Levels of plasma iron available to be utilised by the body are maintained within a tight range under normal circumstances by controlling the rate of iron absorption and storage1. However, there are a number of different factors that can lead to disruption of the iron balance in obstetrics and gynaecology patients (see figure below).
Figure 2. Why patients seen by obstetricians and gynaecologists become iron deficient2
Chronic blood loss
Menstrual blood loss is one of the primary causes of iron deficiency in non-pregnant, premenopausal women2. The average menstrual blood loss of 35 mL over a cycle increases the daily iron requirement by 50–70% relative to the absence of menstruation2. Menstrual blood loss may be considerably higher in adolescents experiencing anovulatory bleeding3, in women using intrauterine contraceptive devices4 and women at a late stage of reproduction5.
Chronic bleeding may also occur as a result of disease. In postmenopausal women, blood loss associated with gastrointestinal lesions or cancer is the most common cause of iron deficiency6 and may partly explain the rise in iron deficiency with age in the postmenopausal group (see 'Gastroenterology Essentials' section).
Iron deficiency may arise as a result of low iron intake from the diet, such as in individuals on a restricted energy diet for weight loss. A diet very high in plant-based foods may also result in iron deficiency due to the low bioavailability of iron from these sources, although vegetarians who eat a varied and well balanced diet are not at significantly greater risk of iron deficiency than non-vegetarians7. Iron deficiency in the elderly may occur as a result of anorexia3.
Chronic diseases associated with inflammation, such as cancer, chronic heart failure or renal disease, can be a cause of iron deficiency. Inflammatory cytokines stimulate an increase in levels of hepcidin, an iron homeostasis hormone responsible for controlling the absorption of iron from the intestine as well as the release of iron from stores within the body1. In the short term, pathological increases in hepcidin impair the release of iron from iron stores resulting in functional iron deficiency8. Over the longer term, absorption of iron from the intestine is also blocked by hepcidin preventing stores from being replenished and leading to absolute iron deficiency.
Pregnancy and postpartum
Insufficient dietary iron, inflammation and blood loss can all contribute to iron deficiency during pregnancy and postpartum.
Pregnant women require approximately 1.2 g of iron, in addition to their normal iron requirements, over the course of pregnancy9. This total comprises the iron requirements of the foetus (270 mg), the placenta (90 mg), and maternal erythrocyte expansion (450 mg)9. Blood volume increases by 30–50%, beginning at Week 6–8 and peaking at Week 28–342,3. Approximately half of the additional iron requirement can be gained by cessation of menses, but a further 600 mg from the diet is required, primarily during the second and third trimesters, to avoid iron deficiency2. Use of antacids during pregnancy may decrease dietary iron bioavailability since gastric acid is needed to maintain iron in its more readily absorbed ferric state10.
Studies show a significant rise in inflammatory markers over the course of pregnancy11 and there is evidence that the presence of inflammation may increase the risk of iron deficiency, particularly in women with chronic co-morbidities. In one study, obese mothers had higher rates of inflammation and hepcidin compared to lean controls, which correlated with a trend toward lower iron levels (serum ferritin and transferrin saturation [TSAT]) and significantly lower iron levels in their offspring12.
Blood loss during delivery can result in iron deficiency and anaemia, with a loss of more than 500 mL sufficient to cause anaemia in women without prior iron deficiency anaemia3. The median blood loss during vaginal delivery is 250 mL but blood loss in excess of 1000 mL occurs in more than 5% of deliveries3.