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The Patient with Anemia and Iron Deficiency
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Haye H. van der Wal, Peter van der Meer
Heart failure (HF) is frequently accompanied by one or more comorbidities, which are associated with poorer quality of life and impaired prognosis. Anemia and iron deficiency are of particular importance, because of their high incidence and severe clinical consequences. Although HF treatment has dramatically improved in recent decades, there is still substantial morbidity and mortality, which is partially attributed to the impact of comorbidities. Thus, comorbidities are an attractive therapeutic target in HF. However, treatment of anemia in HF with erythropoiesis-stimulating agents did not improve outcomes. On the other hand, treating iron deficiency with intravenous iron seems more promising. In this chapter, we describe the etiology and pathophysiology of anemia and iron deficiency in HF, discuss the clinical consequences and diagnostic process, and review established and novel strategies for treatment of anemia and iron deficiency in HF.
Anemia as a Modifiable Risk Factor for NEC
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Use of erythropoiesis-stimulating agents (ESAs), including erythropoietin and darbepoetin, is one approach to prevent anemia by increasing endogenous hemoglobin production. One goal of ESA use is to reduce the need for RBC transfusion. A meta-analysis of 34 RCTs found early ESA use in the first week of life resulted in a decreased need for RBC transfusion (RR 0.79; 95% CI 0.74 to 0.85) and also a decreased risk for NEC (RR 0.69; 95% CI 0.52 to 0.91) (16). There was no similar effect observed in a meta-analysis examining late use of ESAs (after 7 days of age) (17). However, it is important to note that ESAs may have other effects that could mediate the observed effect in reducing NEC with early use, such as reducing intestinal inflammation (18) or regulation of intestinal barrier function (19), autophagy, and apoptosis (20).
Thalidomide
Published in Sarah H. Wakelin, Howard I. Maibach, Clive B. Archer, Handbook of Systemic Drug Treatment in Dermatology, 2015
Elaine Agius, Robert P.E. Sarkany
There is evidence that thalidomide requires cytochrome P450 (CYP450) catalysed biotransfomation to exert its pharmacological activity and that the CYP2C subfamily may be primarily involved. The potential for clinically relevant interactions with medicinal products appears to be low. Special precautions should be taken with: Beta-blockers or anticholinesterase agents (e.g. neostigmine), due to increased risk of bradycardia.Sedatives such as anxiolytics, hypnotics, antipsychotics, antihistamines, opiate derivatives, barbiturates and alcohol, due to thalidomide’s sedative effect.Drugs known to be associated with peripheral neuropathy (e.g. vincristine and bortezomib).Oral contraceptive pills and hormone replacement therapy, due to increased risk of venous thromboembolic disease.Erythropoiesis stimulating agents, due to a higher risk of thromboembolic reactions.Live vaccines since thalidomide is an immunosuppressant.
Is serum hemoglobin level an independent prognostic factor for IgA nephropathy?: a systematic review and meta-analysis of observational cohort studies
Published in Renal Failure, 2023
Kang Zhang, Meng-di Wang, Shang-shang Jiang, Long Tang, Yue-fen Wang, Yuan Meng, Zhen Cai, Xue-yan Sun, Fang-qiang Cui, Wen-jing Zhao
Although decreased Hb was significantly associated with poor prognosis of IgAN patients, whether early clinical intervention to renal anemia has renoprotective effects remains unknown. In IgAN, renal anemia is mainly caused by decreased erythropoietin (EPO) production [13]. Since 1989, erythropoiesis-stimulating agents (ESAs) have been applied to treat renal anemia [37,38]. ESAs have good curative effects in increasing Hb levels and reducing transfusion requirements. However, a large randomized controlled trial (RCT) conducted in 24 countries showed that in CKD patients who do not rely on dialysis, the use of darbepoetin alfa did not reduce ESRD risk and was associated with an increased risk of stroke [39]. As an inhibitor that specifically suppresses the enzymic activity of hypoxia-inducible factor prolyl hydroxylase enzyme, Roxadustat (FG-4592) has been demonstrated to be non-inferior to ESAs for improving hemoglobin in CKD patients [40,41]. Whether using FG-4592 will influence hard renal endpoints, including ESRD and mortality, remains unknown. Although an experimental study found that the HIF pathway might enhance kidney fibrosis [42], FG-4592 use did not suggest an increased risk of kidney fibrosis [43]. In contrast, in a mice model of ischemia/reperfusion（I/R）-induced acute kidney injury (AKI), FG-4592 protected tubular epithelial cells against hypoxia-induced injury by inhibiting inflammation [44]. Therefore, large RCTs are still needed to investigate whether HIF-PHI therapy at an earlier stage of Hb decline could delay the progression of kidney disease.
Approval of biosimilars: a review of unsuccessful regulatory filings
Published in Expert Opinion on Biological Therapy, 2021
Anurag S. Rathore, Hemlata Chhabra, Ankita Bhargava
EMA was the first regulatory agency to start reviewing applications for biosimilars approval. To date, EMA has approved 64 biosimilars within the product classes of 1) human growth hormone, 2) granulocyte colony-stimulating factor, 3) erythropoiesis-stimulating agent, 4) insulin, 5) follicle-stimulating hormone (FSH), 6) parathyroid hormone, 7) tumor necrosis factor (TNF) inhibitor, and 8) monoclonal antibodies for use in the EU [11]. Thus, far nine biosimilar approvals have been withdrawn after approval, one biosimilar has been withdrawn before approval, and two biosimilar applications have been refused by the agency (Table 1). This leaves a total of 55 biosimilars authorized for use in Europe [12]. In spite of the patent expiration in EU for Erbitux (cetuximab) and Aranesp (darbepoetin alfa) in 2014 and 2016, respectively, no biosimilars have been approved for the same. A number of biosimilar products for cetuximab including ABP-494 (Actavis/Amgen) and CT-P15 (Celltrion) are in development [13]. Two products, Retacrit (Hospira) and Silapo (Stada), are being approved by EMA for similar indications such as Aranesp including anemia, chronic kidney failure, cancer, and autologous blood transfusion. The reference medicine for both the products is Eprex/Erypo, which contains epoetin alpha as an active substance. [14]. Other blockbuster drugs that are set to lose their patents in the coming 2 years in Europe include Soliris (2020), Benlysta (2021), Lemtrada (2021), Avastin (2022), and Lucentis (2022) [15].
An evaluation of ferric derisomaltose as a treatment for anemia
Published in Expert Review of Hematology, 2021
Xenophon Kassianides, Richard Bodington, Sunil Bhandari
A number of observational studies have gone on to address re-treatment and erythropoiesis stimulating agent (ESA) requirements. The NIMO Scandinavia consortium reviewed the impact of FDI in NDD-CKD individuals, with regards to avoidance of re-treatment, and showed good efficacy irrespective of CKD stage. Sixty-five percent of participants did not require repeat treatment with iron over a 15-month period. A better result could have been potentially exhibited if all patients had received adequate iron doses to allow for optimal correction of iron deficiency; the most commonly administered dose in this study was 500 mg [39]. Additionally conversion of IV iron preparation from IS to FDI in 190 HD dependent patients indicated non-inferiority in terms of change in mean Hb per mg of iron administered and confirmed the efficacy of FDI (Hb and SF achieving significant increase) over 12 months [40]. Observational studies have suggested that FDI does not increase dose demand for ESAs [41] and can lead to potential cost-saving due to reduction in ESA dose requirements (698 NDD-CKD patients with IDA: Initial mean dose of ESA: 40,688 IU/month, final mean dose 35,665 IU/month, −13.7%; p < 0.001) [42].