Anemia is more than a reduced hemoglobin value. It is a final common expression of nutritional deficiency, chronic inflammation, renal and systemic disease, marrow dysfunction, blood loss, or impaired erythropoiesis. The Global Burden of Disease 2021 analysis estimated that anemia affected nearly one quarter of the world population, with marked differences by age, sex, geography, severity, and cause.^[1] Its clinical impact extends beyond fatigue. Persistent anemia can diminish exercise tolerance, concentration, work capacity, and resilience during acute illness.

The burden remains particularly visible in low- and middle-income countries, where dietary insufficiency, infection, chronic disease, reproductive blood loss, and barriers to early care frequently overlap.^[2] In India, anemia has often been framed as a problem of women and children, yet nationally representative work has shown that adult men also carry a considerable burden.^[3] Hospital-based observations from rural India similarly demonstrate that anemia spans the adult life course and becomes more severe in selected older groups.^[4]

A useful clinical classification begins with red-cell morphology. Microcytosis usually directs attention toward iron-restricted erythropoiesis, whereas a normocytic pattern may accompany chronic inflammation, renal disease, or early deficiency states. Macrocytosis raises a different set of questions, including vitamin B12 or folate deficiency, medication exposure, liver disease, and marrow disorders. The boundaries are not absolute, however. Hemoglobin concentration, age, physiological state, and comorbidity influence how anemia is defined and interpreted in practice.^[5]

Iron deficiency remains a central cause worldwide and typically produces low ferritin, low serum iron, reduced transferrin saturation, and increased iron-binding capacity as depletion progresses.^[6] Anemia of inflammation is mediated largely through hepcidin-driven iron sequestration and impaired erythropoiesis, often producing a normocytic normochromic picture.^[7] Vitamin B12 deficiency, by contrast, can present with macrocytosis and megaloblastic change, although hematological and neurological manifestations do not always appear together.^[8]

The present study examined the clinico-hematological profile of anemia in adults, with emphasis on presenting symptoms, morphological pattern, severity, etiology, red-cell indices, and iron parameters. The aim was to define the dominant patterns within the study population and identify the laboratory features that distinguished the principal morphological groups.

Study Design and Setting A hospital-based cross-sectional observational study was conducted among adults evaluated for anemia. Study Period Three months. Study Population The study population consisted of adults aged 18 years or older diagnosed with anemia. The observed age range was 25-72 years. Sample Size The study included 200 adults who fulfilled the eligibility criteria. Inclusion Criteria Adults aged ≥18 years diagnosed with anemia according to World Health Organization hemoglobin thresholds; patients who underwent complete clinical evaluation, complete blood count, peripheral smear examination, and iron-profile assessment; and patients with complete clinical and laboratory records. Exclusion Criteria Patients younger than 18 years, pregnant women, patients who had received a blood transfusion or treatment for anemia before evaluation, and patients with incomplete clinical or laboratory information. Clinical and Laboratory Assessment Clinical presentation was recorded at evaluation. Hematological assessment included hemoglobin concentration, red blood cell count, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red-cell distribution width, total leukocyte count, and platelet count. Iron status was assessed using serum ferritin, serum iron, total iron-binding capacity, and transferrin saturation. Morphological and Etiological Classification Anemia was categorized as microcytic hypochromic, normocytic normochromic, or macrocytic. Severity was classified as mild, moderate, or severe. Etiological categories comprised iron deficiency, anemia of chronic disease, vitamin B12 deficiency, and folate deficiency, based on the integrated clinical and laboratory assessment. These were treated as working clinical classifications; a category was not reassigned solely because one automated index or iron parameter appeared discordant. Statistical Analysis Analysis was performed using Python 3.13 with pandas and SciPy. Continuous variables were summarized as mean ± standard deviation, while categorical variables were expressed as number and percentage. Symptom frequencies were calculated separately because more than one symptom could be recorded for an individual. Associations between categorical variables were tested with the chi-square test. Continuous variables were compared across morphological groups using the Kruskal-Wallis test because several laboratory measures, particularly ferritin, showed non-normal distributions. A p-value <0.05 was considered statistically significant.

The study comprised 200 adults aged 25-72 years. Mean age was 44.08 ± 13.22 years. Women constituted 115 (57.5%) participants and men 85 (42.5%). The largest age group was 31-40 years (56; 28.0%), followed by 41-50 years (43; 21.5%). Pallor was recorded in 115 (57.5%) participants, fatigue in 79 (39.5%), and weakness in 60 (30.0%). The demographic and clinical profile is summarized in Table 1, while the relative frequency of presenting features is displayed in Figure 1.

Normocytic normochromic anemia was the most frequent morphological type, affecting 86 (43.0%) participants. Microcytic hypochromic anemia was present in 61 (30.5%), and macrocytic anemia in 53 (26.5%). The leading etiological category was anemia of chronic disease (86; 43.0%), followed by iron deficiency (61; 30.5%), vitamin B12 deficiency (27; 13.5%), and folate deficiency (26; 13.0%). Distribution by morphology, severity, and etiology is shown in Table 2. The morphological proportions are illustrated in Figure 2.

Mild anemia was present in 91 (45.5%) participants, moderate anemia in 85 (42.5%), and severe anemia in 24 (12.0%). The severity distribution is presented in Figure 3. Mean hemoglobin for the full cohort was 9.63 ± 1.19 g/dL. The microcytic group showed the lowest ferritin (18.59 ± 3.59 ng/mL), serum iron (42.36 ± 5.15 µg/dL), and transferrin saturation (10.59 ± 1.50%), together with the highest TIBC (401.10 ± 10.30 µg/dL). Its mean MCH was low (24.33 ± 0.36 pg), although mean MCHC was 33.60 ± 0.90 g/dL. The normocytic group had ferritin of 34.05 ± 3.80 ng/mL and transferrin saturation of 16.15 ± 1.20%, indicating that the assigned morphological and etiological categories were not uniformly represented by every biochemical measure. The macrocytic group had the highest MCV (98.92 ± 3.01 fL), RDW (16.73 ± 0.22%), ferritin (478.23 ± 20.22 ng/mL), and transferrin saturation (49.46 ± 1.77%). Hematological and biochemical differences across morphological groups are detailed in Table 3; all comparisons were statistically significant (p<0.001).

Severity differed substantially across morphological categories (Table 4). All 86 participants with normocytic normochromic anemia were classified as mild. Among those with microcytic hypochromic anemia, 46 (75.4%) had moderate and 10 (16.4%) had severe anemia. In the macrocytic group, 39 (73.6%) had moderate and 14 (26.4%) had severe anemia. The association between morphology and severity was statistically significant (χ²=183.54, degrees of freedom=4, p<0.001), as visualized in Figure 4.

This study depicts adult anemia as a mixed clinical problem rather than a single nutritional diagnosis. Normocytic normochromic anemia was the most frequent morphological pattern, anemia of chronic disease was the leading etiological category, and nearly one third of participants had microcytic hypochromic iron-deficiency anemia. Macrocytic anemia also formed a sizeable subgroup. Most cases were mild or moderate, yet severe anemia clustered within the microcytic and macrocytic categories. Expected trends were evident in the low iron stores of the iron-deficiency group and the higher MCV and RDW of macrocytic cases, but individual indices were not uniformly concordant with the assigned categories. The predominance of a normocytic pattern differs from the global hierarchy in which iron deficiency is usually the leading cause. The difference is clinically plausible in a hospital-attending adult population, where chronic inflammatory, renal, infectious, and other systemic disorders are over-represented. Global analyses have repeatedly shown that the relative contribution of anemia causes changes sharply with age, sex, and geographical setting.[9] Thus, a hospital series should not be read as a prevalence survey of the surrounding community. It instead reflects the case mix reaching clinical evaluation. Hospital-based studies illustrate how strongly the morphological spectrum depends on age and referral pattern. Warghane et al. studied 207 elderly patients and found normocytic normochromic anemia in 60.4%, anemia of chronic disease in 62.3%, and moderate anemia in 45.9%. These proportions were higher than the corresponding 43.0%, 43.0%, and 42.5% observed in the present study, plausibly because their cohort was restricted to older adults with a greater burden of chronic illness.[10] A tertiary-care study of 250 patients by Kumar et al. reported a contrasting distribution: microcytic hypochromic anemia accounted for 55%, normocytic normochromic anemia for 29%, and macrocytic anemia for 16%.[11] The present pattern, with normocytic anemia predominating but substantial microcytic and macrocytic components, lies between these profiles and supports the view that local case mix materially influences the apparent hierarchy of anemia. Iron deficiency nevertheless accounted for 30.5% of the cohort and produced a persuasive biochemical signature. Low ferritin and transferrin saturation, accompanied by increased TIBC, indicate reduced iron stores and restricted availability for erythropoiesis. Contemporary reviews emphasize that ferritin remains a central diagnostic marker, while its interpretation becomes more difficult when inflammation is present.[12] The pattern becomes more convincing when several measures point in the same direction. A low ferritin concentration or low transferrin saturation with raised TIBC is therefore more informative than serum iron alone.[13] Two discordant findings deserve explicit attention. First, the microcytic hypochromic group had a low MCH and elevated RDW, but its mean MCHC remained 33.60 g/dL. Morphological terminology and automated red-cell indices were therefore not fully interchangeable in this series, and MCHC alone would not support the hypochromic label. Second, the normocytic group categorized as anemia of chronic disease had mean ferritin of 34.05 ng/mL and transferrin saturation of 16.15%. These relatively low values may reflect concurrent iron restriction or a mixed phenotype rather than isolated inflammation. Ferritin can be difficult to interpret in inflammatory states, particularly without inflammatory markers.[12] The etiological proportions should consequently be regarded as working clinical classifications rather than biochemically pure disease groups. The clinical implications extend beyond prescribing iron. In adults, especially men and postmenopausal women, iron deficiency should prompt evaluation for chronic blood loss, gastrointestinal disease, malabsorption, and other underlying conditions rather than being treated as an isolated laboratory abnormality.[14] Among younger Indian women, menstrual loss and dietary insufficiency remain common concerns, but they should not become automatic explanations that delay investigation. The present findings support a structured approach: identify the morphological pattern, examine iron indices, then pursue the likely source of deficiency. Macrocytic anemia represented 26.5% of participants, with vitamin B12 and folate deficiency contributing almost equally. This proportion was considerably higher than the 3.6% prevalence of megaloblastic anemia reported by Kaur et al. among 1,150 adult anemic patients at an Indian tertiary-care hospital.[15] Differences in referral pattern, diagnostic thresholds, and the deliberate grouping of vitamin B12 and folate deficiency within the macrocytic category may partly explain the gap. In the current cohort, macrocytic cases were older on average and were predominantly moderate or severe. This matters because vitamin B12 deficiency can produce neurological injury even when hematological abnormalities are modest or partially corrected by folate exposure.[16] Clinical enquiry regarding diet, gastrointestinal symptoms, medication use, and neurological complaints should therefore accompany laboratory confirmation. Age also shaped the observed profile. Macrocytic cases had a mean age above 60 years, while the normocytic group was younger. Older adults frequently have multiple potential contributors, including nutritional deficiency, chronic kidney disease, inflammation, occult blood loss, and marrow disorders. Population-based work has demonstrated that anemia becomes progressively more common with advancing age and that a substantial proportion remains unexplained after routine classification.[17] Reviews of anemia in later life similarly caution against dismissing a low hemoglobin concentration as a normal consequence of aging.[18] The symptom pattern was unsurprising but clinically useful. Pallor, fatigue, weakness, dizziness, breathlessness, and palpitations were frequent, yet none is specific to a particular anemia mechanism. Warghane et al. recorded pallor in 97.1%, generalized weakness in 89.9%, and fatigue in 85.5% of their elderly cohort, markedly higher than the corresponding frequencies in the present study.[10] The difference is likely related to older age, comorbidity, and hospital acuity rather than a fundamentally different symptom complex. Symptom intensity also does not necessarily track hemoglobin concentration alone; the rate of decline, cardiopulmonary reserve, age, and comorbidity influence presentation. In busy outpatient practice, especially where patients have adapted to longstanding symptoms, routine hemoglobin testing and red-cell indices may uncover clinically meaningful anemia that history alone underestimates. Several limitations should be considered. The hospital-based cross-sectional design limits generalizability and does not allow prevalence estimation or causal inference. The symptom field captured the leading complaints rather than an exhaustive symptom inventory. Reticulocyte counts, renal function, inflammatory markers, stool blood testing, measured vitamin B12 and folate concentrations, and marrow findings were not available as analyzable variables, restricting independent confirmation of etiological categories. The normal-range mean MCHC in the microcytic group and the relatively low ferritin and transferrin saturation in the normocytic group further indicate possible mixed phenotypes or constraints in classification. Referral patterns may also have influenced the strong separation of age, morphology, and severity groups. Even so, the study offers a practical message: adult anemia should be evaluated through a combined clinical, morphological, and biochemical framework.

Normocytic normochromic anemia associated with chronic disease was the most frequent assigned pattern in this adult cohort, followed by microcytic hypochromic iron-deficiency anemia and macrocytic megaloblastic anemia. Pallor and fatigue were common, but the clinical presentation remained non-specific. Moderate-to-severe anemia was concentrated in the microcytic and macrocytic categories. Morphology, red-cell indices, and iron parameters were informative but not completely concordant, particularly in the microcytic and normocytic groups. A stepwise assessment, followed by targeted confirmation when findings conflict, is more clinically defensible than reliance on hemoglobin, MCV, MCHC, or ferritin alone.

Source of Funding

Nil.

Conflict of Interest

None declared.

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