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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 9  |  Issue : 1  |  Page : 11-15

Iron deficiency and iron deficiency anemia in the adult omani population


1 Department of Haematology, Sultan Qaboos University Hospital; College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman
2 Department of Haematology, Sultan Qaboos University Hospital, Muscat, Oman

Date of Web Publication22-Mar-2018

Correspondence Address:
Dr. Anil V Pathare
Department of Haematology, Sultan Qaboos University Hospital, P. O. Box35, Muscat 123
Oman
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joah.joah_65_17

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  Abstract 

Context: The prevalence of iron deficiency anemia (IDA) in adults from the Sultanate of Oman is unknown.
Aims: The aim of this study was to assess the prevalence of IDA and latent iron deficiency (ID) in students admitted to a university hospital.
Settings and Design: This is a prospective, cross-sectional cohort study.
Subjects and Methods: In asymptomatic university students, blood samples were obtained for blood counts and iron status after obtaining consent. Students who were found to have IDA or ID were given oral iron therapy for a minimum of 3 months to study the response to treatment.
Statistical Analysis Used: Student's t-test (continuous variables) and Chi-square test (categorical variable) were used for statistical analysis.
Results: The mean age + standard deviation was 21 + 1.3 years with a range from 17 to 29 years in 350 students, with 274 students being females (78.8%). Using the World Health Organization criteria, 91 (26%), 133 (38%), and 126 (36%) students, respectively, were classified as IDA, ID, and normal. HPLC showed that 28 students had sickle cell trait (HbS: 26%–35%), and one each had sickle cell disease (HbS 92%), Hb C trait (31%), Hb D trait (30%), Hb E trait (19%), and delta gene variant (HbA2 – 1.6%). Among the students who received treatment (52 IDA and 20 ID), Hb, mean corpuscular volume, mean corpuscular hemoglobin, and serum ferritin showed statistically significant improvement after oral iron therapy (P < 0.001, paired Student's t-test).
Conclusions: The prevalence of IDA was 26% and that of ID was 38%, with a preponderance of females.

Keywords: Iron deficiency, iron deficiency anemia, latent iron deficiency, Oman


How to cite this article:
Alkindi S, Al Musalami A, Al Wahaibi H, Althuraiya A, Al Ghammari N, Panjwani V, Fawaz N, Pathare AV. Iron deficiency and iron deficiency anemia in the adult omani population. J Appl Hematol 2018;9:11-5

How to cite this URL:
Alkindi S, Al Musalami A, Al Wahaibi H, Althuraiya A, Al Ghammari N, Panjwani V, Fawaz N, Pathare AV. Iron deficiency and iron deficiency anemia in the adult omani population. J Appl Hematol [serial online] 2018 [cited 2018 Oct 22];9:11-5. Available from: http://www.jahjournal.org/text.asp?2018/9/1/11/228334


  Introduction Top


Despite the rapid development in the Middle East during the last two decades,[1],[2],[3] anemia still represents one of the most prevalent disorders in this region, with hematological features that mimic iron deficiency (ID). In the Eastern Mediterranean region, >140 million individuals are considered to be anemic according to the World Health Organization (WHO) estimates, with the highest prevalence among women of reproductive age, infants, and children, especially those with low socioeconomic status.[4] If not corrected, anemia can lead to school absenteeism, diminished learning capacity, and enhanced susceptibility to infection, all with consequent impact on cognitive development.[5]

Anemia resulting from lack of sufficient iron for synthesis of hemoglobin (Hb) is the most common hematologic disease of infancy and childhood.[6],[7],[8] Ingested iron is either in the form of nonheme iron or heme iron. Nonheme iron derived from plants is mainly composed of inorganic ferric Fe (III) iron and is absorbed into enterocytes through the divalent metal transporter 1 after reduction of Fe (III) to Fe (II) by duodenal cytochrome b.[6],[7],[8],[9] In contrast, heme-iron derived from meat is absorbed through a heme carrier protein into enterocytes, where it is degraded by hemeoxygenase-1.[8],[9],[10] Since absorption of dietary iron is about 10%, a diet containing 8–10 mg of iron daily is necessary for optimal nutrition.[8],[10] However, vegetarian women are at a high risk of ID anemia and should be always checked and supplemented.

Chronic iron deficiency anemia (IDA) from occult bleeding may be caused by a lesion of the gastrointestinal tract, such as a peptic ulcer, Meckel's diverticulum, a polyp, or hemangioma, or by inflammatory bowel disease.[10] Blood loss must be considered a possible cause in every case of IDA, particularly in older children. However, the most common cause in females is menorrhagia and increased demand such as pregnancy and frequent childbirths. In some geographic areas, hookworm infestation is an important cause of ID.[8],[11] Pulmonary hemosiderosis may be associated with unrecognized bleeding in the lungs and recurrent ID after treatment with iron.[12]

In progressive ID, a sequence of biochemical and hematologic events occurs.[6],[7],[8] First, the tissue iron stores represented by bone marrow hemosiderin disappear. The level of serum ferritin, an iron storage protein, provides a relatively accurate estimate of body iron stores in the absence of inflammatory disease.[13],[14],[15] Normal ranges are age dependent, and decreased levels accompany ID. Next, serum iron level decreases (also age dependent), the iron-binding capacity of the serum increases, and the percent saturation falls below normal (also varies with age). When the availability of iron becomes rate limiting for hemoglobin synthesis, a moderate accumulation of heme precursors, free erythrocyte protoporphyrins, results. As the deficiency progresses, the red blood cells (RBCs) become smaller than normal and their hemoglobin content decreases.

The morphologic characteristics of RBCs are best quantified by the determination of mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV). With increasing deficiency, the RBCs become deformed and misshapen and present characteristic microcytosis, hypochromia, poikilocytosis, and increased RBC distribution width (RDW).[8] The reticulocyte percentage may be normal or moderately elevated, but absolute reticulocyte counts indicate an insufficient response to anemia. Nucleated RBCs may occasionally be seen in the peripheral blood. White blood cell counts are normal. Thrombocytosis, sometimes of a striking degree (600 × 109/L–1000 × 109/L), may be seen.[8],[9],[10]

The prevalence of IDA in adults from the Sultanate of Oman is unknown.[16] We therefore prospectively enrolled students admitted to a university in this study to ascertain the prevalence of IDA and ID and observe the effect of iron therapy on Hb and red cell indices, namely, MCV and MCH.


  Subjects and Methods Top


A total of 350 students studying at a university were prospectively enrolled in this cross-sectional cohort study after an informed consent and approval from the institutional Medical Research and Ethical Committee. None of the students included in the study had been on any hematinics in the last 6 months or had any infection in the past 1 month.

Blood was obtained by venipuncture into Becton Dickinson K2ETDA anticoagulated Vacutainer ® and plain tubes. Complete blood counts were performed with an electronic cell counter (Abbott CELL-DYN ® 4000, Abbott Diagnostics, Abbott Park, IN). A fresh hemolysate was prepared from each sample and subjected to cation-exchange high-performance liquid chromatography (Bio-Rad VARIANT, Bio-Rad Laboratories, Hercules, CA). Serum ferritin was estimated by a commercial Elisa Kit and serum C-reactive protein (CRP) was estimated based on nephelometry and turbidimetry, both implemented on an automated analyzer.

The WHO defines anemia as blood hemoglobin values of <7.7 mmol/l (13 g/dl) in men and 7.4 mmol/l (12 g/dl) in women.[8],[17] Thus, based on the results of hemoglobin and serum ferritin, all the students were divided into three groups; (1) Normal group with the Hb >12.0 g/dl for women and >13.0 g/dl for men with serum ferritin 30.0 ng/ml or more,[8] (2) ID group with Hb >12.0 g/dl for women and >13.0 g/dl for men with serum ferritin <30.0 ng/ml, and (3) IDA group with Hb <12.0 g/dl for women and <13.0 g/dl for men with serum ferritin <30.0 ng/ml. The utility of serum ferritin as an accurate measure of body iron stores was validated by the simultaneous estimation of CRP using a cutoff of 30 mg/mL.[8] After the blood test results were obtained, students with a serum ferritin below 30 ng/ml were given one capsule containing ferrous fumarate 350 mg (elemental iron 112 mg), every day for the period of 3 months, and were requested to provide with a repeat blood sample.

Statistical analysis

Data were analyzed with IBM Statistical Package for the Social Sciences (SPSS), Version 23 (IBM Corp., Armonk, New York, USA). Continuous variables were expressed as mean + standard deviation (SD), whereas categorical variables were expressed as numbers (percentages). Baseline values of various parameters in three groups of students were compared and any changes in the values of various parameters as a result of treatment were analyzed for statistical significance using unpaired and paired Student's t-test as applicable. P<0.05 was considered statistically significant.


  Results Top


In this study on 350 consecutive university students, the mean age + SD was 21 + 1.3 years (range 17–29 years). Totally 276 students were females (78.8%). All students had a CRP level below 30 mg/mL. It was observed that 91 (26%), 133 (38%), and 126 (36%) students satisfied the diagnostic criteria for IDA, ID, and normal groups, respectively, as described above [Table 1]. Furthermore, among the IDA, ID, and normal groups, 87 (95.6%), 122 (91.7%), and 67 (53.2%) were females, respectively. In addition, based on the HPLC results, 28 students concomitantly had sickle cell trait (HbS: 26%–35%), and one each had sickle cell disease (HbS 92%), Hb C trait (31%), Hb D trait (30%), Hb E trait (19%), and delta gene variant (HbA2 – 1.6%).
Table 1: Baseline values of the various parameters in the three groups, distributed by gender

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[Table 2] summarizes the differences in the various parameters among the three groups. Hb, MCV, MCH, Mean Corposcular Hemoglobin Concentration (MCHC), and serum ferritin were statistically significantly lower in ID and IDA groups compared to normal group, whereas RDW and platelet counts were significantly higher (unpaired Student's t-test).
Table 2: Statistical significance of differences in the various parameters in the three groups

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[Table 3] summarizes the differences seen following hematinic treatment in a small subgroup of the IDA and ID students (n = 52, 57% and n = 15, 15% respectively) who volunteered for the same. Hb, MCV, MCH, and serum ferritin all showed statistically significant improvement posthematinic therapy (P< 0.001, paired Student's t-test). In the IDA group, the increase in Hb, MCV, MCH, and ferritin values ranged between 0.6 and 2.8 g/dL, 1.7 and 7.7 fl, 0.1 and 3.6 pg, and 3 and 22 ng/mL, respectively, whereas, in the ID group, the increase in Hb, MCV, MCH, and ferritin values ranged between 0.4 and 1.6 g/dL, 1.1 and 4.1 fl, 0.1 and 2 pg, and 1 and 25 ng/mL, respectively.
Table 3: Statistical significance of differences in the various parameters in IDA (n=52; 57%) and ID students (n=20; 15%) before and after hematinic therapy

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  Discussion Top


Nutritional condition of a population constitutes an important health indicator. Children and adolescents are particularly at risk of suffering from deficient nutritional status because of increased needs. The prevalence of IDA worldwide, especially in the developing world, is increasingly seen.[1],[2],[3],[4],[5] IDA is the end stage of negative iron balance. It is preceded by a latent stage known as ID, where serum ferritin is below the normal reference range with normal hemoglobin level.

Our study showed that the prevalence of ID among the students at the university was 26% [Figure 1]. Moreover, although enrollment was consecutive, females constituted almost 80% of this student cohort, with 44% and 32% showing ID and IDA, respectively. In contrast, in the males in this cohort, only 15% and 5% had ID and IDA, respectively (P< 0.01, Chi-square test). Our results are in agreement with several other studies.[18],[19],[20] Napolitano et al.[18] attributed low menstrual blood loss to lower the chance of having ID in women of childbearing age in a Spanish study, whereas, Al-Buhairan and Oluboyede in a study from Saudi Arabia [19] have attributed the lower prevalence of IDA in males to the high intake of meat in addition to no menstrual blood loss in males.
Figure 1: Distribution of iron deficiency and iron deficiency anemia in the student community at Sultan Qaboos University

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In IDA, besides Hb, MCV and MCH are also reduced. However, in ID, while Hb is normal, it is yet to be clearly established whether MCV and MCH are in normal range or subtly reduced. Moreover, given the inter-subject variations, influenced by a multitude of environmental factors, a large epidemiological investigation will be necessary to clarify the issue. However, our study, although with a smaller sample size, was able to show that in fact in ID students, the MCV and MCH were also correspondingly reduced. Furthermore, supplementation of oral iron was able to improve these parameters concomitantly in both the IDA and ID cohorts [Figure 2], further emphasizing the fact that both these cohorts had ID at the tissue level as evidenced by a similar increase in the serum ferritin levels ranging from 3 to 22 ng/mL and 1 to 25 ng/mL, respectively. However, treatment for 3 months was clearly not adequate to reverse the ID as only 4 and 2 students, respectively, from the IDA and ID cohorts were seen to improve the serum ferritin levels to reach the normal reference range [Figure 2].
Figure 2: Pre- and post-serum ferritin levels in iron deficiency anemia (a) and iron deficiency (b)

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  Conclusions Top


In the asymptomatic student community at university, the prevalence of ID was 26%, with a distinctly high preponderance in females as compared to males. Response to oral iron therapy significantly improved serum ferritin and red cell indices, although 3-month period was inadequate to even improve the serum ferritin levels within the normal reference range.

Acknowledgments

We wish to thank the hospital administration for allowing to use hospital data. This work was supported by a research grant no. IG/MED/HAEM/11/02.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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Halterman JS, Kaczorowski JM, Aligne CA, Auinger P, Szilagyi PG. Iron deficiency and cognitive achievement among school-aged children and adolescents in the United States. Pediatrics 2001;107:1381-6.  Back to cited text no. 5
    
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McKie AT, Latunde-Dada GO, Miret S, McGregor JA, Anderson GJ, Vulpe CD, et al. Molecular evidence for the role of a ferric reductase in iron transport. Biochem Soc Trans 2002;30:722-4.  Back to cited text no. 6
    
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Trinder D, Fox C, Vautier G, Olynyk JK. Molecular pathogenesis of iron overload. Gut 2002;51:290-5.  Back to cited text no. 7
    
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Cook JD. Diagnosis and management of iron-deficiency anaemia. Best Pract Res Clin Haematol 2005;18:319-32.  Back to cited text no. 8
    
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Zoller H, Pietrangelo A, Vogel W, Weiss G. Duodenal metal-transporter (DMT-1, NRAMP-2) expression in patients with hereditary haemochromatosis. Lancet 1999;353:2120-3.  Back to cited text no. 9
    
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Mehta BC. Iron deficiency. In: Shah SN, editor. API Textbook of Medicine. 7th ed. Mumbai: Association of Physicians of India; 2003. p. 930-4.  Back to cited text no. 10
    
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Hershko C, Bar-Or D, Gaziel Y, Naparstek E, Konijn AM, Grossowicz N, et al. Diagnosis of iron deficiency anemia in a rural population of children. Relative usefulness of serum ferritin, red cell protoporphyrin, red cell indices, and transferrin saturation determinations. Am J Clin Nutr 1981;34:1600-10.  Back to cited text no. 12
    
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Holyoake TL, Stott DJ, McKay PJ, Hendry A, MacDonald JB, Lucie NP, et al. Use of plasma ferritin concentration to diagnose iron deficiency in elderly patients. J Clin Pathol 1993;46:857-60.  Back to cited text no. 13
    
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Nelson R, Chawla M, Connolly P, LaPorte J. Ferritin as an index of bone marrow iron stores. South Med J 1978;71:1482-4.  Back to cited text no. 14
    
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Hallberg L, Bengtsson C, Lapidus L, Lindstedt G, Lundberg PA, Hultén L, et al. Screening for iron deficiency: An analysis based on bone-marrow examinations and serum ferritin determinations in a population sample of women. Br J Haematol 1993;85:787-98.  Back to cited text no. 15
    
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Padmanabhan A, Thomas S, Sheth H, Venugopalan P. High prevalence of microcytic anaemia in Omani children: A prospective study. Ann Trop Paediatr 2001;21:45-9.  Back to cited text no. 16
    
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Napolitano M, Dolce A, Celenza G, Grandone E, Perilli MG, Siragusa S, et al. Iron-dependent erythropoiesis in women with excessive menstrual blood losses and women with normal menses. Ann Hematol 2014;93:557-63.  Back to cited text no. 18
    
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Al-Buhairan AM, Oluboyede OA. Determination of serum iron, total iron-binding capacity and serum ferritin in healthy Saudi adults. Ann Saudi Med 2001;21:100-3.  Back to cited text no. 19
    
20.
Blanco-Rojo R, Toxqui L, López-Parra AM, Baeza-Richer C, Pérez-Granados AM, Arroyo-Pardo E, et al. Influence of diet, menstruation and genetic factors on iron status: A cross-sectional study in Spanish women of childbearing age. Int J Mol Sci 2014;15:4077-87.  Back to cited text no. 20
    


    Figures

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    Tables

  [Table 1], [Table 2], [Table 3]



 

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