−11.1, −0.3]), whereas 30 min/day more of LPA were related to lower GDF‐15 when replacing both sleep (−3.6% [−6.1, −1.0]) and SB (−4.2% [−6.7, −1.7]). In the more active participants, 30 min/day more of MVPA were also associated with lower GDF‐15 when replacing sleep (−2.9% [−5.3, −0.3]), SB (−2.4% [−4.6, −0.2]) and LPA (−3.5% [−6.6, −0.3]), but no associations were found for more time in LPA. Spending more time in SB was associated with higher GDF‐15 levels only among those less active (1.9% [0.9, 2.9] per 30 min/day increment). Sleep time did not appear to be associated with GDF‐15. Conclusions The MVPA was inversely associated with GDF‐15, with stronger associations at lower PA volumes. Also, more LPA and less SB time were linked to lower GDF‐15 in the less active individuals. This suggests that simply moving more and sitting less may reduce chronic disease burden in older adults.

Resumen: Ya han transcurrido veinte años desde la identificación del klotho y del factor de crecimiento fibroblástico 23 (FGF23), el binomio regulador de la homeostasis del fosfato. Al ser el riñón la principal fuente de klotho y el órgano diana regulador del fosfato, la mayoría de los estudios sobre este y el FGF23 tuvieron una vertiente «nefrocéntrica». Gracias al sesgo de este enfoque, los exagerados niveles circulantes de FGF23 observados en la enfermedad renal crónica (ERC) permitieron reconocer el efecto nocivo «off target», independiente de klotho, que ejerce el FGF23. Todo esto ha revolucionado nuestra visión previa sobre la homeostasis mineral y al día de hoy, nos encontramos ante un nuevo escenario en el abordaje clínico del paciente renal, en el que el FGFG23 emerge como marcador precoz de retención de fosfato y simultáneamente como diana terapéutica. En esta revision, se abordan las alteraciones del FGF23 en la ERC y se plantea cómo el mantenimiento del FGF23 circulante en rango adaptativo suprafisiológico desde los estadios iniciales de ERC y el control del «hiperfosfatonismo ilimitado», generado por la resistencia a la acción del FGFG23 en los estadios avanzados, deberían surgir como nuevos paradigmas de tratamiento en chronic kidney disease - mineral and bone disorders (CKD-MBD). El reciente desarrollo de un método automatizado para cuantificar el FGF23, validado para uso clínico, marca el punto de partida para individualizar todo lo que sabemos por los estudios epidemiológicos y utilizarlo adecuadamente desde la cabecera del paciente. Ahora nos toca establecer los límites que discriminen el incremento adaptativo fisiológico de FGF23, para cada estadio de ERC, frente al aumento exagerado, reflejo de una maladaptacion, y que requiera la adopción de medidas terapéuticas. Abstract: Twenty years have passed since the identification of klotho and the fibroblast growth factor 23 (FGF23), the regulatory binomial of phosphate homeostasis. Being kidney the main source of klotho as well as a target organ in the phosphate regulation, most studies involving klotho and FGF23 had a «nephrocentric» focus. Considering that circulating FGF23 can reach exaggerated levels at the end stage of chronic kidney disease (CKD), the bias of this approach allowed to recognize the harmful «off target» klotho-independent effect of FGF23. All of these findings have caused a revolution on our previous knowledge about mineral homeostasis and currently, we are facing a new scenario in the clinical management of CKD, where FGF23 emerges simultaneously as an early biomarker of phosphate retention but also as a therapeutic target. In this review, we describe the disturbances of FGF23 in the CKD and we focus on how the maintenance of circulating FGF23 into a supraphysiological adaptive range from the initial stages of CKD and the control of «unlimited hyperphosphatonism» generated by the resistance to FGF23 action at end stages should emerge as new treatment paradigms in chronic kidney disease - mineral and bone disorders (CKD-MBD). The recent development of an automated FGF23 assay, already validated for clinical use, should be the starting point to individualize all our knowledge from epidemiological studies and will allow us to use it properly for the patient's personalized care. Then, now we are in the momentum to assess the discriminating thresholds to distinguish the physiological adaptive FGF23 elevation related to each CKD stage from the exaggerated increase that would be interpreted as a poor regulatory compensation that will requires the adoption of therapeutic intervention.

Twenty years have passed since the identification of klotho and the fibroblast growth factor 23 (FGF23), the regulatory binomial of phosphate homeostasis. Being kidney the main source of klotho as well as a target organ in the phosphate regulation, most studies involving klotho and FGF23 had a “nephrocentric” focus. Considering that circulating FGF23 can reach exaggerated levels at the end stage of chronic kidney disease (CKD), the bias of this approach allowed to recognize the harmful “off target” klotho-independent effect of FGF23. All of these findings have caused a revolution on our previous knowledge about mineral homeostasis and currently, we are facing a new scenario in the clinical management of CKD, where FGF23 emerges simultaneously as an early biomarker of phosphate retention but also as a therapeutic target. In this review, we describe the disturbances of FGF23 in the CKD and we focus on how the maintenance of circulating FGF23 into a supraphysiological adaptive range from the initial stages of CKD and the control of “unlimited hyperphosphatonism” generated by the resistance to FGF23 action at end stages should emerge as new treatment paradigms in CKD-MBD. The recent development of an automated FGF23 assay, already validated for clinical use, should be the starting point to individualize all our knowledge from epidemiological studies and will allow us to use it properly for the patient’s personalized care. Then, now we are in the momentum to assess the discriminating thresholds to distinguish the physiological adaptive FGF23 elevation related to each CKD stage from the exaggerated increase that would be interpreted as a poor regulatory compensation that will requires the adoption of therapeutic intervention. Resumen: Ya han transcurrido veinte años desde la identificación del klotho y del Factor de crecimiento fibroblástico 23 (FGF23), el binomio regulador de la homeostasis del fosfato. Al ser el riñón la principal fuente de klotho y el órgano diana regulador del fosfato, la mayoría de estudios sobre klotho y FGF23 tuvieron una vertiente “nefrocéntrica”. Gracias al sesgo de este enfoque, los exagerados niveles circulantes de FGF23 observados en la enfermedad renal crónica (ERC) permitieron reconocer el efecto nocivo “off target” independiente de klotho que ejerce el FGF23. Todo esto ha revolucionado nuestra visión previa sobre la homeostasis mineral y a día de hoy, nos encontramos ante un nuevo escenario en el abordaje clínico del paciente renal, en el que el FGFG23 emerge como marcador precoz de retención de fosfato y simultáneamente como diana terapéutica. En esta revisión se abordan las alteraciones del FGF23 en la ERC y se plantea cómo el mantenimiento del FGF23 circulante en rango adaptativo suprafisiológico desde los estadios iniciales de ERC y el control del “hiperfosfatonismo ilimitado”, generado por la resistencia a la acción del FGFG23 en los estadios avanzados, deberían emerger como nuevos paradigmas de tratamiento en la CKD-MBD. El reciente desarrollo de un método automatizado para cuantificar FGF23, validado para uso clínico, marca el punto de partida para individualizar todo lo que sabemos por los estudios epidemiológicos y utilizarlo adecuadamente desde la cabecera del paciente. Ahora nos toca establecer los límites que discriminen el incremento adaptativo fisiológico de FGF23, para cada estadio de ERC, frente al aumento exagerado reflejo de una maladaptacion y que requiera la adopción de medidas terapéuticas.

Abstract Elevated concentrations of acylcarnitines have been associated with higher risk of obesity, type 2 diabetes and cardiovascular disease. The aim of the present study was to assess the association between L-carnitine and acylcarnitine profiles, and 2-year risk of incident lower-extremity functional impairment (LEFI). This case–control study is nested in the Seniors-ENRICA cohort of community-dwelling older adults, which included 43 incident cases of LEFI and 86 age- and sex- matched controls. LEFI was assessed with the Short Physical Performance Battery. Plasma L-carnitine and 28 acylcarnitine species were measured. After adjusting for potential confounders, medium-chain acylcarnitines levels were associated with 2-year incidence of LEFI [odds ratio per 1-SD increase: 1.69; 95% confidence interval: 1.08, 2.64; p = 0.02]. Similar results were observed for long-chain acylcarnitines [odds ratio per 1-SD increase: 1.70; 95% confidence interval: 1.03, 2.80; p = 0.04]. Stratified analyses showed a stronger association between medium- and long-chain acylcarnitines and incidence of LEFI among those with body mass index and energy intake below the median value. In conclusion, higher plasma concentrations of medium- and long-chain acylcarnitines were associated with higher risk of LEFI. Given the role of these molecules on mitochondrial transport of fatty acids, our results suggest that bioenergetics dysbalance contributes to LEFI.

Summary: The SARS-CoV-2 virus has caused tremendous healthcare burden worldwide. Our focus was to develop a practical and easy-to-deploy system to predict the severe manifestation of disease in patients with COVID-19 with an aim to assist clinicians in triage and treatment decisions. Our proposed predictive algorithm is a trained artificial intelligence-based network using 8,427 COVID-19 patient records from four healthcare systems. The model provides a severity risk score along with likelihoods of various clinical outcomes, namely ventilator use and mortality. The trained model using patient age and nine laboratory markers has the prediction accuracy with an area under the curve (AUC) of 0.78, 95% CI: 0.77–0.82, and the negative predictive value NPV of 0.86, 95% CI: 0.84–0.88 for the need to use a ventilator and has an accuracy with AUC of 0.85, 95% CI: 0.84–0.86, and the NPV of 0.94, 95% CI: 0.92–0.96 for predicting in-hospital 30-day mortality.

The synovial fluid (SF) analysis involves a series of chemical and physical studies that allow opportune diagnosing of septic, inflammatory, non-inflammatory, and other pathologies in joints. Among the variety of analyses to be performed on the synovial fluid, the study of viscosity can help distinguish between these conditions, since this property is affected in pathological cases. The problem with viscosity measurement is that it usually requires a large sample volume, or the necessary instrumentation is bulky and expensive. This study compares the viscosity of normal synovial fluid samples with samples with infectious and inflammatory pathologies and classifies them using an ANN (Artificial Neural Network). For this purpose, a low-cost, portable QCR-based sensor (10 MHz) was used to measure the viscous responses of the samples by obtaining three parameters: Δf, ΔΓ (parameters associated with the viscoelastic properties of the fluid), and viscosity calculation. These values were used to train the algorithm. Different versions of the ANN were compared, along with other models, such as SVM and random forest. Thirty-three samples of SF were analyzed. Our study suggests that the viscosity characterized by our sensor can help distinguish infectious synovial fluid, and that implementation of ANN improves the accuracy of synovial fluid classification.

Introduction: Androgens have been described as important players in the regulation of vascular function/structure through their action on the release and effect of vasoactive factors, such as prostanoids. Patients with prostate cancer (PCa) under androgen deprivation therapies (ADTs) present increased risk of cardiovascular mortality. Since thromboxane A2 (TXA2) is one of the most studied prostanoids and its involvement in different cardiovascular diseases has been described, the aim of this study was to investigate: (i) the effect of ADT on the serum levels of TXA2 in PCa patients and its possible link to the redox status and (ii) the effect of the non-hydrolyzable TXA2 analog U-46619 on the function of the aorta of male rats.Methods: The levels of TXA2 and total antioxidant status in 50 healthy subjects, 54 PCa patients, and 57 PCa under ADT were evaluated. These determinations were accompanied by levels of testosterone and C-reactive protein as an inflammation marker. In aortic segments from male rats, the U46619-induced effects on: (i) the vasomotor responses to acetylcholine (ACh), to the NO donor sodium nitroprusside (SNP), to the carbon monoxide-releasing molecule-3 (CORM-3), and to noradrenaline (NA) and (ii) the expression of cyclooxygenase-2 (COX-2), heme oxygenase-1 (HO-1), and phosphorylated ERK1/2 were analyzed.Results: The serum level of TXA2 in patients with PCa was increased with respect to healthy subjects, which was further increased by ADT. There was no modification in the total antioxidant status among the three experimental groups. In aortic segments from male rats, the TXA2 analog decreased the endothelium-dependent relaxation and the sensitivity of smooth muscle cells to NO, while it increased the vasoconstriction induced by NA; the expression of COX-2, HO-1, and pERK1/2 was also increased.Conclusions: ADT increased, along with other inflammatory/oxidative markers, the serum levels of TXA2. The fact that TXA2 negatively impacts the vascular function of the aorta of healthy male rats suggests that inhibition of TXA2-mediated events could be considered a potential strategy to protect the cardiovascular system.

Objective: We aimed to evaluate the results of key performance indicators (KPIs) for a period of over three years, as well as their effectiveness as an improvement tool, to provide information about Point-of-Care Testing (POCT) management system performance and quality assurance. Design and methods: KPIs regarding the global POCT process, extra-analytical phase, quality assurance and staff training and competency were evaluated for blood gases, HbA1c, sweat test and non-connected and connected glucose in an ISO 22870 accredited network. We established the definition of every KPI and its corresponding target. The results of KPIs from all clinical settings were appraised every month during the study period, taking corrective actions when necessary. Results: Annual global results were generally acceptable. However, some clinical areas displayed deviations in specific months. The monitoring of these KPIs allowed us to detect the deviations immediately and identify their causes. These included errors in patient identification, consumables, strips, reagents, analyzers, calibration, internal and external quality control, sample management, connectivity, and operator identification strategy, among others. Conclusions: The evaluation of these KPIs over time has shown their appropriateness. This set of quality indicators could be a useful tool for laboratory medicine leading POCT networks for better and safer patient care.

INTRODUCTION:The present study describes the distribution of selected micronutrients and anaemia among school-aged children living in Libo Kemkem and Fogera (Amhara State, Ethiopia), assessing differences by socio-demographic characteristics, health status and dietary habits. METHODS:A cross-sectional survey was carried out during May-December 2009. Socio-demographic characteristics, health status and dietary habits were collected. Biomarkers were determined for 764 children. Bivariate and multivariable statistical methods were employed to assess micronutrient deficiencies (MD), anaemia, and their association with different factors. RESULTS:More than two thirds of the school-aged children (79.5%) had at least one MD and 40.5% had two or more coexisting micronutrient deficiencies. The most prevalent deficiencies were of zinc (12.5%), folate (13.9%), vit A (29.3%) and vit D (49%). Anaemia occurred in 30.9% of the children. Children living in rural areas were more likely to have vit D insufficiency [OR: 5.9 (3.7-9.5)] but less likely to have folate deficiency [OR: 0.2 (0.1-0.4)] and anaemia [OR: 0.58 (0.35-0.97)]. Splenomegaly was positively associated with folate deficiency and anaemia [OR: 2.77 (1.19-6.48) and 4.91 (2.47-9.75)]. Meat and fish consumption were inversely correlated with zinc and ferritin deficiencies [OR: 0.2 (0.1-0.8) and 0.2 (0.1-0.9)], while oil consumption showed a negative association with anaemia and deficiencies of folate and vitamin A [0.58 (0.3-0.9), OR: 0.5 (0.3-0.9) and 0.6 (0.4-0.9)]. Serum ferritin levels were inversely correlated to the presence of anaemia (p

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