INTRODUCTION:
The diagnosis of anemia is simple and objective: the World 
Health Organization (WHO) denes anemia as the decline in 
blood hemoglobin to a concentration below 13 g/dL in men 
and 12 g/dL in women. However, to conrm that iron deciency 
(ID) is the origin of the anemia is not always easy (1,2). 
Usually, the simple complete blood count (CBC) strongly 
suggests this origin with typical pattern of microcytic 
hypochromic and elevation of red cells distribution width 
(RDW). However, microcytic hypochromic picture may be 
found in other anemias, like thalassemia, sideroblastic 
anemia and also in anemia of chronic inammation. Few pure 
and many dimorphic IDA cases are normocytic. Therefore, a 
normal mean corpuscular volume (MCV) does not exclude ID 
from being the cause of the anemia. Moreover, the presence of 
microcytosis does not necessarily imply ID and can be 
produced by other anemias (chronic process, sideroblastic 
anemia) and diseases (e.g. thalassemia). RDW measures the 
degree of anisocitosis (size difference) of the population of red 
cells and its elevation is neither sensitive nor specic for ID (3, 
4, 5). The next step is to determine the so-called iron 
metabolism (in addition to all other necessary determinations, 
including levels of vitamin B12 and folic acid) and in many 
cases the level of C-reactive protein. A typical pattern is a 
decrease in decreased serum iron (sideremia) serum ferritin, 
and transferrin saturation. However, this is not the usual case. 
Serum ferritin, in the absence of inammation (usually 
dened as a normal C-reactive protein level), reects total 
body iron deposits. Thus, a low serum ferritin (< 30 ng/mL) 
unequivocally means ID, whether accompanied by anemia or 
not. However, as serum ferritin is an acute phase reactant, a 
normal or even elevated ferritinemia does not exclude the 
presence of ID (6, 7,8). Thus, in the presence of an 
inammatory process (usually dened by an elevated C-
reactive protein level), ID could exist even with levels of ferritin 
up to 100 ng/mL. Another parameter of the normal “iron 
metabolism”, especially useful when the determination of 
ferritin is equivocal, is the transferrin saturation index. This  
shows the percentage of transferrin that transports iron and 
thus a decrease (< 20%) implies ID, either absolute or 
functional.

In some cases, even taking into account all these 
determinations, ID can be difcult to diagnose. It generally 
occurs in situations where the anemia has a multifactorial 
origin. This is typical in cases of anemia of mixed origin, a 
chronic process that coexists with ID, which is a frequent 
scenario in gastrointestinal inammatory disease or cancer 
(9,10,11). These other factors include the determination of 
soluble transferrin receptor, reticulocyte hemoglobin 
concentration, the percentage of hypochromic red cells, the 
concentration of erythropoietin and even the determination of 
hepcidin(12,13,14). The soluble transferrin receptor is one of 
the most useful as it is the least inuenced by the presence of 
inammation and it correlates well with concentration of 
transferrin receptor in the cell plasma membrane. If the levels 
are high, ID is likely to be a major component of anemia, while 
in those cases with normal or low levels; anemia is probably 
not associated with ID (15, 16). 

Patients with inammatory conditions such as inammatory 
bowel disease (IBD), chronic heart failure (CHF), and chronic 
kidney disease (CKD) have high rates of iron deciency with 
adverse clinical consequences. Under normal circumstances, 
serum ferritin levels are a sensitive marker for iron status but 
ferritin is an acute-phase reactant that becomes elevated in 
response to inammation, complicating the diagnosis. 
Proinammatory cytokines also trigger an increase in 
hepcidin, which restricts iron absorption and promotes 
sequestration of iron by ferritin within storage sites. Patients 
with inammatory conditions may thus have restricted 
availability of iron for erythropoiesis and other cell functions 
due to increased hepcidin expression, despite normal or high 
levels of serum ferritin. The standard threshold for iron 
deciency (<30� �g/l) , therefore does not apply and 
transferrin saturation (TSAT), a marker of iron availability, 
should also be assessed. A serum ferritin threshold of 
<100��g/l or TSAT < 20% can be considered diagnostic for 
iron deciency in CHF, CKD, and IBD. If serum ferritin is 
100–300� �g/L, TSAT < 20% is required to conrm iron 
deciency. Routine surveillance of serum ferritin and TSAT in 
these at-risk groups is advisable so that iron deciency can be 
detected.

INTERPRETATION OF SERUM IRON PROFILE AND CBC FINDINGS IN 
IRON DEFICIENCY ANEMIA

Original Research Paper

Dilip Kumar Pandey
Assistant Professor, Department Of Pathology, Anugrah Narain Magadh 
Medical College, Gaya, Bihar

Pathology

BACKGROUND: Iron deciency anaemia is most common anemia worldwide. It is most common in 
female. In male IDA occurs most commonly due to gastrointestinal disease. Diagnosis of IDA on clinical 

suspicion is easy with CBC report and iron prole .Few dimorphic anemias and anemias in complex clinical settings pose 
difculty in diagnosis, thus other investigations are also needed. 
MATERIALS AND METHODS: we prospectively collected clinical data, CBC ndings and iron prole results of patients of IDA in 
tertiary teaching institutes of Bihar. EDTA peripheral blood samples were run on Sysmex XT-1800i and CBC ndings were 
noted, whenever needed peripheral blood smears were made to know morphology of red blood cells; serum samples of all 
cases were run for serum iron prole (iron, ferritin and transferritin saturation) and values noted and tabulated.
RESULT:  All patients have both decreased serum iron and ferritin. They revealed classical microcytic hypochromic picture with 
raised RDW. Female outnumbered male. Male female ratio was 1:1.4. In this study CBC ndings (MCV, MCH and RDW) were 
well correlated with iron prole ndings. Minimum hemoglobin level was 5.4gm/dl. 
CONCLUSION: Iron deciency anemia is major public health problem worldwide .In majority of cases, CBC and iron prole 
study can clinch the diagnosis, however few cases need further investigations and clinical correlation.

ABSTRACT

KEYWORDS : IDA, Ferritin, Iron, CBC, Peripheral Blood Smear, Hemoglobin

VOLUME-8, ISSUE-10, OCTOBER-2019 • PRINT ISSN No. 2277 - 8160 • DOI : 10.36106/gjra

Subhash Chandra 
Jha*

Dr Subhash Chandra Jha, Assistant Professor, Department Of Pathology, 
Government Medical College, Bettiah, West Champaran, Bihar. 
* Corresponding Author

60 X GJRA - GLOBAL JOURNAL FOR RESEARCH ANALYSIS



The clinical picture varies greatly from one case to another. 
Pallor of varying grades may be found. It is produced both by 
the anemia and by the lack of iron, which is essential for 
cellular energy metabolism. Symptoms depend greatly on the 
speed of onset of anemia, its severity and the characteristics of 
the patient. Thus, IDA or ID can be detected in a person with 
symptoms that include general weakness, fatigue, irritability, 
poor concentration, headache, and intolerance to exercise. 
Some iron-decient patients, with or without anemia, might 
have alopecia, atrophy of lingual papillae, or dry mouth due to 
loss of salivation. Other symptoms, such as weakness or 
koilonychia, chlorosis, or the syndromes of Plummer-Vinson or 
Paterson-Kelly (dysphasia with esophageal membrane and 
atrophic glossitis) have virtually disappeared. These changes 
were caused by reduction of iron-containing enzymes in the 
epithelia and the gastrointestinal tract. Pica can cause iron 
deciency.[17,18,19]. 

MATERIAL AND METHODS: 
we prospectively collected clinical data, CBC ndings and 
iron prole results of 11 patients of IDA in tertiary teaching 
institutes of Bihar. EDTA peripheral blood samples were run 
on Sysmex XT-1800i and CBC ndings were noted, whenever 
needed peripheral blood smears were made to know 
morphology of red blood cells; serum samples of all cases 
were run for serum iron prole (iron, ferritin and transferritin 
saturation) and values noted and tabulated. Further 
investigations were done in those Patients that had normocytic 
and dimorphic blood picture with clinical features of iron 
deciency and or dimorphic anemia .In few cases, bone 
marrow study was also done to know cause of microcytic 
anemia, especially in oral iron refractory patients. 

Table 1.IRON   PROFILE IN IRON DEFICIENCY ANEMIA

RESULT:  
Male female ratio was 1:1.4. In this study CBC ndings (MCV, 
MCH and RDW) were well correlated with iron prole ndings. 
Minimum hemoglobin level was 5.4gm/dl. Severity of anemia 
i.e. hemoglobin concentration was proportional to MCV and 
MCH values. Serum ferritin level was well correlated with 
severity of microcytic hypochromic anemia. Minimum serum 
ferritin was 3.6mcg/L 

Table.2    RBC INDEXEX IN IRON DEFICIENCY ANEMIA

Figure  1. PBS shows microcytic hypochromic picture and 
tear drop cell

DISCUSSION:
Ferritin is the best indicator of iron deciency and a low ferritin 
alone is diagnostic of IDA. Iron is stored intracellularly as 
ferritin and in the presence of infection, malignancy or chronic 
inammation; the ferritin rises as acute phase protein. 
Therefore, the diagnosis of IDA is challenging when there is 
coexisting inammation, as the ferritin can be up to 100 �g/L  ,
even in the presence of iron deciency. In this case, further 
tests can help clarify the diagnosis. Total iron-binding  
capacity, transferrin saturation, serum iron, and serum 
transferrin receptor levels may be helpful if the ferritin level is 
between, 46 and 99 mcg/ L (12,13). 

Iron prole studies include serum iron level, transferrin 
saturations and total iron-binding capacity (TIBC) or 
transferrin concentration, in addition to ferritin. In the 
bloodstream, serum iron is carried bound to transferrin. The 
TIBC (expressed in �g/dL ) is the maximum  iron that can be 
bound by transferrin if this were 100% saturated. The 
transferrin saturation is the concentration of iron that is bound 
to transferrin, expressed as a percentage of the TIBC  In IDA, .
the ferritin, serum iron and transferrin saturations are low, but 
the TIBC increases. The serum transferrin concentration 
(expressed in mg/dL) increases in IDA, as the body tries to 
compensate for low iron levels and this correlates positively 
with the TIBC. In contrast, in anaemia of chronic disease 
(ACD) the ferritin is raised, owing to an increase in the iron 
regulator hepcidin (14, 15,16). Studies have shown that 
hepcidin expression is unregulated when there is infection or 
inammation, via inammatory cytokines such as IL-6. 
Hepcidin binds to ferroportin (the iron exporter on cells) which 
results in internalization and degradation of this transporter, 
which reduces iron release from cells. This failure of release of 
iron from the ferritin stores results in a low iron, low transferrin 
saturation and low TIBC, with a high ferritin 

The mean cell volume (MCV) and mean cell hemoglobin 
(MCH) are very sensitive for IDA in the absence of B12 
deciency or folate deciency. However, they may also be 
reduced in ACD, haemoglobinopathies and sideroblastic 
anemia. The MCH may be more reliable than the MCV as it is 
less inuenced by storage and the counting machine. In 
patients with an MCV disproportionately low for the Hb, Hb 
electrophoresis should be performed to exclude a 
haemoglobinopathy. If iron deciency coexists with B12 or 
folate deciency, the MCV can be high, normal or low. The red 
cell distribution width (RDW) is a measure of the variation in 
the diameter of the red cells. The normal diameter of a red cell 
is 6–8��m. A high RDW occurs in conditions such as IDA, B12 
deciency and folate deciency. The RDW would be expected 
to be normal in ACD and haemoglobinopathies. 
Measurement of soluble transferrin receptor is more reliable 
at identifying IDA than TIBC and iron. The discovery of the 
iron-regulatory hormone hepcidin in 2001 has revolutionized 
our understanding of iron disorders. Nevertheless, promising 
applications can already be glimpsed, ranging from the use of 
hepcidin levels for diagnosing iron-refractory iron deciency 
anemia to global health applications such as guiding safe 
iron supplementation in developing countries with high 
infection burden (18, 19, 20, 21).

VOLUME-8, ISSUE-10, OCTOBER-2019 • PRINT ISSN No. 2277 - 8160 • DOI : 10.36106/gjra

CASE 
NO.

IRON 
µg/dL

FERRITIN
ng/mL

TIBC Transferrin
Saturation %

RETIC
%

AGE/SEX
Year

1 17 8.6 337 5.0 1.0 5/M

2 28 3.6 371 8.0 1.5 22/F

3 20 7.5 355 10.0 1.0 40/F

4 18 9.0 354 9.5 1.4 20/M

5 17 8.5 353 7.9 1.2 35Y/F

6 19 8.0 355 7.6 1.5 3/F

7 18 9.0 388 8.6 2.0 78/F

8 17 8.5 380 8.7 2.0 80/M

9 16.9 7.4 389 7.7 1.0 67Y/F

10 16.9 7.4 389 7.7 1.0 30/F

11 18 4.1 272 8.0 60Y/M

CASE RBC HB HCT MCV MCH MCHC RDW

1 3.8 7.1 25.3 66.6 18.7 28.1 18.7

2 3.3 5.4 20.6 64.0 18.3 29.6 16.8

3 3.5 5.6 20.8 65.0 18.3 28.5 19.0

4 3.6 7.8 21.5 63.0 17.5 27.9 18.5

5 3.7 6.8 22.0 62.5 18.0 28.0 19.0

6 3.5 6.6 23.8 63.0 19.5 27.7 18.8

7 3.6 7.0 22.9 63.0 18.9 26.00 19.6

8 3.9 7.5 23.8 63.0 17.0 27.0 19.0

9 3.7 7.2 23.5 62.0 16.0 26.0 18.0

10 3.4 5.7 20.1 64.0 18.1 28.2 18.5

11 3.3 5.8 21.0 64.5 18.5 29.0 19.0

  X 61GJRA - GLOBAL JOURNAL FOR RESEARCH ANALYSIS



CONCLUSION: 
Iron deciency anaemia is major public health problem. In 
majority of cases, CBC and iron prole study(serum iron,  
transferrin, ferritin and TIBC) can clinch the diagnosis, 
however few cases need further investigations and clinical 
correlation. Ferritin is the best indicator of iron deciency and 
a low ferritin alone is diagnostic of IDA. It has not diagnostic 
importance in clinical setting of chronic inammation and 
infection. 

REFERENCES:
1. Sayer JM, Long RG. A perspective on iron deciency anaemia. Gut. 

1993;34:1297–1299. [PMC free article] [PubMed] [Google Scholar]
2. McIntyre AS, Long RG. Prospective survey of investigations in outpatients 

referred with iron deciency anaemia. Gut. 1993;34:1102–1107. [PMC free 
article] [PubMed] [Google Scholar]

3. Beutler E, Hoffbrand AV, Cook JD. Iron deciency and overload. Hematology 
Am Soc Hematol Educ Program. 2003;34:40–61. [PubMed] [Google Scholar]

4. Yates JM, Logan EC, Stewart RM. Iron deciency anaemia in general practice: 
clinical outcomes over three years and factors inuencing diagnostic 
investigations. Postgrad Med J. 2004;80:405–410. [PMC free article] [PubMed] 
[Google Scholar]

5. Kepczyk T, Kadakia SC. Prospective evaluation of gastrointestinal tract in 
patients with iron-deciency anemia. Dig Dis Sci. 1995;40:1283–1289. 
[PubMed] [Google Scholar]

6. Ioannou GN, Rockey DC, Bryson CL, Weiss NS. Iron deciency and 
gastrointestinal malignancy: a population-based cohort study. Am J Med. 
2002;113:276–280. [PubMed] [Google Scholar]

7. Hershko C, Hoffbrand AV, Keret D, Souroujon M, Maschler I, Monselise Y, 
Lahad A. Role of autoimmune gastritis, Helicobacter pylori and celiac 
disease in refractory or unexplained iron deciency anemia. Haematologica. 
2005;90:585–595. [PubMed] [Google Scholar]

8. Barabino A. Helicobacter pylori-related iron deciency anemia: a review. 
Helicobacter. 2002;7:71–75. [PubMed] [Google Scholar]

9. Sarker SA, Mahmud H, Davidsson L, Alam NH, Ahmed T, Alam N, Salam MA, 
Beglinger C, Gyr N, Fuchs GJ. Causal relationship of Helicobacter pylori with 
iron-deciency anemia or failure of iron supplementation in children. 
Gastroenterology. 2008;135:1534–1542. [PubMed] [Google Scholar]

10. Rector WG Jr. Pica: its frequency and signicance in patients with iron-
deciency anemia due to chronic gastrointestinal blood loss. J Gen Intern 
Med. 1989;4:512–513. [PubMed] [Google Scholar]

11. Skikne BS. Serum transferrin receptor. Am J Hematol. 2008;83:872–875. 
[PubMed] [Google Scholar]

12. Rockey DC, Cello JP. Evaluation of the gastrointestinal tract in patients with 
iron-deciency anemia. N Engl J Med. 1993;329:1691–1695. [PubMed] 
[Google Scholar]

13. Sawhney MS, Lipato T, Nelson DB, Lederle FA, Rector TS, Bond JH. Should 
patients with anemia and low normal or normal serum ferritin undergo 
colonoscopy? Am J Gastroenterol. 2007;102:82–88. [PubMed] [Google 
Scholar]

14. Kautz L, Nemeth E. . Molecular liaisons between erythropoiesis and iron 
metabolism. Blood 2014;124(4):479-482

15. Young MF, Glahn RP, Ariza-Nieto M, et al. Serum hepcidin is signicantly 
associated with iron absorption from food and supplemental sources in 
healthy young women. Am J Clin Nutr 2009;89(2):533-538.

16. Roe MA, Collings R, Dainty JR, Swinkels DW, Fairweather-Tait SJ. Plasma 
hepcidin concentrations signicantly predict interindividual variation in iron 
absorption in healthy men. Am J Clin Nutr 2009;89(4):1088-1091

17. Prentice AM, Doherty CP, Abrams SA, et al. Hepcidin is the major predictor of 
erythrocyte iron incorporation in anemic African children. Blood 
2012;119(8):1922-1928.

18. Donker AE, Raymakers RA, Vlasveld LT, et al Practice guidelines for the 
diagnosis and management of microcytic anemias due to genetic disorders 
of iron metabolism or heme synthesis. Blood 2014;123(25):3873-3886

19. Aue Macdougall I, Macdougall I, Mast A Iron deciency: what are the future 
trends in diagnostics and therapeutics? Clin Chem 2013;59(5):740-745.

20. L. A. Cohen, L. Gutierrez, A. Weiss et al., “Serum ferritin is derived primarily 
from macrophages through a nonclassical secretory  pathway,” Blood, vol. 
116, no. 9, pp. 1574–1584, 2010.  

21. F. M. Torti and S. V. Torti, “Regulation of ferritin genes and protein,” Blood, vol. 
99, no. 10, pp. 3505–3516, 2002. 

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62 X GJRA - GLOBAL JOURNAL FOR RESEARCH ANALYSIS