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Iron is involved in many types of metabolism, including oxygen transport in hemoglobin. Iron deficiency (ID), ie a decrease in circulating iron, can have severe consequences. We provide an update on iron metabolism and ID, highlighting the particularities in older adults (OAs). There are three iron compartments in the human body: 1) the functional compartment, which consists of heme proteins including hemoglobin, myoglobin and respiratory enzymes; 2) iron reserves (IR), which consist mainly of liver stocks and are stored as ferritin; and 3) transferrin. There are two types of ID. Absolute ID is characterized by a decrease in IR. Its main pathophysiological mechanism is bleeding, which is often digestive and can be due to neoplasia, frequent in OAs. Biological assessment shows low serum ferritin and transferrin saturation (TS) levels. Furthermore, hypochromic microcytic anemia is frequent, and the serum-soluble transferrin receptor (sTfR) level is high. Functional ID, in which IR are high or normal, is due to inflammation, which is also frequent in OAs, particularly in its chronic form. Biological assessments show high serum ferritin, normal or low TS, and normal sTfR levels. Moreover, C-reactive protein is elevated, and there is moderate non-regenerative non-macrocytic anemia. The main characteristics of iron metabolism anomalies in the elderly are the high frequency of ID (20% of ID with anemia in adults ≥85 years) and the severity of its consequences, which include cognitive impairment in case of ID or iron overload and decrease of physical activity in case of ID. In conclusion, causes of ID are frequently intertwined in OAs as a result of the polymorbidity that characterizes them. ID can have dramatic consequences, especially in frail OAs. Thus, measuring the appropriate biological markers prevents errors in the positive diagnosis of ID type, clarifies etiology, and informs treatment-related decision-making.

Cardiovascular (CV) events are particularly frequent after acute pneumonia (AP) in the elderly. We aimed to assess whether cardiac troponin I, a specific biomarker of myocardial injury, independently predicts CV events and death after AP in older inpatients. Among 214 consecutive patients with AP aged ≥75 years admitted to a university hospital, 171 with a cardiac troponin I sample in the 72 h following diagnosis of AP were included, and 71 (42%) were found to have myocardial injury (troponin > 100 ng/L). Patients with and without myocardial injury were similar in terms of age, gender and comorbidities, but those with myocardial injury had more severe clinical presentation (median (interquartile range) Pneumonia Severity Index: 60 (40–95) vs. 45 (30–70), p = 0.003). Myocardial injury was strongly associated with in-hospital myocardial infarction (25% vs. 0%, p < 0.001), CV mortality (11 vs. 1%, p = 0.003) and all-cause mortality (34 vs. 13%, p = 0.002). After adjustment for confounders, myocardial injury remained a strong predictive factor of in-hospital mortality (odds ratio (95% confidence interval): 3.32 (1.42–7.73), p = 0.005) but not one-year mortality (1.61 (0.77–3.35), p = 0.2). Cardiac troponin I elevation, a specific biomarker of myocardial injury, was found in nearly half of an unselected cohort of older inpatients with AP and was associated with a threefold risk of in-hospital death.

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