Scientific Clinical Institutes Maugeri, IRCCS Lumezzane, Cardiac Rehabilitation Division, Lumezzane, 25065 Brescia, Italy.
Division of Human Anatomy and Physiopathology, Department of Clinical and Experimental Sciences, University of Brescia, 25065 Brescia, Italy.
Nutrients. 2021 Jan 15;13(1):237. doi: 10.3390/nu13010237.
Chronic diseases are characterised by altered autophagy and protein metabolism disarrangement, resulting in sarcopenia, hypoalbuminemia and hypo-haemoglobinaemia. Hypo-haemoglobinaemia is linked to a worse prognosis independent of the target organ affected by the disease. Currently, the cornerstone of the therapy of anaemia is iron supplementation, with or without erythropoietin for the stimulation of haematopoiesis. However, treatment strategies should incorporate the promotion of the synthesis of heme, the principal constituent of haemoglobin (Hb) and of many other fundamental enzymes for human metabolism. Heme synthesis is controlled by a complex biochemical pathway. The limiting step of heme synthesis is D-amino-levulinic acid (D-ALA), whose availability and synthesis require glycine and succinil-coenzyme A (CoA) as precursor substrates. Consequently, the treatment of anaemia should not be based only on the sufficiency of iron but, also, on the availability of all precursor molecules fundamental for heme synthesis. Therefore, an adequate clinical therapeutic strategy should integrate a standard iron infusion and a supply of essential amino acids and vitamins involved in heme synthesis. We reported preliminary data in a select population of aged anaemic patients affected by congestive heart failure (CHF) and catabolic disarrangement, who, in addition to the standard iron therapy, were treated by reinforced therapeutic schedules also providing essential animo acids (AAs) and vitamins involved in the maintenance of heme. Notably, such individualised therapy resulted in a significantly faster increase in the blood concentration of haemoglobin after 30 days of treatment when compared to the nonsupplemented standard iron therapy.
慢性疾病的特征是自噬和蛋白质代谢紊乱,导致肌肉减少症、低白蛋白血症和低血红蛋白血症。低血红蛋白血症与疾病影响的靶器官无关,与预后较差相关。目前,贫血治疗的基石是铁补充剂,可与促红细胞生成素联合使用以刺激造血。然而,治疗策略应包括促进血红素的合成,血红素是血红蛋白(Hb)和许多其他人类代谢基本酶的主要成分。血红素合成受复杂的生化途径控制。血红素合成的限速步骤是 D-氨基-γ-酮戊酸(D-ALA),其可用性和合成需要甘氨酸和琥珀酰辅酶 A(CoA)作为前体底物。因此,贫血的治疗不应仅基于铁的充足性,还应基于血红素合成所需的所有前体分子的可用性。因此,适当的临床治疗策略应整合标准铁输注以及涉及血红素合成的必需氨基酸和维生素的供应。我们在一组患有充血性心力衰竭(CHF)和分解代谢紊乱的老年贫血患者中报告了初步数据,除了标准铁治疗外,这些患者还接受了强化治疗方案,该方案还提供了维持血红素所需的必需氨基酸(AAs)和维生素。值得注意的是,与未补充标准铁治疗相比,这种个体化治疗在 30 天的治疗后可使血红蛋白的血液浓度更快地增加。