Introducción: El objetivo de este trabajo fue determinar la prevalencia de anemia ferropénica según el componente dinámico y estático, identificando de esta manera los deportes con mayor prevalencia de anemia y determinar la asociación entre el sexo, la edad y anemia.Material y métodos: Estudio observacional de tipo corte transversal analítico. Se utilizó la base de datos de la Dirección Nacional de Servicios Biomédicos del Instituto Peruano del Deporte, en el periodo de enero a diciembre de 2013. De un universo de 1833 deportistas, se seleccionaron aquellos entre 18 y 35 años de edad. Las variables numéricas se evaluaron usando la prueba de t de Student o la prueba de Mann-Whitney dependiendo del estado de normalidad de las variables. Las variables categóricas fueron evaluadas usando χ2. Razones de prevalencias crudas y ajustadas fueron calculadas usando regresión de Poisson con varianza robusta, para evaluar la asociación entre sexo y anemia.Resultados: Se analizaron 633 deportistas, siendo en su mayoría varones (68,4%). Las variables que se incluyeron en el modelo bivariado fueron sexo, edad deportiva y suplementación con hierro, las cuales fueron también incluidas en el modelo multivariado, encontrándose asociación entre anemia y edad deportiva (p=0,01). No se encontró asociación entre sexo y anemia (RPa= 0,96; IC95%: 0,60-1,40; p=0,85), sin embargo, la prevalencia de anemia fue por encima del 15% (17,9% hombres y 16,8% mujeres).Conclusiones: Se halló mayor prevalencia de anemia ferropénica en los deportes de alto componente estático y dinámico. No se encontró asociación entre anemia ferropénica y sexo en deportistas seleccionados del Instituto Peruano del Deporte en el año 2013.

The objective of this study was to evaluate copper sulphate densitometry as a screening method for anaemia in children. The accuracy of copper sulphate densitometry was also compared to clinical assessment for the presence of pallor and haemoglobin measurement with a BMS-haemoglobinometer. Different observers performed these three screening tests independently. For the purposes of this study, anaemia was defined as a laboratory haemoglobin (Hb) concentration below 10 g/dl. A cross-sectional screening study was undertaken, where the results of the different screening tests were compared to laboratory haemoglobin determination (gold standard). The study sample consisted of one hundred consecutive children, aged between 6 months and 6 years, whose parents had given informed written consent for participation. The study was conducted in the Paediatric Outpatient Department of Pretoria Academic Hospital (73 children) and a local creche (27 children). In this study sample, the prevalence of anaemia (Hb < 10 g/dl) was 17% (95% Confidence Interval (95%CI) 10.2; 25.8). Clinical assessment by students for the presence of pallor had a sensitivity of 41.2% (95%CI 19.4; 66.5), specificity of 81.9% (95%CI 71.6; 89.2), positive predictive value of 31.8% (95% CI14.7; 54.9) and negative predictive value of 87.2%(95%CI 77.2; 93.3). The likelihood ratio for detection of anaemia by clinical assessment was 2.3. Copper sulphate densitometry had a sensitivity of 88.2% (95%CI 62.3; 97.9), specificity of 89.2% (95%CI 79.9; 94.6), positive predictive value of 62.5% (95% CI 40.8; 80.5) and negative predictive value of 97.4% (95%CI 90.0; 99.5) to screen for anaemia. The Likelihood Ratio of a positive copper sulphate-screening test was 8.17. On average, haemoglobin concentration was underestimated by 0.29 g/dl with the BMS-haemoglobinometer, with the 95% limits of agreement ranging from underestimation by 1.3 g/dl to over-estimation by 1.9 g/dl. Logistic regression analysis revealed that both the copper sulphate test and measurements with the BMS-haemoglobinometer predicted anaemia accurately. The area under the Receiver Operating Characteristic (ROC) curve for the haemoglobinometer was 0.94 (95%CI 0.87; 1), while the area under the curve for copper sulphate densitometry was 0.89 (95% CI 0.73; 1). Used together, the area under the ROC curve was 0.95 (95% CI 0.89; 1). In resource-poor settings, copper sulphate densitometry could be an accurate, inexpensive and simple screening method for anaemia in children. / Dissertation (MSc (Clinical Epidemiology))--University of Pretoria, 2005. / Clinical Epidemiology / unrestricted

Pregnancy is a condition leading to an important strain on thyroid morphology and function.A normal functioning of the thyroid gland in the mother is essential for the early fetal development, since the fetal thyroid does not produce thyroid hormones until the end of the first trimester (approximately 12 to 14 weeks).The impact of thyroid dysfunction (and especially hypothyroidism) during pregnancy is well documented and has been associated with a number of obstetrical complications, such as premature delivery, low birth weight and even fetal death. In view of all changes in thyroid physiology during pregnancy the ATA (American Thyroid Association) guidelines recommend using trimester- and population-specific normality ranges, to define thyroid dysfunction. It is proposed to determine them in pregnant women without thyroid antibodies (TPO) and without severe iodine deficiency. Due to the few numbers of randomized clinical trials, there is still no consensus whether all pregnant women should be screened or only women at risk for the development of thyroid dysfunction during pregnancy.Thyroid dysfunction during pregnancy is caused in most cases by the presence of thyroid autoimmunity (TAI) and also the altered pregnancy outcomes in most studies are associated with the presence of TAI.Besides the presence of TAI, other factors might also change, influence and/or modify thyroid function. When we started our research, there were only few studies that investigated the impact of other variables, such as iron, BMI, smoking habit and/or the background of the pregnant women on the prevalence of thyroid dysfunction during the first trimester of pregnancy.The aims of the thesis were therefore, to investigate: • the association between the iron reserve status (ferritin levels), thyroid (dys)function and autoimmunity, corrected for confounders such as age, BMI, smoking habit and the time of blood sampling;• the impact of the ethnic background of the pregnant woman on thyroid function and autoimmunity, corrected for confounders such as age, BMI, smoking habit, and the time of blood sampling. Furthermore, to determine ethnic-specific reference ranges and investigate their impact on the diagnosis of thyroid dysfunction;• the impact of changes in thyroid function within the normal reference range in women free of thyroid autoimmunity on pregnancy outcomes, corrected for established covariates (age, BMI, smoking) and iron reserve as candidate new variable.• whether targeted high-risk screening for thyroid dysfunction during pregnancy could be improved with the inclusion of iron status and ethnicity to the actual risk factors defined in the ATA-GL.The results can be summarized as follows:Thyroid function during pregnancy can be influenced by variables others than thyroid antibodies such as the iron status and the ethnical background of the women. However, their impact on thyroid function is less important compared to that of thyroid antibodies. No significant impact of well-known variables (BMI, age, smoking) and others such as iron has been shown on clinical pregnancy outcomes when thyroid function remained within the normal range and no thyroid antibodies were present.We have shown that adding variables such as iron deficiency, ethnic background and obesity to the currently provided list of factors leading to a high-risk for the development of thyroid dysfunction during pregnancy, might improve the detection rate of subclinical hypothyroidism to comparable rates obtained in case of universal screening. / Doctorat en Sciences médicales (Médecine) / info:eu-repo/semantics/nonPublished

INTRODUCTION: Anemia is a frequent complication in patients with inflammatory bowel disease (IBD). The inflammation observed in IBD negatively impact absorption of iron. This could lead to increased hospitalizations, affect growth and development, and decrease overall quality of life. This is especially pronounced in the pediatric population. The screening and treatment of iron deficiency anemia (IDA) varies between centers, and as a result, roughly 40-60% of pediatric IBD patients are iron deficient. OBJECTIVES: The objective of this study is to assess the efficacy and safety profile of intravenous and enteral iron therapy in a population of iron deficient patients with IBD. The secondary aim of this study is to determine if oral or intravenous iron therapy can improve hematologic and iron parameters. We will also examine the longitudinal changes in gastrointestinal (GI) symptoms and quality of life in patients receiving oral and intravenous iron supplementation. METHODS: We conducted a prospective cohort study in pediatric patients with IBD admitted to the inpatient GI service at Boston Children’s Hospital from 09/05/2017 to 03/05/2018. Forty-six IBD patients were screened, and twenty-nine (63%) were identified as iron deficient and were consented for data collection through chart review and administration of the IMPACT-III quality of life questionnaire. RESULTS: Out of the twenty-nine IBD patients, eighteen (62%) received intravenous iron, seven (24%) received oral iron, and four (14%) were untreated and served as controls. The mean change in hemoglobin in patients receiving parenteral, oral, or no iron therapy was 1.6g/dl±0.5, 1.1g/dl±0.4, and 0.2g/dl±0.5, respectively. The change in hemoglobin was significant between the parenteral and oral iron group (P<0.05). The mean change in health-related quality of life scores in patients receiving parenteral or oral iron therapy was 11.6±11.4 and 3.8l±7.5, respectively. CONCLUSION: Our study demonstrates that intravenous iron therapy was more efficacious than oral iron in improving hematologic and iron parameters in IBD patients. This improvement was concomitant with higher scores on the IMPACT-III quality of life questionnaire, suggesting that iron supplementation improves health-related quality of life in IBD patients with iron deficiency anemia.

The objectives of this thesis were: 1) to assess the iron status of piglets, 2) to thoroughly evaluate the blood profile, growth performance, and tissue mineral concentration of young pigs during the pre and postweaning periods after receiving various dosages of iron (0, 50, 100, 200, and 300 mg iron) at birth, 3) as well as evaluate the effects of an additional iron injection before weaning on hematological measures, growth performance, and tissue mineral concentration postweaning. In the initial experiment, there was a 60% incidence of iron deficiency at weaning after administration of a 150 mg iron injection at birth. Also at weaning, hemoglobin concentration was negatively correlated with BW and BW gain (r = -0.53, P < 0.0001, and r = -0.60, P < 0.0001 respectively). In the second experiment, pigs that were not injected with iron at birth had a major reduction in hematological measures, growth performance, and tissue iron concentration until d 52 where iron status was recovered but growth was not. Overall, ADG was improved in a linear and quadratic manner (P = 0.02 and P = 0.01 respectively) as the iron dosage increased with the largest improvement from the 0 mg to 50 mg iron treatment. The improvement observed in ADG let to similar increases (P = 0.02 and P = 0.01 respectively) in final BW as iron dosage treatments increased. Hemoglobin (Hb) concentration improved (P = 0.01) with increasing injectable iron as early as d 1 and continued to d 38, thereafter (d 52) no differences in Hb concentration were observed. Iron concentration for all tissues (liver, spleen, heart, and kidneys) at weaning was greater (P ≤ 0.01) as the iron dosage increased. In the third experiment, pigs that were supplemented with an additional iron injection 4 days before weaning had an increased ADG for the overall experimental period (31 to 34 d). The improved ADG during the experiment led to a heavier (P < 0.001) final BW (~1 kg) for pigs injected with an additional iron injection. At weaning, pigs injected with a second iron injection had higher (P < 0.001) hemoglobin concentration and other complete blood count measures. The improved Hb concentration observed at weaning continued 14 days later (P ≤ 0.02). Additionally, liver iron concentration was greater (P = 0.02) at weaning for the pigs receiving an additional iron injection. In summary, the initial iron injection administered at birth may not be adequate to satisfy all individual iron requirements of piglets before weaning, however, hematological measurements and tissue iron concentration do improve as the iron dosage increases at birth. Furthermore, injecting an additional iron injection before weaning improves nursery growth performance.

No description available.

Iron depletion (ID) is the most common nutrient deficiency worldwide and is the leading cause of anemia. Chronic arsenic (As) exposure is a major public health problem in Bangladesh and triggers inflammatory responses that render iron status assessment challenging. We assessed the prevalence of ID and iron deficiency anemia (IDA) in 147 arsenic-exposed Bangladeshi women (75 skin lesion cases; 72 controls), ages 18-33 years, who were part of a skin lesion study. Hemoglobin (Hb) was measured in whole blood; ferritin and hs-c-reactive protein (CRP) were measured in serum. The prevalence of anemia (Hb<120g/L) was 18%. Although the prevalence of ID (ferritin≤12mcg/L) did not differ between cases and controls, anemia was more common among cases (25% vs. 10%; p=0.02). Of anemic women, 27% (N=7) also had ID (Hb<120g/L and ferritin≤12mcg/L), indicating IDA. Women with normal iron status had higher toenail arsenic compared to iron-depleted women (2.9 vs 1.4 µg As/g toenail; p=0.00), and their water arsenic concentration was higher than that of iron-depleted women (18.8 vs 6.2 µg As/L; p=0.03); every 1µg increase in toenail As was associated with a 45% lowered risk of ID (OR=0.55, 95%CI=0.33,0.94). Much of the anemia in this cohort appears unrelated to ID, but could be linked to other nutrients, such as folate and vitamin B12, which are involved in both hematopoiesis and arsenic metabolism. It is possible that arsenic exposure in this cohort compromised folate and vitamin B12 status.

To determine effects of iron deficiency on AMPK activation and signaling, as well as the AMPKα subunit composition in skeletal muscle, rats were fed a control (C=50-58 mg/kg Fe) or iron deficient (ID=2-6 mg/kg Fe) diet for 6-8 wks. Their respective hematocrits were 47.5% ± 1.0 and 16.5% ± 0.6. Iron deficiency resulted in 28.3% greater muscle fatigue (p<0.01) in response to 10 min of stimulation (1 twitch/sec) and was associated with a greater reduction in phosphocreatine (C: Resting 24.1 ± 0.9 micromol/g, Stim 13.1 ± 1.5 micromol/g; ID: Resting 22.7 ± 1.0 micromol/g, Stim 3.2 ± 0.7 micromol/g; p<0.01) and ATP levels (C: Resting 5.89 ± 0.48 micromol/g, Stim 6.03 ± 0.35 micromol/g; ID: Resting 5.51 ± 0.20 micromol/g, Stim 4.19 ± 0.47 micromol/g; p<0.05). AMPK activation increased with stimulation in muscles of C and ID animals. A reduction in Cytochrome c and other iron-dependent mitochondrial proteins was observed in ID animals (p<0.01). The AMPK catalytic subunit (alpha) was also examined because both isoforms are known to play different roles in responding to energy challenges. In ID animals, AMPK alpha2 subunit protein content was reduced to 71.6% of C (p<0.05), however this did not result in a significant difference in resting AMPK alpha2 activity. AMPK alpha1 protein was unchanged, however an overall increase in AMPK alpha1 activity was observed (C: 0.91 pmol/mg/min; ID: 1.63 pmol/mg/min; p<0.05). Resting phospho Acetyl CoA Carboxylase (pACC) was unchanged. This study indicates that chronic iron deficiency causes a shift in the expression of AMPK alpha subunit composition and potentially altered sensitivity to cellular energy challenges.

Oral iron replacement therapy is often used as a first-line modality for the treatment of iron deficiency anemia (IDA). Oral iron replacement options include tablets, capsules, and liquid formulations. Esophagitis due to iron tablet administration is a well-documented phenomenon, yet peptic ulcer disease secondary to iron tablet administration is less well-known. An 83-year-old female with a past medical history of chronic kidney disease stage V, anemia of inflammatory disease, heart failure with preserved ejection fraction, and gastroesophageal reflux disease presented to the hospital with diffuse abdominal pain and dark red emesis. She was started on ferrous sulfate supplementation two weeks ago and described progressive abdominal pain and nausea since beginning the medication. She was not taking nonsteroidal anti-inflammatories (NSAIDs), antiplatelets, or anticoagulants. Six months ago, she had an unremarkable upper endoscopy performed for new-onset gastroesophageal reflux disease. Laboratory studies revealed a hemoglobin of 7.3 mg/dL and due to a concern for rapid blood loss, she was given one unit of packed red blood cells. A non-contrast computed tomography was performed showing wall thickening of the stomach and the first two portions of the duodenum. A possible ulcer was seen in the distal posterior stomach. The patient was made NPO, and twice daily intravenous pantoprazole was started. An upper endoscopy was performed which revealed a 2.5 cm clean-based ulcer in the duodenal bulb. Biopsies showed acute inflammation and positivity for iron debris but were negative for Helicobacter pylori. Once daily pantoprazole was continued, and her ferrous sulfate tablets were discontinued. Her symptoms did not return. Ferrous sulfate may erode and ulcerate the gastric and duodenal mucosa like that of a chemical burn. Iron deposits may be seen on biopsies performed with Prussian blue staining. Brown crystalline deposits may be seen on hematoxylin and eosin staining. Iron injury may be seen in pill or capsule formulations due to a concentration effect, but this is typically not seen with solution forms. Treatment includes discontinuation of tablet or capsule formulations and substitution with liquid forms.

Food insecurity is a growing issue in the United States. Iron deficiency is the most common form of nutritional deficiency in patients with endothelial dysfunction and vascular-related diseases. This preliminary study lays the groundwork for the “Nutrient deficiency-on-a-chip” model. Endothelial cells are cultured on mechanically tunable, enzymatically cross-linked gelatin and treated with deferoxamine, an iron chelator, or angiotensin II were used to simulate a nutrient deficient and diseased environment, respectively. As oxidative stress and disturbed barrier function are the most prevailing mechanism of angiotensin II and iron deficiency induced endothelial dysfunction, to test our model we investigated the changes in reactive oxygen species production and VE-cadherin expression in engineered endothelium. Both angiotensin II and deferoxamine treated engineered endothelium showed an increase in oxidative stress and disturbed barrier function. This in vitro model can be a useful tool to better understand disease mechanisms associated with nutrient deficiency and identify novel therapeutics.