Ferritin as a diagnostic point-of-care marker in iron deficiency anemia: a narrative review and clinical implications

Introduction

Background

Anemia is the most common blood disorder in pregnancy, affecting more than one third of all pregnant patients (1,2). Anemia is typically characterized by a reduction in hemoglobin, hematocrit, or red blood cell count (1). During pregnancy, physiologic increases in blood volume result in hemodilution and a corresponding decline in hemoglobin levels. Accordingly, anemia in pregnancy is defined as a hemoglobin concentration of below 11.0 g/dL in the first trimester and below 10.5–11.0 g/dL in later trimesters (1). Aside from natural hemodilution, iron deficiency is the most common cause of anemia in pregnancy (1). Iron deficiency anemia (IDA) occurs when iron intake is insufficient to meet iron utilization requirements. IDA is a potentially reversible risk factor associated with significant maternal and perinatal morbidities, warranting early identification, aggressive treatment, and intensive follow up in the prenatal period for symptomatic patients (3). However, the US Preventive Services Task Force concluded that current evidence is insufficient to assess the net benefit of routine screening for IDA and iron supplementation for asymptomatic pregnant patients (4). Research is needed to address this gap, as untreated iron deficiency may progress quickly, leaving asymptomatic patients at risk for delayed diagnosis and treatment.

The American College of Obstetricians and Gynecologists recommends routine screening for anemia with a complete blood count in the first trimester and again at 24–28 weeks gestation (5). If anemia is identified, the severity of anemia must be assessed. Hemoglobin levels ranging from 10.0–10.9 g/dL are considered mild; 7.0–9.9 g/dL are considered moderate; and 4.0–6.9 g/dL are considered severe (1). Patients with mild anemia and normal to mildly low mean corpuscular volume are likely to have IDA (1). However, hemoglobin alone is an imperfect marker of iron deficiency. Patients with normal hemoglobin levels may still be iron deficient; in fact, iron deficiency without anemia is estimated globally to be at least twice as common as IDA (6). Conversely, patients with low hemoglobin levels, such as those with inherited hemoglobinopathies, may not necessarily be iron deficient (1).

Increasingly, serum ferritin has been considered a more reliable marker for IDA than hemoglobin, as it serves as an estimate of the body’s iron stores. In fact, a low serum ferritin level is now the gold standard for detecting IDA in patients with moderate or severe anemia (1). While challenges remain in testing ferritin levels, such as determining a cutoff for serum ferritin levels and standardizing testing methods, ferritin still proves to be a strong method for screening and diagnosing IDA. Thus, hemoglobin and ferritin are often used in conjunction to diagnose IDA.

Although labs for complete blood count and ferritin levels are frequently ordered for pregnant patients at prenatal visits, financial or physical barriers may prevent particularly high-risk pregnant patients from returning for laboratory testing to confirm IDA. Point-of-care (POC) testing may present more accessible alternatives to standard laboratory tests. However, research on ferritin POC devices is lacking, especially for use in pregnant patients.

Rationale and knowledge gap

This narrative review aims to fill the gaps in research on the role of ferritin in IDA screening, diagnosis, and management in pregnancy. In particular, this review focuses on the use of ferritin POC devices in pregnancy.

Objective

The objective of this review is to address the following questions:

• What is the biology and pathophysiology of ferritin?
• What is the role of ferritin in IDA?
• How do ferritin levels differ in pregnant patients?
• How are ferritin levels used to screen for and diagnose IDA?
• How are ferritin levels measured using non-POC and POC methods?
• How are ferritin levels used to manage IDA?

We present this article in accordance with the Narrative Review reporting checklist (available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0122/rc).

Methods

A series of PubMed and Google Scholar searches were performed to find articles addressing the role of ferritin in IDA screening, diagnosis, and management, especially in pregnancy. Combinations of keywords, such as “ferritin”; “iron deficiency anemia” or “IDA”; “screening” or “diagnosis” or “management”; “point-of-care” or “POC”, and “iron status” were used. An example of a search equation used for this review is (“ferritin”) AND (“point of care” OR “point-of-care” OR “POC”). Titles and abstracts were screened for relevance. Included articles were reviewed in full text. References within these articles and related articles were screened for inclusion. Articles from database inception to June 2026 were reviewed, but inclusion preference was given to articles published after 2016. Articles not available in English or not related to iron status, anemia, or POC testing were excluded (Table 1).

J.N.D., M.S., C.H., E.C., and D.S. conducted literature reviews within assigned topic areas. J.N.D. subsequently verified the eligibility and quality of the included studies to ensure consistency in study selection and interpretation throughout the manuscript.

Findings

Biology of ferritin

Ferritin structure and function

Ferritin is a 24-subunit protein complex that serves as the primary intracellular iron storage molecule. The protein comprises two distinct subunits: the L (light) subunit aids in iron nucleation and storage, whereas the H (heavy) subunit is essential for the oxidation of ferrous iron (Fe²⁺) to ferric iron (Fe³⁺). The ferritin molecule has a spherical structure that can encapsulate up to 4,500 iron atoms in a bioavailable and non-toxic form. Systemic iron balance is largely dependent on iron storage, which reduces the potentially detrimental effects of free iron that can produce reactive oxygen species via the Fenton reaction (7,8).

Ferritin is essential for regulating iron release in accordance with the physiological needs of the body (9). The release of iron is carefully regulated, particularly during erythropoiesis and other cellular processes, to meet metabolic demands. Serum ferritin levels indicate the body’s iron reserves and are affected by factors including iron availability, inflammatory cytokines, and specific hormonal signals (9,10).

Ferritin as an iron storage protein

Ferritin functions as a key intracellular iron storage component found in the bone marrow, liver, spleen, and several other tissues. Ferritin efficiently captures soluble iron, known as ferrous iron (Fe²⁺), and converts it to the ferric form (Fe³⁺) for storage to prevent the occurrence of free iron, which can be harmful due to its involvement in oxidative damage. When tissues need iron for cellular processes, ferritin can be mobilized from the ferritin core and subsequently exported from cells by ferroportin. This iron is essential for various processes, such as hemoglobin synthesis, mitochondrial function, and DNA replication (11).

Ferritin acts as a key regulator of iron levels, and the two exist in a bidirectional regulatory relationship. In response to high intracellular iron levels, ferritin is upregulated via post-transcriptional mechanisms, increasing iron storage capacity. In states of low intracellular iron, ferritin expression is decreased, leading to reduced iron storage. This regulation system is essential for biological processes and prevents excess amounts of iron from causing toxicity. Similarly, serum ferritin reflects total iron stores, with lower ferritin levels indicating iron reserve depletion and higher ferritin levels indicating iron overload (11,12). Of note, ferritin levels are not always representative of iron reserves because they can be temporarily elevated by inflammation or dietary choices (i.e., spinach and red meat).

Role of ferritin in IDA

Pathophysiology of ferritin in IDA

In IDA, insufficient dietary intake, poor absorption, or excessive iron loss leads to depletion of iron stores. As iron stores become depleted, ferritin synthesis decreases and iron is mobilized less efficiently, resulting in compromised iron availability for erythropoiesis and hemoglobin production. This process ultimately leads to the characteristic microcytic, hypochromic anemia seen in IDA. Because ferritin concentrations typically decline in parallel with the depletion of iron stores, serum ferritin is considered an accurate indicator of total body iron status, particularly in healthy individuals (13). Ferritin correlates strongly with bone marrow biopsy results and outperforms other biomarkers, including hemoglobin, mean corpuscular volume, transferrin, and transferrin saturation, in predicting depleted iron stores (14). Serum ferritin levels are also strongly associated with hemoglobin content of reticulocytes, which is another known indicator of IDA (15).

Clinically, the hallmark features of IDA include fatigue, pallor, and weakness. Additional symptoms may include headache, dizziness, brittle nails, cold hands or feet, pica, decreased cognitive function, and restless leg syndrome (16). Pregnant women may also experience symptoms such as low breast milk production and decreased thermoregulation (17).

Comparison with other anemias (non-pregnant individuals)

Ferritin levels in IDA differ from those in other forms of anemia. In anemia of chronic disease, ferritin levels are typically elevated or within normal range, despite a lack of available iron. These increased ferritin levels are largely due to the inflammatory cytokine-driven upregulation of ferritin as part of the acute-phase response to systemic stress. Iron becomes sequestered and is unavailable for erythropoiesis, resulting in anemia. This contrast in ferritin status can be helpful in distinguishing IDA from anemia of chronic disease, as both conditions may present with similar clinical symptoms, such as fatigue and pallor, but require different treatment strategies (13,18).

In conditions such as thalassemia or sickle cell disease, ferritin levels may be elevated due to chronic blood transfusions or ineffective erythropoiesis, leading to secondary iron overload. In these cases, ferritin serves as a marker of iron excess rather than deficiency, which requires different therapeutic approaches, including iron chelation therapy to prevent iron toxicity (19,20).

Ferritin in pregnancy

Pregnant women experience substantial changes in iron metabolism to meet the increased demands of the developing fetus and placenta (21). These changes are influenced by the hormone hepcidin, which is considered the master regulator of iron homeostasis, controlling the storage versus mobilization of iron based on the body’s demands (22). Typically, hepcidin levels correlate directly with ferritin levels, with greater levels reflecting the sequestration of iron in storage (22). During pregnancy, maternal hepcidin is significantly suppressed, especially during the second and third trimesters, to allow for the release of iron into the bloodstream, coinciding with a decline in serum ferritin levels (23). This released iron is necessary to accommodate hematopoiesis for increasing plasma volume, as well as the active transfer of iron to the developing fetus (21). Specifically, a longitudinal study looked at serum ferritin throughout pregnancy and found a consistent decline as pregnancy advanced (24). Median ferritin concentrations decreased from 56.5 µg/L at 15 weeks gestation to 34.3 µg/L at 20 weeks and 14.7 µg/L at 33 weeks. The statistical analysis following this study also demonstrated that a ferritin of <60 µg/L was predictive of <15 µg/L in the third trimester, further demonstrating this longitudinal decline throughout pregnancy (24).

Still, serum ferritin levels are considered the most reliable marker of iron status during pregnancy (16). In this regard, reduced serum ferritin levels can be indicative of IDA in pregnant patients, which contributes to increased risk of detrimental maternal and fetal consequences, such as postpartum hemorrhage and blood transfusion (25), preterm delivery, low birth weight, and developmental impairments (26). In contrast, elevated ferritin levels during pregnancy may signify underlying inflammation, gestational diabetes, or preeclampsia (27). Consequently, tracking ferritin levels during pregnancy, particularly in anemic patients, is crucial for potentially directing iron supplementation and ensuring optimal health outcomes for both mother and fetus (26).

Ferritin in IDA screening and diagnosis

In many clinical practice settings, hemoglobin is commonly used for primary screening of anemia during pregnancy, while ferritin is subsequently measured to evaluate iron stores and confirm iron deficiency, following the US Preventive Services Task Force recommendations (4). However, growing evidence supports the utility and cost-effectiveness of ferritin-based screening, particularly during the first trimester (24,28-30). Two studies evaluating iron deficiency in non-anemic pregnant patients found that current ferritin thresholds are too low, recommending early ferritin screening to detect iron deficiency before hemoglobin levels fall (24,29). These findings demonstrate that hemoglobin alone is an insufficient screening marker for detecting iron deficiency in pregnancy. Similarly, another study found that first semester ferritin may be preferable to hemoglobin alone or even replacement in settings with low risk of anemia (28). Several guidelines reflect this trend towards ferritin screening, with five guidelines recommending ferritin screening in addition to a complete blood count, and one guideline recommending universal ferritin screening (31). However, the literature remains limited; more research is needed to establish the optimal role of ferritin in screening and diagnosis of IDA in pregnancy.

Threshold levels

A serum ferritin level of less than 30 µg/L is generally considered diagnostic of iron deficiency in otherwise healthy pregnant and non-pregnant women (5,32,33). However, because ferritin is an acute-phase reactant, this threshold may vary depending on the clinical context, particularly in the presence of inflammation and chronic disease (see the “Ferritin in inflammatory conditions” section) (34). This threshold also raises to <50 µg/L in women with inherited bleeding disorders to ensure detection of iron deficiency (32). The potential for ferritin concentrations to fluctuate in disease states supports the importance of properly assessing a patient’s condition before making a diagnosis with ferritin values alone (35).

It is also crucial to acknowledge that thresholds for diagnosing IDA tend to vary between organizations and institutions. Laboratory reference ranges can be variable and inaccurate, leading to inconsistencies in identifying and managing dangerously low iron stores. There even lacks consensus among international clinical guidelines on the appropriate cutoff values for diagnosing IDA in pregnancy (23,36). The World Health Organization recommends a ferritin threshold of <12 µg/L to diagnose iron deficiency in most healthy individuals and <15 µg/L in first trimester individuals with no recommendations for second or third trimesters. These recommendations are based on expert opinion and historical data last updated in 1993 (37,38). Meanwhile, the American College of Obstetricians and Gynecologists supports the <30 µg/L cutoff for IDA diagnosis in pregnancy (5).

More recent investigations, specifically those that correlate bone marrow iron stores with serum ferritin levels, suggest higher thresholds are necessary to improve the sensitivity of ferritin screening and IDA diagnosis. Research indicates that a threshold of 15 µg/L may miss up to 50% of iron deficient individuals (37). One study of diagnostic accuracy compared serum ferritin levels with bone marrow biopsy results in 54 anemic patients and found sensitivity improved from 25% to 92% when the ferritin threshold was raised from 12 to 30 µg/L. Moreover, they noticed that among five patients with absent bone marrow iron stores, only one had a ferritin threshold of <12 µg/L, further discrediting this long-accepted cutoff value (39).

The discussion of ferritin threshold values is especially pertinent in the pregnant population, as ferritin levels decline throughout pregnancy, as discussed in the “Ferritin in pregnancy” section. Thus, physiologically based trimester-specific thresholds may be needed. One study identified physiologic thresholds of <25 µg/L during the first trimester and <20 µg/L during later trimesters (23), while other studies have recommended thresholds of <60 µg/L in the first trimester (24,29). Regardless, these studies show that despite normal hemoglobin levels, pregnant patients with ferritin below either threshold showed progressively worsening iron status. Therefore, by the time a pregnant patient reaches the lower threshold cutoffs, her iron stores may already be substantially depleted. Early ferritin screening may better identify pregnant women at risk before the onset of anemia (23,24,29). Furthermore, research also demonstrates that a higher screening ferritin threshold of <30 µg/L is more cost-effective than both a lower threshold of <15 µg/L and no ferritin screening in pregnant patients (30). Further research is needed for establishing standardized ferritin cutoffs to improve the screening, diagnosis, and treatment of pregnancy-related anemia (23,32,36).

Sensitivity and specificity

Ferritin is a highly specific screening tool for IDA. A cutoff of <30 µg/L yields a specificity as high as 97–98% in women (14,39), demonstrating that low ferritin levels are highly indicative of depleted iron stores and strongly support the diagnosis of IDA.

The sensitivity of ferritin for diagnosing IDA, however, can vary depending on the patient population. In otherwise healthy individuals, a serum ferritin value of <30 µg/L has demonstrated a 92% sensitivity for diagnosis of iron deficiency (37). However, in patients with inflammatory or hematologic conditions, serum ferritin can be elevated independent of iron status. Therefore, ferritin levels above 30 µg/L do not definitively exclude IDA. For example, a study evaluated the diagnostic accuracy of serum ferritin for IDA in a population of patients with known hematologic conditions, including hematologic malignancies and myeloproliferative disorders. They found that ferritin has a much lower sensitivity of 54% in women of this population (14). In other words, iron deficient patients with seemingly normal ferritin levels may be easily overlooked by this screening test.

In all, these specificity and sensitivity values communicate that serum ferritin is generally a proficient estimate of iron stores, especially in healthy populations. However, there are still limitations in using ferritin for diagnosis; exclusion of IDA may warrant thoughtful clinical evaluation. When ruling out IDA in patients with inflammatory conditions or potentially inflated serum ferritin, additional measures should be used alongside ferritin.

Ferritin in inflammatory conditions

As previously mentioned, serum ferritin levels may increase in the presence of inflammation, reducing its reliability as a biomarker of iron status (15). Ferritin is an acute-phase reactant that, by definition, is elevated during inflammation. The mechanism behind this increase can also be tied to the peptide hormone hepcidin. In states of inflammation, hepcidin and ferritin may increase alongside one another (22). Inflammatory conditions in pregnancy, such as preeclampsia, infection, and obesity, have been associated with increased hepcidin levels (40). Increased hepcidin levels lead to the sequestration of iron within cells, diminishing iron bioavailability and increasing ferritin levels independent of iron status (41). Generally, IDA tends to be overlooked in patients with inflammatory states, like inflammatory bowel disease, chronic kidney disease, or congestive heart failure, as the high ferritin values result in a false negative (41).

Due to the difficulty of accurate testing, serum ferritin level standards are not widely regarded or known in patients with inflammatory conditions. For instance, European guidelines support diagnosis of IDA in patients with inflammatory bowel disease, chronic kidney disease, or congestive heart failure at ferritin levels of <100 µg/L or 100–300 µg/L if iron deficiency is confirmed via transferrin saturation (41). Additionally, a review of 38 studies found that individuals with IDA and preexisting inflammatory conditions had a mean ferritin level of 82.43 µg/L, suggesting that the standard diagnostic threshold of <30 µg/L is inadequate to detect IDA in these individuals (42). It must also be considered that pregnancy alone is already an inflammatory state, and serum ferritin may experience unexpected elevation as a result (40,43). One study found that in iron deficient pregnant patients, mean serum ferritin increased from 9.7 µg/L at 48 hours prepartum to 16.9 µg/L at 48 hours postpartum, representing a 74% increase in ferritin and demonstrating the fluctuation of ferritin in the peripartum period (44). A different longitudinal study of iron biomarkers during pregnancy compared serum ferritin concentrations between patients with inflammatory marker C-reactive protein (CRP) levels of <5 mg/L, 5–10 mg/L, and >10 mg/L (24). They found no significant difference in serum ferritin concentrations throughout pregnancy between patients in the CRP <5 mg/L group and the 5–10 mg/L group, but differences appeared when comparing the lower inflammation groups to the >10 mg/L group (24). These findings indicate that the mild-to-moderate inflammation typically associated with pregnancy may not necessarily impact ferritin levels. In summary, serum ferritin should be used with caution in pregnant women, especially those with additional inflammatory conditions.

Measuring ferritin levels

Non-POC methods

Currently, ferritin levels are largely measured by centralized laboratory technology. Three commonly-used contemporary techniques for evaluating ferritin levels include the enzyme-linked immunosorbent assay (ELISA), chemiluminescent immunoassays, and immunoturbidimetric assays (45). There is no single gold standard method nor a most common method for assessing ferritin levels; therefore, specific methods for measuring ferritin levels vary by laboratory standards and available technology (45).

ELISA acts on the specific interaction between an antigen (ferritin) and an antibody, subsequently employing an enzyme-linked secondary antibody to identify the antibody-antigen complex. ELISA-based assays have shown high precision and low detection limits; however, performance characteristics vary based on assay format and degree of automation. ELISA necessitates substantial laboratory equipment and may entail significant time and financial resources (46).

Chemiluminescent immunoassay employs a chemiluminescent substrate for the detection of the ferritin-antibody complex. Chemiluminescent immunoassay, akin to ELISA in principle, yields highly accurate results; however, this test also necessitates significant time and financial investment for implementation (47).

The immunoturbidimetric assay represents a modern approach for evaluating ferritin levels, measuring the turbidity produced by the interaction between ferritin and specific antibodies. Turbidity correlates with the concentration of ferritin in the sample, as quantified by spectrophotometry. This process can be executed quickly and yields results that agree with established laboratory methods (48).

Each of these methods demonstrates comparable accuracy and reliability, as proven by a recent meta-analysis including 148 studies (45). When assessing the major ferritin assay methods, including ELISA, chemiluminescence, and immunoturbidimetry, they exhibited a between-run imprecision rate of 8.9%±8.7% and a within-run imprecision rate of 6.2%±3.4% (45). The methods also demonstrated a high linear correlation with one another, as proven by a pooled regression coefficient of 0.985, suggesting they are interchangeable at the population level (45). Laboratory assay methodology is not known to be a driver of differences in accuracy of ferritin measurement, as analytical bias largely arises from variation in ferritin threshold level and inconsistency between commercial laboratory platforms (49,50). Each immunochemical technique presents unique advantages and limitations.

Overall, laboratory-based technologies excel due to high quality and accuracy, management by laboratory-trained personnel, and their capacity to meet the high demands of a busy setting (51,52). However, they are limited in that they are often expensive, sophisticated, large in size, and time-consuming. Turnaround time for centralized laboratory results in the hospital setting is often hours, as the specimen must be collected at bedside, transported to the centralized laboratory, queued, processed, and analyzed before clinicians can access results (51,52). Similarly, in the outpatient setting, laboratory testing typically requires a separate appointment, costing the patient additional time, money, and effort. This process reduces the efficiency of a hospital course or management plan and may ultimately delay necessary patient care.

POC methods

POC devices are portable screening or diagnostic tools to be used at or near the site of patient care, offering providers real-time results to enhance clinical decision making. These devices are ideally rapid, user-friendly, and necessitate minimal training, rendering them appropriate for application in both clinical and field environments (48,52). However, POC devices specifically for the measurement of ferritin are still in development and have not yet been integrated into routine clinical care.

Ferritin monitoring has been strictly laboratory-based to date, but by the early-mid 2010s, research prototypes and proof-of-principles for POC ferritin devices began emerging (53). Multiple studies have demonstrated the feasibility of POC ferritin devices by describing assay methods, including lateral flow immunoassay (LFIA), fluorescence-based immunoassay, electrochemical biosensing, and chemiluminescence immunoassays (53-59). More innovative models include an antibody-free fluorescence assay and smartphone-coupled LFIA, ironPhone (60,61). Although this technology remains in the research phase, ironPhone is a promising example of a handheld device that can assess iron status from finger-prick blood. In a small human validation study with 20 participants, this mobile phone attachment and app duo demonstrated a 0.92 correlation (P<0.0001) with a standard laboratory analyzer and a sensitivity of 90% for detecting iron deficiency at a ferritin threshold of <15 µg/L (61). Another example of a POC ferritin device in the phase of small human validation study is IronScan™, an LFIA device that demonstrated strong agreement with the standard laboratory analyzers and 90% sensitivity for diagnosing iron deficiency at a ferritin threshold of <30 µg/L (59).

Despite these examples, there generally exist limited data on the clinical validity of a majority of these models, as these studies do not report diagnostic performance metrics such as sensitivity and specificity values. Most of these tools remain in research and clinical trial phases, with none yet approved by the United States Food and Drug Administration. A limited number of POC devices, including fluorescence-based immunoassay systems and rapid lateral flow tests, are commercially available in other countries, such as Australia and Switzerland (Table 2). However, no ferritin POC technology has reached widespread commercialization or clinical use in the United States. Furthermore, accuracy and validity measures for these devices have been compiled in Table 2 as reported by the commercial retailers, but limited research has been published confirming these values. Research is available for only two commercially available devices; the accuracy and validity values from these studies have been reported in Table 2.

A major reason that POC ferritin devices lag behind other POC devices is the necessity of serum or plasma separation from whole blood before analysis (49). This separation requires the integration of a microfluidic device or other separation mechanism into the POC tool to remove cellular components that interfere with accurate ferritin detection (49,53,56).

Currently, there are no studies that evaluate the use of POC ferritin devices in pregnancy. With further development and research, POC ferritin devices have potential to be pivotal in the diagnosis of IDA during pregnancy. A primary benefit of POC ferritin devices is their capacity to deliver rapid results, with result times typically ranging from 5 to 30 minutes. These rapid results would allow healthcare providers to make prompt decisions concerning the initiation of iron supplementation or alternative treatment strategies. One potential sensor technology reports the ability to detect ferritin from plasma in 0.1 second (55). Timeliness is significant for vulnerable populations at elevated risk of iron deficiency, including pregnant women, children, and the elderly (52,53). Additionally, these devices could hold significant value in contexts where laboratory-based testing is not easily accessible, including rural, remote, or resource-limited environments (53). POC ferritin devices allow opportunities to facilitate extensive screening initiatives, enhancing the identification of undiagnosed anemia and alleviating the global impact of IDA. Further study and development of these devices for use in pregnancy represents a potential advancement for the field.

Nevertheless, POC ferritin devices exhibit limitations (76). POC devices, in general, rely on high quality specimen collection, minimal inter-operator variation, and avoidance of extreme temperatures, all of which can influence device accuracy. For instance, POC devices are typically designed for optimal operation at about 20–25 ℃, and they are often sensitive to variation in ambient temperature. While there is no published data on the thermal stability of POC ferritin devices specifically, studies on other comparable rapid testing devices indicate that temperatures below 15 ℃ may cause POC devices to slow or fail, and temperatures above 37 ℃ may diminish reagent stability, device accuracy, and overall reliability of results (77-79). Additionally, although these POC ferritin tests can rapidly measure ferritin levels, they do not offer a comprehensive assessment of iron status, which may necessitate the inclusion of further biomarkers like serum iron and transferrin saturation. Consequently, POC ferritin devices primarily serve as preliminary screening instruments, with subsequent laboratory testing advised for confirmation (52,80,81). However, when used during pregnancy, POC ferritin devices may provide sufficient evidence for a diagnosis and treatment with supplementation since IDA is often empirically treated without ferritin or iron studies currently.

Although all POC ferritin devices serve as effective tools for the rapid and efficient diagnosis of IDA, their performance may differ based on the clinical context and the particular requirements of the patient population. These factors must be carefully considered to determine the most suitable device. Advancements in POC technology are anticipated to enhance the accuracy and usability of these devices, thereby improving the diagnosis and management of IDA worldwide (80).

Ferritin in IDA management

Monitoring the response to iron therapy is essential in the management of IDA, ensuring effective treatment and minimizing the risk of complications, such as iron overload. A reliable indicator of effective iron therapy is generally an elevation in serum ferritin levels; however, improvement in ferritin levels should be evaluated no less than 4 weeks after starting iron supplementation and could require months for complete ferritin normalization (82,83). An increase of 50–100% in ferritin levels during treatment typically indicates an enhancement in iron reserves. As discussed, inflammatory states may affect ferritin levels. It is therefore essential to evaluate hemoglobin levels in conjunction with ferritin for patients with inflammatory conditions. A 1 g/dL increase in hemoglobin is typically anticipated within 4 weeks following effective treatment (83).

Insufficient response, as evidenced by stable ferritin levels or persistently low hemoglobin despite intervention, may be attributed to factors such as iron malabsorption, ongoing blood loss, or non-adherence to supplementation (6). Individuals exhibiting persistent symptoms or abnormal test results may necessitate additional diagnostic evaluations, including endoscopy or stool analysis to investigate gastrointestinal bleeding (84). A tailored approach to monitoring ferritin, hemoglobin, and clinical response is essential for maximizing the efficacy of iron therapy while preventing both iron deficiency and toxicity.

Conclusions

Ferritin serves as a crucial biomarker for the diagnosis and management of IDA; however, its clinical utility is affected by factors, such as inflammation and comorbidities, complicating interpretation. The introduction of POC ferritin testing devices presents a considerable opportunity for enhancing screening and diagnosis of IDA, especially in underserved or resource-limited environments. These advancements provide the potential for more timely and accessible management of IDA, particularly among pregnant individuals. Future research and innovation in ferritin measurement techniques may enhance treatment strategies, thereby improving patient outcomes and addressing the global issue of IDA.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0122/rc

Peer Review File: Available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0122/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0122/coif). H.K.A. received grant from NIH related to tranexamic acid (R01HD110109) and consulting fees from Takeda, Sanofi, Hemosonics and COR2ED. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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