What GPs need to know about iron deficiency in women

Many women in Australia have difficulty getting enough iron in their diet, with iron deficiency affecting women at different stages of life.

Iron deficiency state, with or without anaemia, is a common clinical problem in women in Australia. Studies have documented iron deficiency in 11–35% of women under 50 years of age and in about 3% of women over 50 years (here and here).

About 15% of non-pregnant women of reproductive age and 12% of pregnant women in Australia have anaemia, with iron deficiency as the major cause (here). Higher incidence of pregnancy-related iron deficiency anaemia has been reported in Tasmania (18%) and Far North Queensland (29%) (here and here). In addition, nearly 50% of pregnant Aboriginal and Torres Strait Islander women were found to have iron deficiency anaemia (here).

Common causes of iron deficiency in Australian women under 50 years of age include suboptimal dietary intake, menstrual blood loss, pregnancy and breast feeding (here). Gastrointestinal bleeding is a major cause in post-menopausal women (here), while increased physiological demand and dietary deficiency are the likely causes in the adolescent age group. In all cases, the general practitioner should ascertain the cause before contemplating remedial therapy.

The clinical features of iron deficiency state commonly include tiredness, lethargy, fatigue, irritability, inability to cope with day-to-date activities, hair loss, and even depression (here). The severity of the symptoms, however, vary from patient to patient. Women with iron deficiency anaemia may present with conjunctival pallor and nail changes (koilonychia) (here).

Diagnosis of iron deficiency state requires full blood count, examination of the blood film and serum iron studies, including ferritin (here). A low serum iron saturation (< 5%) and low serum ferritin (below the lower limit of the normal range) are indicative iron deficiency. A low haemoglobin level (< 110 g/L), hypochromic and microcytic red cell indices, and presence of microcytic and hypochromic red cells in the blood film are features of iron deficiency anaemia. These typical features, however, may be masked by coexisting vitamin B₁₂ or folate deficiency, systemic disease (eg, renal failure) or thyroid disease. Hence the need to include assay of serum B₁₂ and folate, serum chemistry, and liver function and thyroid-stimulating hormone tests as part of the investigation of women with suspected iron deficiency. In women without obvious history of dietary cause, increased physiological demand or excessive menstrual blood loss, possible gastrointestinal bleeding should be ruled out (here).

In women with borderline or mild iron deficiency attributable to suboptimal diet, optimising the dietary source may suffice. In other cases, oral iron therapy should be initiated. Iron tablet should be taken on an empty stomach or two hours after a meal. Concurrent intake of vitamin C (eg, orange juice) will optimise the absorption, whereas coffee, tea or coke will impair the absorption and, hence, should be avoided. Intake of iron tablets on alternate days or thrice weekly is preferable (to a daily schedule) to minimise gastrointestinal side effects such as nausea, constipation or diarrhoea (attributable to hepcidin effect), thus improving patient compliance (here). The intermittent intake of oral iron therapy has been shown to be as effective as the daily regimen (here).

In cases of suboptimal response, poor compliance, or troublesome side effects, total dose iron infusion therapy should be considered. As a general rule, 150 mg of elemental iron is required to improve the haemoglobin level by 10 g/L, plus 500 mg to replete the iron stores. Total dose iron infusion therapy requires optimum clinical supervision, and the patient should be made aware of possible side effects, including hypophosphataemia – a complication more commonly reported with ferric carboxymaltose therapy (here).

If response to iron supplementation therapy is suboptimal, further clinical evaluation and investigations are warranted to address the causative medical problem.

Professor Arumugam Manoharan is a clinical haematologist at St George Private Hospital in Sydney.  

The statements or opinions expressed in this article reflect the views of the authors and do not necessarily represent the official policy of the AMA, the MJA or InSight+ unless so stated. 

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