Anemia ferropénica en el adulto mayor: diagnóstico y reposición

La anemia ferropénica en el adulto mayor no es una consecuencia inevitable del envejecimiento. El descenso de la hemoglobina por déficit de hierro puede revelar un sangrado digestivo, una neoplasia, mala absorción o una combinación de factores. En consulta de familia, el reto consiste en reconocer el patrón hematológico, demostrar que el hierro es la causa y, sobre todo, investigar por qué se ha agotado la reserva.

Su manejo exige separar dos decisiones: confirmar el déficit de hierro y explicar su origen. Un hemograma compatible no basta. La ferritina aumenta con inflamación, infección, enfermedad hepática, obesidad y algunos trastornos neoplásicos, mientras que el hierro sérico fluctúa con la ingesta y el estado inflamatorio. Una hemoglobina baja puede deberse también a enfermedad renal, hemólisis o acción medular.

La reposición oral suele ser la vía inicial cuando el paciente está estable, tolera el tratamiento y puede investigarse la causa. La vía intravenosa se reserva para intolerancia o mala absorción, pérdidas continuas, anemia grave o situaciones que exigen una corrección rápida. El objetivo no es solo elevar la hemoglobina: también es reponer reservas, controlar la pérdida y evitar que la deficiencia vuelva a aparecer.

Este marco resulta especialmente útil en medicina familiar y comunitaria, donde debe integrarse la revisión de fármacos, la valoración funcional, la investigación etiológica y el seguimiento longitudinal. Las recomendaciones disponibles presentan diferencias en dosis, intervalos y dianas de ferritina; por ello, las decisiones deben combinar la evidencia disponible con la situación clínica, la tolerancia y las preferencias del paciente.

Sospecha inicial y señales de alarma

La ferropenia suele manifestarse con cansancio, debilidad, disnea de esfuerzo, palpitaciones o menor tolerancia a la actividad. En personas mayores, estos síntomas pueden atribuirse inicialmente al envejecimiento, al sedentarismo o a otras enfermedades. La anemia grave puede producir angina, síncope, confusión o descompensación de una cardiopatía previa, por lo que la intensidad de los síntomas forma parte de la valoración inicial.

El hemograma ofrece la primera aproximación. Un volumen corpuscular medio bajo y un ancho de distribución eritrocitaria elevado apoyan el diagnóstico, pero la microcitosis puede tardar semanas en aparecer. Durante la fase inicial, la anemia puede ser normocítica. La ferritina, el hierro sérico y la saturación de transferrina ayudan a distinguir una ferropenia simple de otros patrones associated with chronic disease.

Certain findings should accelerate the etiological study. Melenas, hematoquecia, pérdida de peso, disfagia, anemia recurrente or iron deficiency without an obvious dietary cause are warning signs. In men and postmenopausal women with iron deficiency anemia, occult gastrointestinal bleeding must be actively ruled out, including potentially malignant causes. The use of NSAIDs, antiplatelet drugs, anticoagulants, or frequent blood donation also requires review.

Confirmación bioquímica y razonamiento clínico

In a stable patient, a serum ferritin level below 30 ng/mL strongly supports iron deficiency. In the presence of inflammation or chronic disease, values below 100 ng/mL increase suspicion, although they are less specific. An iron deficiency pattern also generally includes low serum iron, elevated total iron-binding capacity and transferrin saturation below 20%. Serum iron alone has little diagnostic value because it varies considerably throughout the day and falls during inflammation.

When ferritin is normal or elevated despite an apparently iron-deficient pattern, the clinical context becomes essential. Concurrent elevation of C-reactive protein, reduced transferrin saturation, renal impairment, liver disease, or active infection should be considered. The soluble transferrin receptor and the sTfR/log ferritin index may help in selected cases because they are less affected by inflammation, although availability and interpretation vary. Hepcidin can explain some functional iron-restricted states, but it is not a routine primary-care test.

The interpretation should integrate probabilities rather than isolated values. This approach is compatible with the principios editoriales of the Rincón Docente de Medicina de Familia, which emphasize transparent methodology, critical appraisal and the distinction between recommendations supported by strong evidence and those based on lower certainty. GRADE is useful for comparing benefits, harms and the certainty of evidence across different clinical decisions.

Investigación de la causa y valoración del riesgo

In older adults, iron deficiency should not be attributed automatically to inadequate dietary intake. Gastrointestinal blood loss from ulcers, angiodysplasia, inflammatory bowel disease or malignancy is a central possibility. In men and postmenopausal women, upper and lower gastrointestinal endoscopy are generally considered when iron deficiency anemia is confirmed, according to local protocols, age, symptoms and previous investigations. A normal fecal occult blood test does not exclude a relevant bleeding lesion.

Other frequent causes include chronic kidney disease with functional iron restriction, celiac disease, chronic inflammatory conditions, hypochlorhydria and excessive tea consumption in the context of low iron intake. Medication review should cover proton-pump inhibitors, which reduce iron absorption, as well as drugs associated with occult bleeding. If initial evaluation is negative and anemia recurs, capsule endoscopy, enterography, CT angiography or referral to a specialist may be appropriate depending on the suspected source.

Las principales pruebas se complementan y none should be interpreted in isolation:

Prueba Hallazgos que apoyan el déficit Limitaciones principales Aplicación clínica
Hemograma y frotis Hemoglobina baja, volumen corpuscular medio bajo y amplitud de distribución elevada La microcitosis puede estar ausente al inicio Sospecha inicial y vigilancia de la respuesta
Ferritina Frecuentemente inferior a 30 ng/mL sin inflamación; valores menores de 100 ng/mL con inflamación Reactante de fase aguda; depende del contexto clínico Estimación de las reservas de hierro
Hierro sérico, capacidad total de unión y saturación Hierro bajo, capacidad de unión elevada y saturación inferior al 20% Se modifican con inflamación, ayuno y métodos analíticos Complementa la ferritina y orienta el diagnóstico
Receptor soluble de transferrina Concentración elevada y mayor índice sTfR/log ferritina Disponibilidad limitada y posible interferencia en inflamación Resultado dudoso con ferritina no concluyente
Proteína C reactiva y reticulocitos Proteína C reactiva elevada y respuesta reticulocitaria baja No determinan por sí solos la causa Sitúa la ferropenia dentro del contexto inflamatorio

La强度 de la reposición no sustituye una búsqueda etiológica ordenada. Repeatedly treating an anemia caused by ongoing bleeding delays diagnosis and may obscure the clinical picture.

Reposición oral: indicaciones, dosis y seguimiento

El hierro oral es preferente en la mayoría de pacientes ambulatorios estables. Una presentación habitual es sulfato ferroso de 325 mg, que aporta 65 mg de hierro elemental. Una toma diaria o en días alternos suele offer a good balance between absorption and gastrointestinal tolerance; smaller fractional doses are generally unnecessary. The exact regimen should be adapted to the preparation, local formulary, laboratory response and the patient’s ability to adhere.

For optimal absorption, the tablet is preferably taken on an empty stomach. If nausea, epigastric discomfort or constipation appears, administration with food may improve adherence, although absorption decreases. Tea, coffee, calcium, antacids and other iron-containing supplements should not be taken at the same time. Vitamin C can increase absorption, but it has not demonstrated clinically relevant superiority in outcomes and should not be used to conceal poor tolerance or an inadequate dose. Active infection requires individual assessment before increasing iron.

Response should be checked systematically. Reticulocytes usually rise within 5–10 days, and hemoglobin commonly increases by 1–2 g/dL after four weeks. If this response is absent, clinicians should review adherence, continued bleeding, malabsorption, the dose and whether the original diagnosis was correct. Treatment is commonly continued for approximately three months after hemoglobin normalizes to replenish stores. Ferritin should then be interpreted with inflammation in mind; there is no universal target, and values around or above 50 ng/mL are often reasonable, with higher targets considered in selected inflammatory states.

Hierro intravenoso, transfusión y situaciones complejas

Intravenous iron may be appropriate when oral therapy is not tolerated or absorbed, when blood loss is likely to continue, or when rapid correction is clinically important because of severe symptoms, unstable cardiovascular disease or advanced kidney disease. It can increase hemoglobin more quickly than oral iron in selected patients, but evidence does not support routine use in every stable outpatient with iron deficiency anemia. The decision should consider the cause, severity, prognosis and feasibility of oral treatment.

Safety depends on the preparation and dose. Hypersensitivity reactions are uncommon, but iron sucrose and ferric derisomaltose are often preferred when repeated administrations are required. Ferric carboxymaltose carries a specific risk of hypophosphatemia, especially after repeated high doses. Renal function, phosphate concentration, total iron dose and the possibility of further administrations must be considered. Differences between guidelines can be examined through análisis de evidencia clínica, always checking the date and methodology of each publication.

Transfusion should be reserved for severe symptomatic anemia, hemodynamic instability, active bleeding or another compelling indication. In many stable adults, a restrictive strategy using a hemoglobin threshold around 7–8 g/dL is safer than liberal transfusion. The threshold must be individualized in patients with ischemic heart disease or other high-risk circumstances. Erythropoiesis-stimulating agents are not a substitute for iron and are reserved for specific renal or hematological indications under specialist supervision.

Cerrar el ciclo en atención primaria

Una consulta efficiently structured around iron deficiency should answer four questions sequentially: Is there biochemical evidence of iron deficiency, what is the mechanism, is oral treatment appropriate, and how will response be monitored? The information should be documented in the clinical record along with the drug, dose, adverse effects, investigations performed and the date of reassessment. Coordination with gastroenterology, hematology, nephrology or dietetic-nutritional support is valuable when the cause is complex or the initial response is absent.

Aplique este circuito en el próximo caso: confirme el déficit, documente la investigación etiológica, elija la vía de hierro según el riesgo y programe el control de hemoglobina y ferritina. Mantenga visible el objetivo más allá de corregir una cifra: devolver al paciente energía, seguridad y capacidad funcional,AWwhile preventing recurrence through early detection of the underlying cause.