Mixed Nutritional Anaemia in Chronic Alcohol Abuse: A Case Report
Okoli Robertson Onyeka, Osunde Ifechukwude, Orkuma Joseph Aondoawase, Obekpa Solomon, Asor Paul Msugh
Asian Hematology Research Journal · pp. 385–394 · Published 17 Jul 2026
10.9734/ahrj/2026/v9i3267Abstract
Chronic, excessive alcohol consumption exerts direct toxic effects on the haematopoietic system and causes severe nutritional deficiencies. Rarely, multiple nutritional deficiencies coexist, creating a dimorphic red cell population that can normalise standard red cell indices, such as mean corpuscular volume, and result in significant diagnostic delays. A 56-year-old male civil servant with a 30-year history of heavy alcohol consumption (145 units/week) presented with a five-month history of progressive weakness, dizziness, fainting spells, and significant weight loss (>10 kg). Physical examination revealed severe pallor, tachycardia, hypotension, and hepatosplenomegaly. Initial laboratory evaluation revealed bicytopenia (haemoglobin: 8.3 g/dL; platelets: 77 × 109/L) with a deceptively normal mean corpuscular volume (MCV: 84 fL). However, the red cell distribution width (RDW-SD) was markedly elevated at 71.8 fL. A peripheral blood film showed a dual morphology comprising macrocytes, hypochromic microcytes, and pencil cells, while a bone marrow aspirate confirmed combined megaloblastic and micronormoblastic erythropoiesis with absent iron stores. Serum folate (2.3 ng/mL) and vitamin B12 (322 pg/mL) levels were both reduced. Concurrent nutritional deficiencies involving folate, vitamin B12, and iron can morphologically mask one another, yielding a normal MCV that obscures the underlying pathology. Alcohol-induced liver disease may destabilise haemostatic and metabolic balance; in vulnerable patients, nutritional restitution alone may be insufficient, and early, multidisciplinary intervention may be required to reduce the risk of fatal multiorgan failure.
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