RESUMEN

La anemia de las enfermedades crónicas (AEC) se genera por la activación del sistema inmune por autoantígenos, moléculas microbianas o antígenos tumorales, que dan lugar a la liberación de citocinas que originan una elevación de la hepcidina sérica, hiposideremia, supresión de la eritropoyesis, disminución de la eritropoyetina (EPO) y acortamiento de la vida media de los hematíes. La anemia suele ser normocítica/normocrómica, es la más prevalente, después de la anemia ferropénica, y es la más frecuente en los ancianos y en los pacientes hospitalizados. Si la anemia es grave, la calidad de vida del paciente se deteriora y puede tener un impacto negativo en la supervivencia. El objetivo del tratamiento va dirigido a controlar la enfermedad de base y a corregir la anemia. En ocasiones se ha utilizado hierro endovenoso y EPO, pero el futuro terapéutico va dirigido contra la hepcidina, que es la diana responsable final de la anemia. (AU)

Anaemia of chronic disease (ACD) is generated by the activation of the immune system by autoantigens, microbial molecules or tumour antigens resulting in the release of cytokines that cause an elevation of serum hepcidin, hypoferraemia, suppression of erythropoiesis, decrease in erythropoietin (EPO) and shortening of the half-life of red blood cells. Anaemia is usually normocytic and normochromic, which is the most prevalent after iron deficiency anaemia, and it is the most frequent in the elderly and in hospitalized patients. If the anaemia is severe, the patient's quality of life deteriorates, and it can have a negative impact on survival. Treatment is aimed at controlling the underlying disease and correcting anaemia. Sometimes intravenous iron and EPO have been used, but the therapeutic future is directed against hepcidin, which is the final target of anaemia. (AU)

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RESUMEN

Anaemia of chronic disease (ACD) is generated by the activation of the immune system by autoantigens, microbial molecules or tumour antigens resulting in the release of cytokines that cause an elevation of serum hepcidin, hypoferraemia, suppression of erythropoiesis, decrease in erythropoietin (EPO) and shortening of the half-life of red blood cells. Anaemia is usually normocytic and normochromic, which is the most prevalent after iron deficiency anaemia, and it is the most frequent in the elderly and in hospitalized patients. If the anaemia is severe, the patient's quality of life deteriorates, and it can have a negative impact on survival. Treatment is aimed at controlling the underlying disease and correcting anaemia. Sometimes intravenous iron and EPO have been used, but the therapeutic future is directed against hepcidin, which is the final target of anaemia.

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BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder in which airflow is obstructed. Viral or bacterial upper respiratory tract infections (URTIs) may lead to exacerbations. Homeopathic medication administration to COPD patients during the influenza-exposure period may help to reduce the frequency of common URTIs. METHODS: This prospective, observational, multicenter study was carried out in Cantabria, Spain. Patients with COPD were divided into two groups: group 1 received conventional treatment + homeopathic medication (diluted and dynamized extract of duck liver and heart; Boiron) (OG); group 2 received conventional treatment only (CG). The primary endpoint was the number of URTIs between the 4-5 months follow up (mean 4.72 ± 0.96) from basal to last visit. Secondary endpoints included the duration of URTIs, number and duration of COPD exacerbations, use of COPD drugs, changes in quality of life (QoL), compliance, and adverse events (AEs). RESULTS: 219 patients were analyzed (OG = 109, CG = 110). There was a significant reduction in mean number of URTIs during the follow-up period in OG compared to CG (0.514 ±â€¯0.722 vs. 1.037 ±â€¯1.519, respectively; p = 0.014). Logistic regression analysis showed a 3.3-times higher probability of suffering ≥2 URTI episodes in CG (p = 0.003, n = 72). OG patients having ≥1 URTI also had a significant reduction in mean URTI duration per episode (3.57 ±â€¯2.44 days OG vs. 5.22 ±â€¯4.17 days CG; p = 0.012). There was no significant difference in mean number of exacerbations, mean duration of exacerbations, or QoL between OG and CG. There was a greater decrease in proportion of patients using corticosteroids for exacerbations between baseline and visit 2 in OG compared to CG (22.1% vs. 7.5% fewer respectively, p = 0.005). Exacerbator phenotype patients had a significant decrease in number of URTIs (0.54 ±â€¯0.72 vs. 1.31 ±â€¯1.81; p = 0.011), and fewer COPD exacerbations (0.9 ±â€¯1.3 vs. 1.5 ±â€¯1.7; p = 0.037) in OG vs. CG, respectively. CONCLUSIONS: Homeopathic medication use during the influenza-exposure period may have a beneficial impact at reducing URTIs' number and duration in COPD patients and at reducing the number of COPD exacerbations in patients with the exacerbator phenotype. Further studies are needed to confirm the effects observed in this study.

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La hepcidina es el principal regulador del metabolismo del hierro y el factor patogénico más importante en sus trastornos. La deficiencia de hepcidina provoca sobrecarga de hierro, mientras que su exceso da lugar o contribuye al desarrollo de anemias por déficit o restricción de hierro en las enfermedades crónicas. Conocemos los mecanismos implicados en la síntesis de hepcidina y, en condiciones fisiológicas, hay un equilibrio entre las señales activadoras e inhibidoras que regulan su síntesis. Las primeras incluyen las relacionadas con la concentración plasmática de hierro y con las enfermedades inflamatorias. Las señales inhibidoras más importantes están relacionadas con la eritropoyesis activa y con la matriptasa-2. Conocer cómo se sintetiza la hepcidina ha servido para diseñar nuevos tratamientos farmacológicos cuya diana principal es la hepcidina. En un futuro próximo, se dispondrá de tratamientos eficaces dirigidos a corregir el defecto de muchos de los trastornos del metabolismo del hierro (AU)

Hepcidin is the main regulator of iron metabolism and a pathogenic factor in iron disorders. Hepcidin deficiency causes iron overload, whereas hepcidin excess causes or contributes to the development of iron-restricted anaemia in chronic inflammatory diseases. We know the mechanisms involved in the synthesis of hepcidin and, under physiological conditions, there is a balance between activating signals and inhibitory signals that regulate its synthesis. The former include those related to plasmatic iron level and also those related to chronic inflammatory diseases. The most important inhibitory signals are related to active erythropoiesis and to matriptase-2. Knowing how hepcidin is synthesised has helped design new pharmacological treatments whose main target is the hepcidin. In the near future, there will be effective treatments aimed at correcting the defect of many of these iron metabolism disorders (AU)

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RESUMEN

Hepcidin is the main regulator of iron metabolism and a pathogenic factor in iron disorders. Hepcidin deficiency causes iron overload, whereas hepcidin excess causes or contributes to the development of iron-restricted anaemia in chronic inflammatory diseases. We know the mechanisms involved in the synthesis of hepcidin and, under physiological conditions, there is a balance between activating signals and inhibitory signals that regulate its synthesis. The former include those related to plasmatic iron level and also those related to chronic inflammatory diseases. The most important inhibitory signals are related to active erythropoiesis and to matriptase-2. Knowing how hepcidin is synthesised has helped design new pharmacological treatments whose main target is the hepcidin. In the near future, there will be effective treatments aimed at correcting the defect of many of these iron metabolism disorders.

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