Anaemia defined as a haemoglobin level <13 g/dl in men and <12 g/dl in women is common in older people and associated with numerous health consequences. The aim of this study was to systematically review all published data from the past 30 years that studied the association between anaemia and cognitive performance in people aged 65 years and over. An English and French Medline and Cochrane Library search ranging from 1979 to 2011 indexed under the Medical Subject Heading (MeSH) terms 'haemoglobin' or 'anaemia' combined with the terms 'dementia' or 'cognition disorders' or 'memory disorders' or 'orientation' or 'executive functions' or 'attention' or 'brain' or 'neuropsychological tests' was performed. Ninety-eight studies were selected. The following specific conditions were excluded: cancer, chronic kidney diseases, chronic heart disease and post-operative cognitive dysfunction. Five observational studies and six prospective cohort studies were included in the final analysis. According to the studies, the number of participants ranged from 302 to 2250 community-dwelling older people aged 55 years or over. Four studies considered the association between haemoglobin concentration and global cognitive functions, another three examined the association between haemoglobin concentration and the incidence of dementia, and four studies evaluated some specific aspects of cognition. A significant positive association was shown between anaemia and global cognitive decline as well as the incidence of dementia. A significant association was also shown between anaemia and executive functions. This systematic review shows a probable association between anaemia and cognitive performances, particularly with executive functions.

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This study aimed to investigate the association between vitamin D deficiency and anemia in a hospitalized geriatric population. An observational study, at the acute care geriatric unit of Brest Hospital, France, was conducted among 226 patients aged ≥70 years consecutively hospitalized between January 22, 2010 and August 9, 2010. Vitamin D and hemoglobin levels were measured. Vitamin D deficiency was defined as a 25(OH)D level <50 nmol/L and anemia as defined by the World Health Organization. After adjustment for albuminemia, anemia was not significantly associated with vitamin D deficiency (odds ratio (OR) = 1.37; 95 % confidence interval (CI) = 0.72-2.6). But anemia was significantly associated with hypoalbuminemia (OR = 2.08; 95 % CI = 1.11-3.91). Denutrition reflected by hypoalbuminemia could be a possible confounding factor in the previously described association between anemia and vitamin D deficiency.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• CYP2C9 and VKORC1 genetic variants contribute to differences in patients' responses to anticoagulant coumarin derivatives. Patients carrying the VKORC1 1173TT genotype have a decreased time to the first INR within the therapeutic range and to the first INR >4, and also require lower warfarin maintenance doses. Patients carrying the *2 or *3 CYP2C9 allele have lower maintenance warfarin requirements than those carrying the wild-type allele. The role of CYP2C9 and VKORC1 genetic variants in fluindione response is unknown. WHAT THIS STUDY ADDS• Our results showed that VKORC1 genotype had a significant impact on early anticoagulation (INR value Ն2 after the first two intakes) (P < 0.0001), on the time required to reach a first INR within the therapeutic range (P < 0.0001), on the time to obtain a first INR value >4 (P = 0.0002) and on the average daily dose of fluindione during the first period of stability (19.8 mg (Ϯ5.5) for VKORC1 CC, 14.7 mg (Ϯ6.2) for VKORC1 CT and 8.2 mg (Ϯ2.5) for VKORC1 TT, P < 0.0001). CYP2C9, CYP4F2 and EPHX1 genotypes did not significantly influence the response to fluindione. This report provides new information on the respective role of common genetic polymorphisms on anticoagulation induced by another class of anticoagulant drugs rather than coumarin derivatives. AIMGenetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9) and of a key pharmacologic target of vitamin K antagonists, vitamin K epoxide reductase (VKORC1), contribute to differences in patients' responses to coumarin derivatives. The role of these variants in fluindione response is unknown. Our aim was to assess whether genetic factors contribute to the variability in the response to fluindione. METHODSFour hundred sixty-five patients with a venous thromboembolic event treated by fluindione for at least 3 months with a target international normalized ratio (INR) of 2.0 to 3.0 were studied. VKORC1, CYP2C9, CYP4F2 and EPHX1 genotypes were assessed. INR checks, fluindione doses and bleeding events were collected. RESULTSVKORC1 genotype had a significant impact on early anticoagulation (INR value Ն2 after the first two intakes) (P < 0.0001), on the time required to reach a first INR within the therapeutic range (P < 0.0001) and on the time to obtain a first INR value > 4 (P = 0.0002). The average daily dose of fluindione during the first period of stability was significantly associated with the VKORC1 genotype: 19.8 mg (Ϯ5.5) for VKORC1 CC, 14.7 mg (Ϯ6.2) for VKORC1 CT and 8.2 mg (Ϯ2.5) for VKORC1 TT (P < 0.0001). CYP2C9, CYP4F2 and EPHX1 genotypes did not significantly influence the response to fluindione. CONCLUSIONSVKORC1 genotype strongly affected anticoagulation induced by fluindione whereas CYP2C9, CYP4F2 and EPHX1 genotypes seemed less determining.