Serum ferritin at admission in hospitalized COVID-19 patients as a predictor of mortality

IntroductionSome COVID-19 patients have higher mortality and the responsible factors for this unfavorable outcome is still not well understood.ObjectiveTo study the association between ferritin levels at admission, representing an inflammatory state, and hospital mortality in COVID-19 patients.MethodsFrom May through July 2020, SARS-CoV-2 positive patients with moderate to severe clinical symptoms were evaluated at admission, regarding clinical and laboratory data on renal and hepatic function, hematologic parameters, cytomegalovirus co-infection, and acute phase proteins.ResultsA total of 97 patients were included; mean age = 59.9 ± 16.3 years, 58.8% male, 57.7% non-white, in-hospital mortality = 45.4%. Age, ferritin, C-reactive protein, serum albumin and creatinine were significantly associated with mortality. Ferritin showed area under the curve (AUC) of 0.79 (p < 0.001) for the cut-off of 1873.0 ng/mL, sensitivity of 68.4% and specificity of 79.3% in predicting in-hospital mortality. Age ≥60 years had an odds ratio (OR) of 10.5 (95% CI = 1.8–59.5; p = 0.008) and ferritin ≥1873.0 ng/mL had an OR of 6.0 (95% CI = 1.4–26.2; p = 0.016), both independently associated with mortality based on logistic regression analysis.ConclusionThe magnitude of inflammation present at admission of COVID-19 patients, represented by high ferritin levels, is independently predictive of in-hospital mortality.     

The early cardiac involvement in patients with β-thalassemia major

BackgroundCardiac complications, heart failure and arrhythmias remain the major causes of death in thalassemia major.AimTo detect the early cardiac involvement in β-thalassemic patients.Patients and methods56 Patients (pts) with β-thalassemia major and transfusion burden ?12 times/year (age 6–16 years) were included in our study, classified into three groups according to serum ferritin, group I: 21 pts with ferritin level <2500 ng/ml, group II: 23 pts with ferritin level 2500–5000 and group III: 12 pts with ferritin level >5000 ng/ml. They were subjected to detailed clinical evaluation, routine laboratory investigations, serum ferritin level, ECG {corrected QT intervals (QTc) and QT dispersion(QTd)}, echocardiography for measurement of left atrial (LA) active emptying fraction, Systolic (peak systolic wave, Q–S peak duration) and diastolic functions of left ventricle using standard and tissue Doppler imaging (TDI).ResultsGroups III and II showed a significant increase in LV septal and posterior wall thickness than group I while QTc and QTd were increased significantly only in group III compared to group I (P = 0.00, 0.01). LV diastolic function and LA active emptying fraction were significantly impaired in group III and II compared to group I while LV systolic function parameters by TDI were impaired significantly in group III compared to group I with insignificant difference by standard echocardiography.ConclusionThe increase in LV septal and posterior wall thickness precedes ECG changes. Also LV diastolic dysfunction and impaired LA active emptying fraction precede LV systolic dysfunction.     

Circulating Bcl-2 concentrations and septic patient mortality

IntroductionThere are not data on blood B-cell lymphoma 2 (Bcl-2) concentrations (one of the antiapoptotic molecules of the Bcl-2 family in the intrinsic apoptosis pathway) in septic patients. Therefore, this study was carried with the aims to explore whether blood Bcl-2 concentrations at diagnosis of sepsis are different in survivor and non-survivor septic patients, are associated with mortality, and are useful for the mortality prediction.MethodsIntensive Care Units from 3 Spanish hospitals participated in this observational and prospective study with septic patients and serum Bcl-2 concentrations at diagnosis of sepsis were determined. Mortality at 30 days was as outcome variable.ResultsWe found that 30-day non-surviving patients (n = 81) showed lower serum Bcl-2 levels (p = 0.003) than surviving patients (n = 140). We found that serum concentrations of Bcl-2 < 4.4 ng/mL were associated with mortality (OR = 3.228; 95% CI = 1.406–7.415; p = 0.006) in the multiple logistic regression analysis, and that showed an area under the curve for mortality prediction of 62% (95% CI = 55–68%; p = 0.003).ConclusionsIn our study appears novel findings such as higher blood Bcl-2 concentrations in survivor than in non-survivor septic patients, the association between low blood Bcl-2 concentrations and mortality of septic patients, and the ability of blood Bcl-2 concentrations for the prediction of septic patient mortality.     

Association of serum soluble Fas concentrations and mortality of septic patients

IntroductionScarce data on Fas, one of the main receptors that activates the apoptosis extrinsic pathway, in septic patients exists. Higher blood soluble Fas (sFas) concentrations in non-survivor septic patients compared with survivors have been found in small studies; however, the association of blood sFas concentrations with mortality controlling for sepsis severity has not been stablished due to this small sample size in those studies. Thus, our main objective study was to determine whether an association between blood sFas concentrations and sepsis mortality controlling for sepsis severity exists.MethodsWe included septic patients in this observational and prospective study carried out in three Spanish Intensive Care Units. We obtained serum samples at sepsis diagnosis sepsis for sFas levels determination.ResultsThirty-day non-surviving patients (n = 85) compared to surviving patients (n = 151) had higher serum sFas levels (p < 0.001). We found in multiple logistic regression analysis an association of serum sFas levels with mortality controlling for age and SOFA (OR = 1.004; 95% CI = 1.002–1.006; p < 0.001), and for age and APACHE-II (OR = 1.004; 95% CI = 1.002–1.006; p < 0.001). Serum sFas levels showed and area under the curve for mortality prediction of 71% (95% CI = 65–71%; p < 0.001). Kaplan–Meier analysis showed higher mortality rate in patients with serum sFas levels > 83.5 ng/mL (Hazard ratio = 3.2; 95% CI = 2.1–5.0; p < 0.001).ConclusionsThat an association between blood sFas concentrations and sepsis mortality controlling for sepsis severity exists was our main new finding study.     

Viral eradication restores normal iron status in chronic hepatitis C patients with abnormal iron studies

Introduction and objectivesAbnormal serum iron studies are seen in a third or more of patients with chronic hepatitis C infection (HCV), where they have been linked to accelerated fibrosis progression and increased risk of hepatocellular carcinoma and sometimes lead to concern for coexisting hereditary hemochromatosis. The aim of this study was to assess the effect of HCV eradication in patients with abnormal serum iron studies prior to treatment with direct-acting antiviral agents (DAAs).PatientsHCV-infected subjects with iron studies obtained before and after successful treatment with DAAs were identified (n = 27). All had one or more abnormal iron test before treatment.ResultsFollowing HCV eradication, serum iron, transferrin-iron saturation and ferritin levels decreased significantly (pre- versus post-treatment, p < 0.01 for each). Serum iron and/or transferrin-iron saturations normalized in 16/19 subjects and raised ferritin levels returned to the normal range in 14/18 subjects, including several with pretreatment transferrin-iron saturation >90% and/or serum ferritin >1000 ng/mL. Elimination of HCV infection was associated with a significant reduction in post-treatment ferritin levels even among subjects whose ferritin levels were within normal limits at baseline. Risk factors for other conditions associated with abnormal iron status were present in the few cases in which iron studies failed to normalize following DAA treatment.ConclusionsEradication of HCV infection restores normal iron status in most patients with abnormal iron tests, including those whose baseline parameters are suggestive of hemochromatosis.     

Evaluation of trefoil factor 3 as a non-invasive biomarker of gastric intestinal metaplasia and gastric cancer in a high-risk population

BackgroundAdenocarcinoma is preceded by chronic atrophic gastritis, gastric intestinal metaplasia and dysplasia. Trefoil factor 3 (TFF3) is a peptide secreted by goblet cells, which is abundantly present in intestinal metaplasia.AimTo evaluate the utility of serum TFF3 as a non-invasive biomarker for the diagnosis of intestinal metaplasia and gastric cancer.MethodsSingle-center, cross-sectional study of 274 patients who consecutively underwent upper gastrointestinal endoscopy with gastric biopsies (updated Sydney system). TFF3 levels were measured in serum by a commercial ELISA kit. Patients with normal histology or chronic atrophic gastritis without intestinal metaplasia comprised the control group. In addition, 14 patients with invasive gastric cancer were included as a reference group. The association between TFF3 levels and intestinal metaplasia was assessed by logistic regression.ResultsPatients with intestinal metaplasia (n = 110) had a higher median TFF3 level as compared to controls (n = 164), 13.1 vs. 11.9 ng/mL, respectively (p = 0.024). Multivariable logistic regression showed a no significant association between TFF3 levels and intestinal metaplasia (OR = 1.20; 95%CI: 0.87–1.65; p-trend = 0.273). The gastric cancer group had a median TFF3 level of 20.5 ng/mL, and a significant association was found (OR = 3.26; 95%CI: 1.29–8.27; p-trend = 0.013).ConclusionSerum levels of TFF3 do not discriminate intestinal metaplasia in this high-risk Latin American population. Nevertheless, we confirmed an association between TFF3 levels and invasive gastric cancer.     

High serum matrix metalloproteinase-9 level predict increased risk of in-hospital cardiac events in patients with type 2 diabetes and ST segment elevation myocardial infarction

IntroductionThe purpose of this study was to compare serum matrix metalloproteinase (MMP)-9 levels in a population of type 2 diabetic versus non-diabetic patients hospitalized with ST-segment elevation myocardial infarction (STEMI) and to examine the relationship between serum MMP-9 levels and the incidence of in-hospital cardiac events, including death and cardiogenic shock.MethodsWe recruited 120 patients with STEMI, of whom 48 were type 2 diabetic and 72 non-diabetic. Serum MMP-9 levels were measured on admission, using a commercially available ELISA. The primary study endpoint was cardiac death in-hospital and cardiogenic shock.ResultsMean serum MMP-9 levels were significantly higher in type 2 diabetic patients compared to non-diabetic patients (240 ± 52 ng/mL versus 185 ± 47 ng/mL; P < 0.0001). In multivariable analysis, type 2 diabetes was an independent factor for mortality [OR: 1.75 (1.40–2.30); P = 0.005] and cardiogenic shock [OR: 1.55 (1.20–1.70); P = 0.03] when the variable MMP-9 level was not introduced into the model, but it was less significantly associated with mortality [OR: 1.60 (1.40–2.10); P = 0.01] and no longer associated with cardiogenic shock when MMP-9 was in the model.ConclusionAfter STEMI, type 2 diabetes is independently associated with high serum MMP-9 levels. This elevated MMP-9 is strongly associated with the increased incidence of in-hospital mortality and cardiogenic shock observed in type 2 diabetes. Our findings clearly indicate that serum MMP-9 provides a highly valuable prognostic information on in-hospital outcome after STEMI, in particular in type 2 diabetic patients.     

Serum levels of Apelin-36 are decreased in older hospitalized patients with heart failure

PurposeApelin is an endogenous peptide, it is a potent inotropes, a peripheral vasodilator, involved in fluid homeostasis, balancing the harmful effects of Ang-II-AT1 system. The apelin-APJ axis is down regulated in chronic heart failure (CHF), but the role of apelin has not yet been studied in elderly patients with CHF. The aim of our study is to investigate serum levels of apelin-36 in a group of older subjects with CHF.Subjects/Materials and methodsThe study population consisted of 30 consecutive patients aged 80 ± 7.8 years with CHF. Serum apelin levels were quantified by enzyme immunoassay (ELISA). Results were considered significant if P was < 0.05.ResultsMean values of apelin-36 in CHF patients were 0.47 ± 0.21 ng/mL, and 0.95 ± 0.37 ng/mL in control subjects (P < 0.0001). Patients in IV NYHA class showed lower levels of apelin (0.38 ± 0.16 ng/mL). Direct correlations between apelin levels and ADLs (P = 0.0008, r = 0.61), and IADLs (P = 0.008, r = 0.50) were observed.Discussion and conclusionsThis study confirms that apelin levels are decreased in patients with CHF, also in the elderly and frail; since apelin represents a potential, promising novel therapeutic target for patients with CHF, geriatric patients should be considered for future clinical trials.     

Increased level of resistin predicts development of atrial fibrillation

BackgroundResistin is a peptide hormone that is secreted from lipid cells and is linked to type-2 diabetes, obesity, and inflammation. Being an important adipocytokine, resistin was proven to play an important role in cardiovascular disease. We compared resistin levels in patients with and without atrial fibrillation (AF) to demonstrate the relationship between plasma resistin levels and AF.MethodOne hundred patients with AF and 58 control patients who were matched in terms of age, gender, and risk factors were included in the trial. Their clinical risk factors, biometric measurements, echocardiographic work up, biochemical parameters including resistin and high-sensitivity C-reactive protein (hs-CRP) levels were compared.ResultsIn patients with AF, plasma resistin levels (7.34 ± 1.63 ng/mL vs 6.67 ± 1.14 ng/mL; p = 0.003) and hs-CRP levels (3.01 ± 1.54 mg/L vs 2.16 ± 1.28 mg/L; p = 0.001) were higher than control group. In subgroup analysis, resistin levels were significantly higher in patients with paroxysmal (7.59 ± 1.57 ng/mL; p = 0.032) and persistent AF (7.73 ± 1.60 ng/mL; p = 0.006), but not in patients with permanent AF subgroups (6.86 ± 1.61 ng/mL; p = 0.92) compared to controls. However, hs-CRP levels were significantly higher only in permanent AF patients compared to control group (3.26 ± 1.46 mg/L vs 2.16 ± 1.28 mg/L; p = 0.02). In multivariate regression analysis using model adjusted for age, gender, body mas index, hypertension, diabetes mellitus, and creatinine levels, plasma resistin levels [odds ratio (OR): 1.30; 95% confidence interval (CI): 1.01–1.70; p = 0.04] and hs-CRP levels (OR: 1.44; 95% CI: 1.12–1.86; p = 0.004) were the only independent predictors of AF.ConclusionThe elevated levels of plasma resistin were related to paroxysmal AF group and persistent AF group, but not to permanent AF group.     

Serum Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Predicting Worsening Renal Function in Acute Decompensated Heart Failure

BackgroundThe development of worsening renal function (WRF, defined as creatinine rise ≥0.3 mg/dL) occurs frequently in the setting of acute decompensated heart failure (ADHF) and strongly predicts adverse clinical outcomes. Neutrophil gelatinase–associated lipocalin (NGAL) is produced by the nephron in response to tubular epithelial damage and serves as an early marker for acute renal tubular injury. We sought to determine the relationship between admission serum NGAL levels and WRF in the setting of ADHF.Methods and ResultsWe measured serum NGAL levels in 91 patients admitted to the hospital with ADHF. Patients were adjudicated by independent physician into those that did or did not develop WRF over the ensuing 5 days of in-hospital treatment. In our study cohort (68% male, mean age 61 ± 15 years, mean left ventricular ejection fraction 31 ± 14%), median admission serum NGAL level was 165 ng/mL (interquartile range [IQR] 108–235 ng/mL). Thirty-five patients (38%) developed WRF within the 5-day follow-up. Patients who developed WRF versus those without WRF had significantly higher median admission serum NGAL levels (194 [IQR 150–292] ng/mL vs. 128 [IQR 97–214] ng/mL, P = .001). High serum NGAL levels at admission were associated with greater likelihood of developing WRF (odds ratio: 1.92, 95% confidence interval 1.23–3.12, P = .004). In particular, admission NGAL ≥140 ng/mL had a 7.4-fold increase in risk of developing WRF, with a sensitivity and specificity of 86% and 54%, respectively.ConclusionsThe presence of elevated admission serum NGAL levels is associated with heightened risk of subsequent development of WRF in patients admitted with ADHF.     

Intravenous Iron Replacement Improves Exercise Tolerance in COPD: A Single-Blind Randomized Trial

IntroductionIron deficiency affects exercise capacity because of the critical role iron plays in the optimal functioning of skeletal muscle metabolism. We hypothesized that intravenous iron may improve exercise tolerance, quality of life (QoL), and daily physical activity (DPA) in patients with chronic obstructive pulmonary disease (COPD).MethodsThis was a placebo-controlled, single-blind, parallel-group, randomized clinical trial. Iron deficiency was defined as a ferritin level < 100 ng/mL or a ferritin level between 100 and 299 ng/mL with a transferrin saturation < 20%, with or without mild anaemia. Patients were randomized at a 2:1 ratio to receive intravenous ferric carboxymaltose or placebo. The primary objective was to investigate whether intravenous iron replacement improved endurance time from baseline by at least 33%. The secondary objectives were to evaluate impact on QoL using the COPD Assessment Test (CAT) and on DPA by accelerometry.ResultsWe included 66 patients, 44 (66.7%) in the intervention group and 22 (33.3%) in the placebo group. Among patients receiving ferric carboxymaltose, 23 (52.3%) achieved the primary endpoint compared to 4 (18.2%) in the placebo group [p = 0.009; relative risk 3.12, (95% CI, 1.19–8.12)]. CAT score decreased ?3 (?6.0–1.3) points from baseline in the intervention group (p = 0.007), in contrast to placebo group [?1 (?4.0–2.3) points, p = 0.236] with no differences in DPA and adverse events in both groups.ConclusionsIron replacement improved exercise capacity and QoL in stable COPD patients with iron deficiency. The treatment was well tolerated.Clinical Trial registrationEudraCT 2016-001238-89.     

Compare the effects of different visfatin concentration on cardiovascular risk factors,adiponectin and insulin resistance in patients with T2DM

AimThe discovery of new adipokine, visfatin can significantly enhance our knowledge of insulin resistance and diabetes mellitus. We explored the relation of visfatin concentrations to cardiovascular risk factors, adiponectin and insulin resistance criteria in patients with type 2 diabetes mellitus (T2DM).Materials and MethodsFifty-eight patients with T2DM were recruited from the out patients clinic of Shariati Hospital. Laboratory and anthropometric measurements include FBG, OGTT, HbA1c, fasting serum visfatin, insulin and adiponectin, HOMA-IR and hsCRP, weight, height, BMI and WHR were performed in all participants. All of the statistical data were analyzed using the SPSS15 software.ResultsThe log₁₀-transformed (log) plasma visfatin concentration was in significant positive correlation with age (r = 0.286, p = 0.033). Patients were divided in two groups by median log visfatin (0.85 ng/mL): group I had low values and group II had high values. In group I the log visfatin was in significant positive correlation with age (r = 0.436, p = 0.018) and in group II log visfatin was in significant negative correlation with FPG and HbA1c (r > 0.4, p < 0.05).ConclusionIn conclusion high circulating levels of visfatin could be in healthy relations with cardiovascular risk factors, insulin resistance status and adiponectin in diabetic patients.     

Relationship Between Pregnancy-Associated Plasma Protein-A and Lung Cancer

BackgroundPregnancy-associated plasma protein-A (PAPP-A) has insulin-like growth factor (IGF)-dependent IGFBP-4 protease activity and plays an important role in amplifying local IGF-1 activity in wound healing, vascular repair, and bone remodeling. We postulated that PAPP-A may contribute to the availability and activity of IGFs, which affect lung cancer. Therefore, we determined the levels of PAPP-A in patients with lung cancer and their possible clinical significance.MethodsThe study population consisted of 83 patients with lung cancer and 33 healthy subjects as a control group. Serum PAPP-A levels were determined using an ultrasensitive enzyme-linked immunosorbent assay.ResultsThe serum PAPP-A levels were higher in patients with lung cancer [median (interquartile range) 10.7 (7.6–14.2) ng/mL] than in the control group [6.2 (5.2–9.8) ng/mL, P < 0.001]. There was a significant negative correlation between the serum PAPP-A levels and Karnofsky performance status (r = ?0.330; P < 0.001) and a positive correlation with patient age (r = 0.358; P < 0.001).ConclusionPAPP-A is a proatherosclerotic metalloproteinase that is also thought to be an inflammatory marker. We found that the serum PAPP-A levels increased in patients with lung cancer and postulated that PAPP-A levels may be a prognostic factor in such cases.     

Prospective study of matrix metalloproteinase-9 and risk of myocardial infarction and stroke in older men and women

ObjectivesThe endopeptidase matrix metalloproteinase-9 (MMP-9) is implicated in atherosclerotic plaque rupture. We investigate prospective associations between MMP-9 and MI or stroke in an older general population cohort, accounting for established and novel cardiovascular risk factors.MethodsBaseline serum MMP-9 was measured in incident MI (n = 368) and stroke (n = 299) cases and two controls per case, ‘nested’ in prospective studies of 4252 men and 4286 women aged 60–79 years, sampled from General Practices in Britain in 1998–2000, with 7-year follow-up for fatal and non-fatal MI and stroke.ResultsGeometric mean MMP-9 was 528 ng/mL (IQR 397, 743) in MI cases compared to 501 ng/mL (IQR 370, 743) in controls, p = 0.10. Participants in the top compared to bottom third of MMP-9 levels had an age-adjusted odds ratio for MI of 1.53 (95% CI 1.09, 2.13), which attenuated to 1.18 (95% CI 0.81, 1.70) after adjustment for established and novel cardiovascular risk factors. There was weak evidence that OR differed according to pre-existing CVD; the OR for MI in 187 participants with pre-existing CVD was 2.20 (1.04, 4.64) and 1.24 (0.84, 1.82) in 715 participants without (LR test for interaction p = 0.06). Geometric mean MMP-9 levels were higher in stroke cases than controls; 522 ng/mL (IQR 363, 673) vs 487 (IQR 393, 704), p = 0.045; however adjustments similarly attenuated the associations.ConclusionsWhile serum MMP-9 is univariately associated with risk of MI and stroke, it is not a strong independent risk marker for either.     

Seguridad y efectividad del oxihidróxido sucroférrico en pacientes españoles en diálisis: subanálisis del estudio VERIFIE

Background and aimsIn this study, we show the results of the subset of Spanish patients of the VERIFIE study, the first post-marketing study assessing the long-term safety and effectiveness of sucroferric oxyhydroxide (SFOH) in patients with hyperphosphatemia undergoing dialysis during clinical practice.Patients and methodsPatients undergoing hemodialysis and peritoneal dialysis with indication of SFOH treatment were included. Follow-up duration was 12–36 months after SFOH initiation. Primary safety variables were the incidence of adverse drug reactions, medical events of special interest, and variations in iron-related parameters. SFOH effectiveness was evaluated by the change in serum phosphorus levels.ResultsA total of 286 patients were recruited and data from 282 were analyzed. Among those 282 patients, 161 (57.1%) withdrew the study prematurely and 52.5% received concomitant treatment with other phosphate binders. Adverse drug reactions were observed in 35.1% of patients, the most common of which were gastrointestinal disorders (77.1%) and mild/moderate in severity (83.7%). Medical events of special interest were reported in 14.2% of patients, and 93.7% were mild/moderate. An increase in ferritin (386.66 ng/mL vs 447.55 ng/mL; P = .0013) and transferrin saturation (28.07% vs 30.34%; P = .043) was observed from baseline to the last visit. Serum phosphorus levels progressively decreased from 5.69 mg/dL at baseline to 4.84 mg/dL at the last visit (P < .0001), increasing by 32.2% the proportion of patients who achieved serum phosphorus levels ≤ 5.5 mg/dL, with a mean daily SFOH dose of 1.98 pills/day.ConclusionsSFOH showed a favorable effectiveness profile, a similar safety profile to that observed in the international study with most adverse events of mild/moderate severity, and a low-daily pill burden in Spanish patients in dialysis.     

Serum calprotectin as a biomarker for Crohn's disease

Background and aimsIn Crohn's disease, correlation between clinical assessment and disease activity at tissue level is weak. Our aim was to evaluate the value of serum calprotectin as a biomarker for Crohn's disease.MethodsThe STORI trial patients (n = 115) were studied at baseline, in clinical remission before infliximab withdrawal, or at the time of relapse after infliximab withdrawal. Forty healthy controls were also studied. Serum calprotectin level was measured by ELISA. Data were analyzed through correlation analyses, Kaplan Meier curves and Cox model, using available Crohn's Disease Activity Index (CDAI), Crohn's Disease Endoscopic Index of Severity (CDEIS), fecal calprotectin and C-reactive protein levels (hsCRP).ResultsMedian serum calprotectin was 8892 ng/mL (range: 410–125,000 ng/mL) in Crohn disease patients as compared with 1318 ng/mL (range: 215.8–3770 ng/mL) in controls (P < 0.0001). Serum calprotectin was significantly higher for active disease (median = 19,584 ng/mL) than for inactive disease (median = 8353 ng/mL) (P < 0.0001). Serum calprotectin correlated with hsCRP (r = 0.4092, P < 0.0001) and CDAI (r = 0.4442, P < 0.0001), but not with CDEIS, on the contrary to fecal calprotectin (r = 0.6458, 0.5515, 0.2577 with P < 0.0001, P < 0.0001, P = 0.019 respectively). In multivariate analysis, serum calprotectin used as a discrete variable (threshold: 5675 ng/ml), appeared complementary to hsCRP (> 5 mg/l) and fecal calprotectin (> 250 μg/g) to predict relapse after infliximab withdrawal (P = 0.0173, 0.0024 and 0.0002; HR: 3.191, 3.561 and 4.120).ConclusionsAs a CD biomarker, serum calprotectin has a similar profile as hsCRP. It is also complementary to fecal calprotectin and hsCRP for prediction of relapse after infliximab withdrawal.     

Is vitamin D status a predictor glycaemic regulation and cardiac complication in type 2 diabetes mellitus patients?

ObjectiveTo evaluate vitamin D as a predictor of glycaemic regulation in type 2 diabetes mellitus patients.Research design and methodsIn observational study 171 type 2 diabetic patients who are followed for median (range) of 10.15 (3–18) years. Mean ± SD age was 56 ± 10. Plasma 25-hydroxyvitamin D3 levels were determined by high-performance liquid chromatography/tandem mass spectrometry on baseline samples. Vitamin D deficiency was defined as a 25-OHD level of less than 20 ng/ml. Vitamin D levels between 20 and 30 ng/ml are termed ‘insufficient’. Vitamin D levels greater than 30 ng/ml are termed ‘optimal’.Results125 patients have vitamin D deficiency, 14 patients have insufficient and the others have optimal. Vitamin D levels were not associated with sex, age, BMI, HDL, LDL, kreatinin, hypertension and smoking. But vitamin D deficiency patients had more longer duration (p = 0.011), more higher uric acid (p = 0.021), fasting glucose (p = 0.037), postprandial glucose (p = 0.001) and HbA1c (p = 0.026).ConclusionsIn our study type 2 diabetic patients have 73% of vitamin D deficiency. Vitamin D deficiency predicts higher fasting and postprandial blood glucose and diabetes disregulation. Type 2 DM patients and low 25-OH vitamin D levels could increased cardiovascular disease directly or indirectly (low HDL and high uric acid in 25-OH vitamin D <20 ng/ml). Whether vitamin D substitution improves prognosis remains to be investigated.     

Vitamin D levels in patients with Behçet’s disease: Significance and impact on disease measures

Aim of the workThis study aimed to investigate serum levels of vitamin D in patients with Behçet’s disease (BD) and to evaluate their relationship to disease activity as well as different disease measures.Patients and methodsForty-two patients with BD were enrolled into this study. These patients were subjected to detailed history taking, thorough clinical examination including assessment of disease activity according to Behçet’s Disease Current Activity Form (BDCAF) score and performed laboratory investigations including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum calcium, serum phosphorus and serum alkaline phosphatase. Serum 25-hydroxyvitamin D (vitamin D) levels were determined using Enzyme-Linked-Immunosorbent Assay (ELISA). A control group of 41 age and sex matched healthy controls was also included.ResultsThe mean level of 25-hydroxyvitamin D (30.65 ± 12.87 ng/ml) was significantly decreased in BD patients compared to the controls (37.98 ± 15.76 ng/ml) (p = 0.02). Significant negative correlations of serum vitamin D levels with patients’ ages (p = 0.03), ESR (p < 0.001), CRP (p < 0.001) and BDCAF (p = 0.003) were found; whereas, there was no significant correlation with disease duration (p = 0.6). In multivariate regression analysis age (p = 0.02), colchicine therapy (0.008), ESR (0.02) and CRP (0.03) were found to be the independent effectors on vitamin D serum levels.ConclusionSerum levels of vitamin D were significantly lower in BD patients compared to controls. Associations were found between vitamin D levels and age, BDCAF as well as ESR and CRP in BD patients. Low vitamin D may predispose BD patients to active disease, especially in older subjects.     

Obesity,Brain Natriuretic Peptide Levels and Mortality in Patients Hospitalized With Heart Failure and Preserved Left Ventricular Systolic Function

BackgroundAn inverse relationship between brain natriuretic peptide (BNP) levels and body mass index (BMI) has been described for patients with left ventricular (LV) systolic dysfunction. In this study, the association of BMI, BNP levels and mortality in patients hospitalized for heart failure with preserved LV systolic function (HFpLVF) was investigated.MethodsOne hundred fifty consecutive patients (98% men) who were hospitalized with HFpLVF and had BNP levels measured on admission were analyzed. Patients were divided into categories of BMI: normal (BMI < 25 kg/m²), overweight (BMI 25–29.9 kg/m²) and obese (BMI ≥ 30 kg/m²). Relevant clinical and echocardiographic characteristics and all-cause mortality were obtained through chart review.ResultsBNP levels were significantly lower in obese (median = 227 pg/mL) and overweight (median = 396 pg/mL) patients compared with those with normal BMI (median = 608 pg/mL, P = 0.003). Higher BMI predicted BNP levels of <100 pg/mL. Compared with patients with normal BMI, overweight and obese patients had a significantly lower risk of total mortality, even after adjusting for other clinical characteristics, including log-transformed BNP levels, atrial fibrillation, the use of beta-blockers at discharge, age, hemoglobin levels and the presence of pulmonary congestion on admission. Higher BNP levels also independently predicted mortality.ConclusionsAn inverse relationship between BMI and BNP levels exists in patients hospitalized with HFpLVF. Higher BMI is associated with lower mortality, whereas higher BNP levels predict higher mortality in male patients with HFpLVF. These findings should be confirmed in a larger multicenter setting.     

Serum hepcidin concentrations correlate with ferritin in patients with inflammatory bowel disease

Background and aimsAnemia is a frequent complication of inflammatory bowel disease (IBD). Hepcidin, a key mediator in this anemia, is up-regulated by high iron levels and inflammation, and serum levels are elevated in IBD. However, the extent of inflammatory activity and iron deficiency for the regulation of hepcidin is not known. This study aimed to evaluate serum hepcidin levels in anemic and non-anemic IBD patients, with iron or non-iron deficiency, and active or inactive disease.MethodsThis retrospective, observational study analyzed serum hepcidin levels from 247 patients with IBD (130 Crohn's patients and 117 with ulcerative colitis) recruited at Swiss Inflammatory Bowel Disease Cohort Study centers. Patients were divided into 5 different groups using criteria of active and inactive diseases (C-reactive protein, and CDAI/MTWAI = disease activity-index), anemia (hemoglobin) and iron deficiency (ferritin) and compared to healthy controls with no signs of anemia and normal ferritin levels. Hepcidin was measured using enzyme-linked immunosorbent assay.ResultsIndependent of inflammatory activity, all patients with decreased ferritin (< 30 μg/L) had significantly lower hepcidin levels when compared to patients and healthy controls having normal ferritin (> 30 μg/L). A significant correlation between serum ferritin levels and serum hepcidin was found (Spearman's Rho = 0.491; p < 0.001). A backward multi-linear stepwise regression analysis showed that only ferritin, and none of the inflammatory markers or age and sex correlated significantly (p = 0.005) with hepcidin.ConclusionThis retrospective analysis suggests that iron deficiency is the key trigger for hepcidin regulation in IBD patients with anemia.