UNASSIGNED: Anemia has been a common comorbidity in most chronic diseases, but has not been well monitored in type 2 diabetes mellitus (T2DM) patients. In this study, we investigated the prevalence of anemia and its nexus with iron stores among T2DM patients in health facilities in the Ashanti Region of Ghana.
UNASSIGNED: This multicenter cross-sectional study recruited 213 T2DM out-patients attending the diabetic clinics at the Kumasi South Hospital and St. Michaels Hospital, Jachie Pramso, Ghana, for routine check-ups. Self-reported questionnaires were used to collect sociodemographic, lifestyle, and clinical data from study participants. Blood samples were collected to estimate hematological parameters and iron stores. Mann-Whitney U test was used to assess the difference in hematological parameters and iron stores between anemic and nonanemic patients. All p < 0.05 were considered statistically significant.
UNASSIGNED: Of the 213 T2DM participants, the prevalence of anemia was 31.9%. More females 145 (68.1%) were registered than males 68 (31.9%). Anemic patients had significantly lower levels of mean cell volume [79.30/fL vs. 82.60/fL, p = 0.001], mean cell hemoglobin [26.60/pg vs. 27.90/pg, p < 0.0001], and mean cell hemoglobin concentration [33.10/g/dL) vs. 33.80/g/dL, p < 0.0001] than those without anemia. Serum levels of ferritin (p = 0.1140), transferrin (p = 0.5070), iron (p = 0.7950), and total iron binding capacity (p = 0.4610) did not differ significantly between T2DM patients with or without anemia.
UNASSIGNED: Despite the high prevalence of anemia among the T2DM patients in our cohort, patients present with apparently normal iron stores. This unrecognized mild anemia must be frequently monitored among T2DM patients.

暂无摘要。

Preclinical studies indicate iron deficiency (ID) plays an important role in cardiac remodelling. However, the relationship between ID and cardiac remodelling remains unknown in clinical setting. This retrospective study aims to identify a potential biomarker for the myocardial remodelling in patients with ID. Due to limited patients with ID are identified without iron deficiency anaemia (IDA), we analyse the relationship of total iron binding capacity (TIBC) and the left ventricular mass index (LVMI) in patients with iron deficiency anaemia.
A total of 82 patients with IDA exhibiting the diagnostic criteria for IDA were enrolled in the study. Among the patients, 65 had reported LVMI values. Subsequently, these patients were divided into two groups according to abnormal LVMI (> 115 g/m2 in men and > 95 g/m2 in women). Linear bivariate analysis was performed to detect the associations of haemoglobin or TIBC with clinical and echocardiographic characteristics. Simple linear regression analysis was used to evaluate the correlation between LVMI and the parameters of IDA, while multivariable linear analysis was used to assess the association of LVMI with age, TIBC and haemoglobin. Logistic regression analysis was utilized to determine the relationship of LV remodelling with anaemia severity and TIBC.
As compared with control group, the levels of TIBC in abnormal LVMI group are increased. Using log transformed LVMI as the dependent variable, simultaneously introducing age, TIBC, and haemoglobin into the simple linear regression or multivariable linear regression analysis confirmed the positive association among these factors. Bivariate correlation analysis reveals the irrelevance between haemoglobin and TIBC. In logistic regression analysis, TIBC is associated with the risk of LV remodelling.
Results of study indicate that TIBC exhibit an explicit association with LVMI in patients with iron deficiency anaemia. Logistic analysis further confirms the contribution of TIBC to abnormal LVMI incidence among this population with IDA.

Serum iron concentration is usually decreased in true iron deficiency and with inflammatory disease in man and domestic animals. Serum total iron binding capacity (TIBC) may be increased in true iron deficiency and decreased with inflammatory disease. This prospective study was designed to measure serum iron analytes in healthy free-ranging and housed Florida manatees (Trichechus manatus latirostris) of both sexes and various ages and to evaluate the effects of diseases common to manatees on these analytes. Blood samples were collected without anticoagulant from 137 healthy free-ranging manatees, 90 healthy housed manatees and 74 free-ranging diseased manatees, and serum was prepared by centrifugation. Serum iron concentration and unsaturated iron binding capacity were measured colourimetrically, and TIBC and percent transferrin saturation with iron were calculated. Serum amyloid A (SAA) was measured to assist in the health assessment of manatees and provide evidence of inflammation in diseased manatees. Based on the serum iron analytes, iron availability was lower in immature manatees compared with adults, and it was lower in housed manatees compared with free-ranging manatees. In contrast to other mammals studied, serum iron concentration was elevated rather than depressed in late pregnancy. Serum iron concentrations and transferrin saturation with iron percentages were significantly lower, and SAA concentrations were significantly higher, in diseased (ill and injured) manatees compared with healthy manatees. Serum iron concentration and transferrin saturation with iron values were negatively correlated with SAA concentrations, and manatees with the highest SAA concentrations had lower serum TIBC values. These findings indicate that inflammation is the major factor responsible for alterations in iron analytes in diseased manatees. Consequently, hypoferraemia may be used as supportive evidence of inflammatory disease in manatees (unless haemorrhage is also present). A decision threshold of ≤13.8 μmol/l was determined for hypoferraemia using receiver operating curve analysis. Based on studies in man and domestic animals, iron therapy is unnecessary for manatees with hypoferraemia associated with inflammation and has the potential for causing tissue damage and increased susceptibility to bacterial infections.

A range of interactions between gut microbiota and iron (Fe) metabolism is described. Oral probiotics ameliorate host\'s iron status. However, this has been proven for single-strain probiotic supplements. Dose-dependence of beneficial probiotic supplementation effect on iron turnover remains unexplored. Our study aimed to investigate the effects of oral multispecies probiotic supplementation in two doses on iron status in rats. Thirty rats were randomized into three groups receiving multispecies probiotic supplement at a daily dose of 2.5 × 109 CFU (PA group, n = 10) and 1 × 1010 CFU (PB group, n = 10) or placebo (KK group, n = 10). After 6 weeks, rats were sacrificed for analysis, blood samples, and organs (the liver, heart, kidneys, spleen, pancreas, femur, testicles, duodenum, and hair) were collected. The total fecal bacteria content was higher in the PB group vs. PA group. Unsaturated iron-binding capacity was higher in the PB group vs. KK group. Serum Fe was lower in both PA and PB vs. KK group. Iron content in the liver was higher in the PB group vs. KK group; in the pancreas, this was higher in the PB group vs. the KK and PA group, and in the duodenum, it was higher in both supplemented groups vs. the KK group. A range of alterations in zinc and copper status and correlations between analyzed parameters were found. Oral multispecies probiotic supplementation exerts dose-independent and beneficial effect on iron bioavailability and duodenal iron absorption in the rat model, induces a dose-independent iron shift from serum and intensifies dose-dependent pancreatic and liver iron uptake.

The aim of this study was to investigate the relationship between serum ferritin level and antioxidative status and metabolic dysregulation in young adult obese population. This cross-sectional study included 300 subjects of either sex, grouped as obese and non-obese subjects. The body mass index, total iron binding capacity, fasting blood glucose, superoxide dismutase activity, and levels of serum ferritin, iron, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, glutathione, and vitamin C were estimated. Analysis showed a significant alteration in all the parameters in obese adults. The correlation of ferritin level and body mass index showed a positive correlation (r = -0.81, p < 0.001, respectively) with levels of fasting blood glucose, superoxide dismutase, total cholesterol, low-density lipoprotein cholesterol, and triglyceride in obese individuals, whereas an insignificant correlation with vitamin C and glutathione level was observed in obese individuals. The significant positive correlation of ferritin level with the metabolic parameters and some antioxidative parameters in obese individuals signifies the development of metabolic disorders. Therefore, estimation of serum ferritin level will be an important early indicator for the risk of developing metabolic disorders in young adults.

UNASSIGNED: Iron is important for brain development and cognitive function. Iron deficiency may cause alteration of neurotransmitters and may be manifested by different central nervous system disorders including attention deficit hyperactivity disorder (ADHD).
UNASSIGNED: As studies are scarce in the Indian context, we had undertaken this study to find out the association between iron deficiency and ADHD.
UNASSIGNED: Hospital-based cross-sectional study.
UNASSIGNED: Hematological parameters indicating iron status (hemoglobin [Hb], ferritin, Iron, total iron binding capacity [TIBC], mean corpuscular volume [MCV], and mean corpuscular Hb [MCH]) were measured among 119 ADHD patients selected by complete enumeration method and 119 controls.
UNASSIGNED: Shapiro-Wilk test, Mann-Whitney U-test, Spearman\'s correlation, and binary logistic regression were used. P < 0.01 was taken as statistically significant.
UNASSIGNED: Hb, iron, ferritin, MCV, and MCH were lower among cases and negatively correlated to ADHD, while reverse is true for TIBC and ADHD. Iron deficiency anemia makes one 3.82 times more prone for ADHD.
UNASSIGNED: Iron deficiency was associated with ADHD.

In this study, the potential effect of three HFE gene polymorphisms (C282Y, H63D and S65C) and the SLC40A1 A77D polymorphism on iron balance was investigated in 234 subjects (91 Arab beta-thalassemia major (BTM) patients, 34 beta-thalassemia trait (BTT) individuals and 109 health controls). Genotyping was done using restriction-fragment-length polymorphism and direct-sequencing. Serum-iron, total iron binding capacity, transferrin and ferritin were estimated in all BTT and BTM, and in 65 healthy controls. H63D was the only polymorphism detected in our cohort. Allele frequency was 13% in both BTM and BTT and 10% in controls with no significant difference. Serum iron, ferritin and transferrin saturation were significantly higher in normal males heterozygous for H63D as compared to homozygous wild-type males. Ferritin was significantly higher in BTT males with or without H63D polymorphism when compared to the healthy males with H/H genotype. No such difference was observed between H/H versus H/D BTT subgroups. We conclude that H63D is the only significant hemochromatosis-associated polymorphism in the Arabian Gulf region. The heterozygous state of H63D may significantly alter iron parameters in normal males. In BTT, it appears that the beta-thalassemia allele has an overriding influence on ferritin values, and this generally manifest in males.

BACKGROUND: Gestational diabetes mellitus (GDM) is the most common metabolic disorder during pregnancy. GDM causes substantial morbidity and mortality and long- term complications. GDM-related risk factors have not been completely identified yet. Some studies have found relationship between increased serum ferritin and impaired oral glucose tolerance test but the relationship between serum ferritin and risk of GDM has been controversial. The aim of the study was to determine serum iron and ferritin levels and total iron binding capacity (TIBC) in women with GDM and comparison with normal pregnant women.
METHODS: This case-control study was performed among 200 pregnant women (case = 100, control = 100) who were referred to Yahya-Nejad Hospital in the second trimester in Babol from 2008 to 2009. GDM was diagnosed by impaired OGTT based on Carpenter and Coustan criteria. The 2 groups were matched in age, gestational age and parity.
RESULTS: High serum ferritin level increased the risk of gestational diabetes to 2.4-fold [OR = 2.4 (0.83-6.9) CI = 95% (P = 0.10)], while in those with low ferritin levels, the risk of developing gestational diabetes was reduced to 82% [OR = 0.8 with (0.08-0.37) CI = 95% (P = 0.001)]. Using the logistic regression model, after adjustment for BMI, the OR was 2.37 [(0.80-7.01) CI = 95% (P = 0.11)] for low ferritin level and OR = 0.20 [(0.09-0.44) CI = 95% (P = 0.0001)] for high ferritin level, which was statistically significant.
CONCLUSIONS: The serum ferritin level was markedly higher in women with gestational diabetes than in normal pregnant women; therefore, high ferritin can be regarded as a significant risk factor for the development of gestational diabetes.

BACKGROUND: We have examined iron biodistribution and hepatic gene expression in rats following administration of the generic Iron Sucrose Azad (ISA) or the reference iron sucrose drug Venofer®.
METHODS: ISA and Venofer® were administered intravenously to normal, non-anemic, male rats at 15 mg/kg (a supra-therapeutic dose-level). To evaluate biodistribution, tissue iron levels were determined over 28 days for plasma, liver, spleen, bone marrow, heart, kidney, lung and stomach using a validated ICP-MS method. Hepatic gene expression was evaluated by microarray analysis of mRNA from samples taken 24 h after drug administration.
RESULTS: Iron concentration/time profiles for plasma and tissues were quantitatively similar for ISA and Venofer. Following administration, circulating iron levels briefly exceeded transferrin binding capacity and there was a transient increase in hepatic iron. Bone marrow iron levels remained elevated throughout the study. No increases in tissue iron levels were observed in the heart, stomach or lungs. Spleen iron levels increased over the course of the study in treated and control rats. Small, transient increases were recorded in the kidneys of treated rats. The effects of ISA and Venofer® on hepatic gene transcription were similar. Principal components analysis showed that there was no systematic effect of either treatment on transcriptional profiles. Only a small number of genes showed significant modulation of expression. No transcriptional pattern matches with toxicity pathways were found in the ToxFX database for either treatment. No modulation of key genes in apoptosis, inflammation or oxidative stress pathways was detected.
CONCLUSIONS: These findings demonstrated that the biodistribution of administered iron is essentially similar for Iron Sucrose Azad and Venofer®, that iron sucrose partitions predominantly into the liver, spleen and bone marrow, and that hepatic gene expression studies did not provide any evidence of toxicity in animals treated at a supra-therapeutic dose-level.