Anaemia in heart failure patients: the prevalence of haematinic deficiencies and the role of ACE inhibitors and aspirin doses as risk factors

Background: Patients with heart failure often have comorbidities that alter the progression of heart failure and impact on prognosis. One such comorbidity is anaemia, and clinicians have started to appreciate the full gravity of its impact on heart failure patients. Yet, the extent of the problem is not fully understood, particularly the role of heart failure therapy itself as a risk factor for developing anaemia. Objective: This study aimed to investigate the prevalence of anaemia in a cohort of heart failure patients. The impact of using different ACEIs and different doses of aspirin was also explored, together with the prevalence of haematinic deficiencies. Methods: Medication lists and pathology results were examined to establish the prevalence of ACEIs use, and the use of aspirin at its most common doses of 100mg and 150mg, together with haematinic deficiencies. Multinomial logistic regression and the Student’s t-test were utilised for the analysis of data. Statistical significance was pre-set at p<0.05. Results: Ninety-six patients were eligible for analysis, with 26% having anaemia. The use of ACEIs had a RR of 17.4 for the presence of anaemia. Perindopril was associated with a RR of 20.8, while the use of ramipril was not significantly associated with such a high RR. Haematinic anaemia occurred only at a rate of 3.3%, but borderline deficiencies were found in more than a third of all patients. An aspirin dose of 150mg was associated with a higher risk for anaemia, compared to a dose of 100mg. Conclusions: ACEIs are associated with the presence of anaemia, with perindopril posing more risk than ramipril when used in heart failure patients. The dose of aspirin may also be a factor in the development of anaemia, with lower doses being safer. Despite the lack of high prevalence of haematinic anaemia among this cohort of patients, borderline haematinic deficiencies were common

Combined Omics Reveals That Disruption of the Selenocysteine Lyase Gene Affects Amino Acid Pathways in Mice

Selenium is a nonmetal trace element that is critical for several redox reactions and utilized to produce the amino acid selenocysteine (Sec), which can be incorporated into selenoproteins. Selenocysteine lyase (SCL) is an enzyme which decomposes Sec into selenide and alanine, releasing the selenide to be further utilized to synthesize new selenoproteins. Disruption of the selenocysteine lyase gene (Scly) in mice (Scly&minus;/&minus; or Scly KO) led to obesity with dyslipidemia, hyperinsulinemia, glucose intolerance and lipid accumulation in the hepatocytes. As the liver is a central regulator of glucose and lipid homeostasis, as well as selenium metabolism, we aimed to pinpoint hepatic molecular pathways affected by the Scly gene disruption. Using RNA sequencing and metabolomics, we identified differentially expressed genes and metabolites in the livers of Scly KO mice. Integrated omics revealed that biological pathways related to amino acid metabolism, particularly alanine and glycine metabolism, were affected in the liver by disruption of Scly in mice with selenium adequacy. We further confirmed that hepatic glycine levels are elevated in male, but not in female, Scly KO mice. In conclusion, our results reveal that Scly participates in the modulation of hepatic amino acid metabolic pathways