The Silent Thief: A Case Study in Iron Deficiency Anaemia

Introduction
Iron deficiency anaemia (IDA), the most common nutritional disorder globally, arises when the body lacks sufficient iron to produce haemoglobin – the oxygen-carrying protein in red blood cells. While often perceived as a simple deficiency, its impact can be profound, masking itself behind vague symptoms until significant depletion occurs. This case study examines the presentation, investigation, diagnosis, and management of IDA in a young adult female, highlighting the critical importance of identifying and addressing both the anaemia and its underlying cause.

Case Presentation
Ms. A, a 28-year-old female office worker, presented to her general practitioner (GP) complaining of persistent fatigue for the past 4 months, worsening over the last 6 weeks. She described feeling “constantly drained,” needing excessive sleep (10-12 hours), and struggling to concentrate at work. She also reported increasing shortness of breath climbing stairs and noticeable pallor noted by her family. Her menstrual history revealed heavy periods (menorrhagia) lasting 7-8 days with clots, requiring frequent pad changes, since her late teens. She described her diet as “busy” – frequent skipped breakfasts, reliance on sandwiches or pasta for lunch, and often takeaway dinners. She rarely consumed red meat and had significantly reduced her intake of green vegetables and legumes over the past year. She was a non-smoker and drank alcohol socially. Physical examination confirmed significant pallor of the conjunctivae and palmar creases. Her vital signs were stable: BP 115/70 mmHg, Pulse 82/min (regular), Respiratory Rate 16/min. Cardiorespiratory examination was unremarkable, and abdominal examination revealed no organomegaly or tenderness. Rectal examination was deferred initially.

Investigation
Based on her symptoms and history, the GP ordered a full blood count (FBC) and iron studies:

1. Full Blood Count (FBC):
   • Haemoglobin (Hb): 88 g/L (Low; Normal range: 115-165 g/L)
   • Mean Corpuscular Volume (MCV): 76 fL (Low; Normal range: 80-100 fL)
   • Mean Corpuscular Haemoglobin (MCH): 24 pg (Low; Normal range: 27-34 pg)
   • Red Blood Cell Distribution Width (RDW): 18% (High; Normal range: 11.5-14.5%)
   • Platelets: 450 x 10^9/L (Mildly elevated)
   • White Cell Count: Normal
   • Conclusion: Microcytic, hypochromic anaemia.
2. Iron Studies:
   • Serum Ferritin: 8 µg/L (Very Low; Normal range: 15-150 µg/L) – The most specific indicator of iron stores.
   • Serum Iron: 6 µmol/L (Low; Normal range: 10-30 µmol/L)
   • Total Iron Binding Capacity (TIBC): 85 µmol/L (High; Normal range: 45-72 µmol/L)
   • Transferrin Saturation: 7% (Very Low; Normal range: 20-50%)
   • Conclusion: Confirmed iron deficiency.

Diagnosis
Based on the classic microcytic, hypochromic anaemia on FBC and the unequivocally low ferritin level alongside low serum iron, high TIBC, and low transferrin saturation, Ms. A was diagnosed with Iron Deficiency Anaemia (IDA).

Discussion of Aetiology and Pathophysiology
The investigation now shifted to identifying the cause of the iron deficiency, guided by her history:

1. Chronic Blood Loss: The history of significant menorrhagia since her teens was a major contributing factor. Chronic, heavy menstrual blood loss directly depletes iron stores over time.
2. Inadequate Dietary Intake: Ms. A’s dietary history revealed insufficient intake of bioavailable iron (heme iron from meat and non-heme iron from plant sources). Skipping meals and reliance on processed foods further exacerbated this.
3. Pathophysiology: Iron is essential for haemoglobin synthesis. Deficiency leads to reduced haemoglobin production, resulting in smaller (microcytic) and paler (hypochromic) red blood cells with reduced oxygen-carrying capacity. This manifests as fatigue, pallor, and shortness of breath. Elevated RDW reflects the variation in red cell size as the bone marrow struggles to produce cells with inadequate iron. Mild thrombocytosis is a common reactive finding in IDA. Low ferritin directly reflects depleted iron stores, while low serum iron and transferrin saturation indicate insufficient iron available for erythropoiesis. High TIBC reflects the body’s attempt to increase iron-binding capacity in response to deficiency.

Differential Diagnoses Considered and Ruled Out
While IDA was clear, other causes of microcytic anaemia were considered:

• Anaemia of Chronic Disease (ACD): Unlikely, as ferritin is typically normal or elevated in ACD (as it’s an acute phase reactant), and she had no history of chronic inflammation/infection.
• Thalassaemia Trait: Typically shows microcytosis and hypochromia but without significant anaemia or low ferritin. Her Hb was severely low, and ferritin was very low, making thalassaemia trait unlikely as the primary cause. Haemoglobin electrophoresis could be considered if there was doubt or family history, but it was not indicated primarily here.
• Sideroblastic Anaemia: Rare; usually shows ringed sideroblasts on bone marrow exam, which was not warranted given the clear evidence of iron deficiency.

Further Investigations
To investigate potential sources of blood loss beyond menorrhagia (especially important in adults with IDA), the following were arranged:

• Coeliac Serology (Anti-tTG IgA): Negative. Ruled out coeliac disease as a cause of malabsorption.
• Faecal Immunochemical Test (FIT): Negative. Suggested no significant current lower gastrointestinal blood loss.
• Referral to Gynaecology: For assessment and management of menorrhagia.
• Referral for Oesophago-Gastro-Duodenoscopy (OGD) and Colonoscopy: Due to her age and the need to exclude occult gastrointestinal bleeding (e.g., peptic ulcer, malignancy, angiodysplasia) despite the negative FIT and heavy menstrual history. Both procedures were performed and reported as normal.

Management Plan

1. Iron Replacement Therapy:
   • Oral Ferrous Sulphate 200mg (65mg elemental iron) twice daily.
   • Education: Take on an empty stomach if tolerated (1 hour before food or 2 hours after) with orange juice (vitamin C enhances absorption). Advised about common side effects (constipation, nausea, dark stools) and to report persistent intolerance.
   • Follow-up FBC: Scheduled for 4 weeks to monitor Hb response, and again at 3 months to assess replenishment of stores (ferritin target >50 µg/L). Expected Hb rise: ~10-20 g/L per week with good adherence.
2. Addressing the Cause:
   • Menorrhagia Management: Gynaecology consultation confirmed dysfunctional uterine bleeding. Options discussed included the Levonorgestrel-releasing Intrauterine System (LNG-IUS), tranexamic acid, or combined oral contraceptive pill. Ms. A opted for the LNG-IUS.
   • Dietary Modification: Referral to a dietitian. Focus on increasing intake of:
     • Heme iron sources: Lean red meat (beef, lamb), poultry, fish (especially oily fish).
     • Non-heme iron sources: Fortified cereals, lentils, beans, tofu, spinach, kale, dried apricots.
     • Vitamin C rich foods (citrus fruits, berries, tomatoes, peppers) consumed with non-heme iron sources to enhance absorption.
     • Reducing inhibitors: Tea/coffee with meals (tannins), excessive bran (phytates).
3. Patient Education: Detailed explanation of IDA, its causes, the importance of completing the iron course (often 3-6 months after Hb normalizes to replenish stores), managing menorrhagia, and maintaining dietary changes long-term.

Outcome and Follow-up
At the 4-week follow-up, Ms. A reported improved energy levels and less breathlessness. Repeat FBC showed Hb 105 g/L, confirming a positive response to therapy. Side effects (mild nausea) were managed by taking iron with a small amount of food. The LNG-IUS was inserted successfully at 6 weeks. At 3 months, Hb was 132 g/L and ferritin had risen to 42 µg/L. Iron therapy was continued for a further 3 months to fully replenish stores. Dietary changes were being maintained. She was discharged to her GP with advice for annual FBC monitoring initially.

Conclusion
Ms. A’s case exemplifies the typical yet often insidious presentation of Iron Deficiency Anaemia. Her symptoms of fatigue, pallor, and breathlessness were classic, but the underlying causes – chronic menorrhagia and inadequate dietary intake – required thorough investigation and targeted management. The diagnosis was confirmed through characteristic FBC findings and unequivocal iron studies. Critically, management extended beyond simple iron replacement to address the root causes: effective treatment of menorrhagia and significant dietary modification. This holistic approach is essential not only to correct the anaemia but also to prevent recurrence. This case underscores IDA as a signpost demanding investigation into its aetiology, particularly in adults where gastrointestinal blood loss must be actively excluded, and highlights the importance of patient education and long-term follow-up for sustained recovery.

References

1. World Health Organization (WHO). (2023). Anaemia Fact Sheet. [Would cite specific data on prevalence]
2. Camaschella, C. (2015). Iron-deficiency anemia. New England Journal of Medicine, 372(19), 1832-1843. [Seminal review]
3. Lopez, A., Cacoub, P., Macdougall, I. C., & Peyrin-Biroulet, L. (2016). Iron deficiency anaemia. The Lancet, 387(10021), 907-916. [Comprehensive overview]
4. National Institute for Health and Care Excellence (NICE). (2021). Anaemia – iron deficiency: Scenario: Management | Management. [Cites specific UK guidelines on IDA management and investigation thresholds]
5. Auerbach, M., & Adamson, J. W. (2016). How we diagnose and treat iron deficiency anemia. American Journal of Hematology, 91(1), 31-38. [Practical clinical guide]