Iron deficiency in non-anemic chronic obstructive pulmonary disease in a predominantly male population: an ignored entity.

Non-anemic iron deficiency has been studied in heart failure, but studies are lacking in chronic obstructive pulmonary disease (COPD). The potential clinical implications of association of iron deficiency with the severity of COPD warrant research in this direction. This was an observational, cross-sectional study on patients with COPD to compare disease severity, functional status and quality of life in non-anemic patients with COPD between two groups - iron deficient and non-iron deficient. Stable non-anemic COPD with no cause of bleeding were evaluated for serum iron levels, ferritin levels, TIBC, 6MWD, SGRQ, spirometry, and CAT questionnaire. The study patients were divided into iron replete (IR) and iron deficient (ID) groups. A total of 79 patients were studied, out of which 72 were men and seven were women. The mean age was 61.5±8.42 years. Of these, 36 (45.5%; 95% CI, 34.3-56.8%) had iron deficiency. Mean 6-minute-walk distance was significantly shorter in ID (354.28±82.4 meters vs 432.5±47.21 meters; p=0.001). A number of exacerbations in a year were more in ID group (p=0.003), and more patients in ID had at least two exacerbations of COPD within a year (p=0.001). However, the resting pO2, SaO2, and SpO2 levels did not differ significantly between the two groups (p=0.15 and p=0.52, respectively). Also, there was no significant difference in the distribution of patients of a different class of airflow limitations between the two groups. Non-anemic iron deficiency (NAID) is an ignored, yet easily correctable comorbidity in COPD. Patients with iron deficiency have a more severe grade of COPD, had lesser exercise capacity and more exacerbations in a year as compared to non-iron deficient patients. So, foraying into the avenue of iron supplementation, which has shown promising results in improving functional capacity in heart failure and pulmonary hypertension, may well lead to revolutionary changes in the treatment of COPD.

Acute toxicity assessment of choline by inhalation, intraperitoneal and oral routes in Balb/c mice.

Studies suggest that choline has potential to be used as a dietary supplement and a drug for immune inflammatory diseases like asthma and rhinitis. But there are apprehensions regarding adverse effects of choline when given orally in high doses. To address this knowledge gap, toxicity assessment of choline chloride was carried out by intranasal (i.n.), oral and intraperitoneal (i.p.) routes in Balb/c mice for 28days. Body weight, food and water consumption of mice were recorded daily. Hematology and clinical chemistry were assessed to check hepatocellular functions and morphological alterations of the cells. Splenocyte counts were analysed for evaluating cellular immunity. Liver function test was performed by assaying different enzyme systems in serum such as, urea, blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Body weight, food and water consumption did not differ between mice treated with choline and the saline control group. Hematologic and biochemical variables were not affected with any increase in serum toxicity marker enzymes indicating normal liver functioning. Choline administration did not affect total cholesterol and high density lipoprotein levels as compared to their respective controls. Urea and blood urea nitrogen levels in choline treated mice were not different than controls. Creatinine level was, however, higher than control in i.p. treatment group, but other parameters were normal. In conclusion, the repeated consumption of choline chloride via i.n. and oral or i.p. routes did not cause toxicity in mice in the toxicological endpoints examined.