NUR 555 Module 5 Comparison Paper Example

An Empty Store and a Locked Store: Iron Deficiency Anemia and Anemia of Inflammation Compared Through Hepcidin

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Southern New Hampshire University

NUR 555: Advanced Clinical Pathophysiology

Comparison Paper

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[Date]

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An Empty Store and a Locked Store: Iron Deficiency Anemia and Anemia of Inflammation Compared Through Hepcidin

Iron deficiency anemia and anemia of inflammation are the two most common anemias worldwide, and both leave the red cells short of iron. The difference is where the iron is. In iron deficiency, the body's stores are empty; in anemia of inflammation, the stores are adequate or full but locked away. This paper argues that a single hormone, hepcidin, explains both conditions and the tests that separate them: hepcidin falls when iron is scarce, opening the gates for absorption and release, and rises with inflammation, closing them, so the pattern of ferritin, transferrin saturation and iron-binding capacity follows directly from which way hepcidin has moved.

Two Patients

Patient G, a 38-year-old woman with two years of heavy menstrual periods, reports fatigue, breathlessness on stairs and an urge to chew ice. Hemoglobin is 9.8 g/dL, mean corpuscular volume (MCV) 72 fL and red cell distribution width high. Ferritin is 6 ng/mL, transferrin saturation 6% and total iron-binding capacity (TIBC) high at 460 mcg/dL.

Patient H, a 61-year-old man with rheumatoid arthritis that has flared for three months, reports fatigue. Hemoglobin is 10.6 g/dL and MCV 86 fL. Serum iron is low and transferrin saturation 12%, but ferritin is 310 ng/mL, TIBC is low at 220 mcg/dL and C-reactive protein is 38 mg/L.

Hepcidin: The Iron Gatekeeper

Because humans lose iron only passively, through shed cells and bleeding, the body manages its iron almost entirely at the points of entry and release (Rogers, 2023). Hepcidin, a peptide hormone made in the liver, attaches to ferroportin, the channel cells use to push iron out, and marks it for destruction inside the cell. Whenever hepcidin runs high, ferroportin disappears from the surface of duodenal cells, which then cannot pass dietary iron into the blood, and from macrophages, which then cannot release iron recycled from old red cells. When hepcidin is low, ferroportin stays in place and iron flows into the plasma (Camaschella, 2015). Hepcidin production falls when iron stores are low or red cell production is stimulated and rises when stores are high or when inflammation signals through interleukin-6 (Weiss et al., 2019).

Patient G: An Empty Store

Patient G's heavy periods removed iron faster than her diet replaced it. As stores emptied, hepcidin fell, maximizing absorption and release, but supply could not keep up with loss. Ferritin, which reflects stored iron, fell to 6 ng/mL, a value that essentially confirms absent stores. With little iron to carry, transferrin saturation fell, while the liver made more transferrin, raising TIBC, as if the body were sending out more trucks to collect a scarce cargo (Camaschella, 2015).

In the marrow, developing red cells without enough iron to make hemoglobin divided an extra time, producing small, pale cells, which explains the low MCV and the high red cell distribution width as new small cells mixed with older normal ones. Fatigue and breathlessness reflect reduced oxygen-carrying capacity. Pica, especially for ice, is a characteristic though poorly understood symptom of iron deficiency.

Patient H: A Locked Store

Patient H's inflamed joints released cytokines, above all interleukin-6, which drove hepcidin up. Ferroportin was degraded in the gut and in macrophages, so dietary iron was absorbed poorly and recycled iron was trapped inside macrophages. Serum iron and transferrin saturation fell even though total body iron was adequate. Ferritin, both a store of iron and an acute-phase protein that rises with inflammation, was high at 310 ng/mL. TIBC fell, because transferrin production decreases in inflammation (Weiss et al., 2019).

Other effects of inflammation add to the anemia. Cytokines blunt the kidney's erythropoietin response and the marrow's response to it, and they shorten red cell survival. The result is usually a mild to moderate, normocytic anemia, as in Patient H, which can become mildly microcytic when iron restriction is prolonged.

Side by Side

Table 1 shows how the direction of hepcidin produces opposite patterns in the iron studies.

Table 1

Iron Deficiency Anemia and Anemia of Inflammation Compared

When the Picture Is Mixed

The comparison is not always clean. A patient with chronic inflammation can also lose blood, for example from the stomach while taking anti-inflammatory drugs, and develop true iron deficiency on top of anemia of inflammation. Ferritin can then be misleading, because inflammation raises it even when stores are low. For this reason, a ferritin that would be normal in a healthy person may still indicate deficiency when inflammation is present, and additional tests such as the soluble transferrin receptor can help, since it rises in iron deficiency but not in inflammation alone (Weiss et al., 2019). Patient H's ferritin of 310 ng/mL makes coexisting deficiency unlikely, but his clinician should keep the possibility in mind if his hemoglobin falls.

Treatment Follows the Hormone

Patient G needs two things: the cause addressed, through evaluation and treatment of heavy menstrual bleeding, and iron replaced. With hepcidin low, her gut is primed to absorb iron, so oral iron works well, and her hemoglobin should rise within weeks (Camaschella, 2015). Patient H is different. With hepcidin high, oral iron is poorly absorbed, and giving it does little. The main treatment is control of the inflammation, here more effective treatment of his rheumatoid arthritis; as inflammation falls, hepcidin falls and iron is released from macrophages (Weiss et al., 2019). Intravenous iron can bypass the gut block if true deficiency coexists, but it is not routine for anemia of inflammation alone.

Conclusion

Patient G and Patient H both have anemia with low serum iron, but for opposite reasons. In Patient G, empty stores lowered hepcidin, opened the iron gates and still could not keep up with blood loss, leaving low ferritin, high TIBC and small red cells. In Patient H, inflammation raised hepcidin through interleukin-6, locking iron in macrophages and the gut, leaving high ferritin, low TIBC and normal-sized cells. Reading the iron studies as the footprint of hepcidin separates the two and explains why oral iron helps only the first.

References

Camaschella, C. (2015). Iron-deficiency anemia. New England Journal of Medicine, 372(19), 1832-1843. https://doi.org/10.1056/NEJMra1401038

Rogers, J. L. (Ed.). (2023). McCance & Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.

Weiss, G., Ganz, T., & Goodnough, L. T. (2019). Anemia of inflammation. Blood, 133(1), 40-50. https://doi.org/10.1182/blood-2018-06-856500