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Background: Fecal calprotectin assays are widely used to exclude inflammatory bowel disease (IBD) in patients with suspected IBD. A problem with the fecal calprotectin assays is the rather long test-turnaround times. A particle enhanced turbidimetric immunoassays (PETIA) for fecal calprotectin would reduce test-turnaround times and would permit more laboratories to perform the measurements. The aim of this study was to evaluate a new feces calprotectin PETIA., Method: Using routine fecal samples the feces calprotectin PETIA was validated on two chemistry analyzers, Mindray BS-380 and Cobas 501., Results: The assay is linear in the range 11-2000 μg/g, with a limit of quantitation of approximately 10 μg/g. No antigen excess hook effect was observed up to 10 000-15 000 μg/g depending on the instrument used. The turbidimetric method showed a good agreement with the Bühlmann ELISA. The total coefficient of variation was 3%-8% in the 50-100 μg/g range., Conclusion: The fecal calprotectin PETIA, fCal Turbo, is well suited for rapid analysis of fecal calprotectin on Mindray BS-380 or Cobas 501 clinical chemistry analyzers. The test results are commutable with Bühlmann fecal MRP8/14 ELISA., (© 2016 Wiley Periodicals, Inc.)

Introduction: Cardiovascular disease (CVD) is a major cause of premature mortality among Systemic lupus erythematosus (SLE) patients. Many studies have measured and evaluated risk factors for premature subclinical atherosclerosis, but few studies are prospective and few have evaluated risk factors for hard endpoints, i.e. clinically important cardiovascular events (CVE). We investigated the impact of traditional and lupus associated risk factors for the first ever CVE in a longitudinal cohort of SLE patients., Methods: A total of 182 SLE patients (mean age 43.9 years) selected to be free of CVE were included. Cardiovascular and autoimmune biomarkers were measured on samples collected after overnight fasting at baseline. Clinical information was collected at baseline and at follow up. End point was the first ever CVE (ischemic heart, cerebrovascular or peripheral vascular disease or death due to CVD). Impact of baseline characteristics/biomarkers on the risk of having a first CVE was evaluated with Cox regression., Results: Follow up was 99.5% after a mean time of 8.3 years. Twenty-four patients (13%) had a first CVE. In age-adjusted Cox regression, any positive antiphospholipid antibody (aPL), elevated markers of endothelial activation (von Willebrand factor (vWf), soluble vascular cellular adhesion molecule-1 (sVCAM-1)) and fibrinogen predicted CVEs. Of SLE manifestations, arthritis, pleuritis and previous venous occlusion were positively associated with future CVEs while thrombocytopenia was negatively associated. Among traditional risk factors only age and smoking were significant predictors. In a multivariable Cox regression model age, any positive aPL, vWf and absence of thrombocytopenia were all predictors of the first CVE., Conclusions: In addition to age, positive aPL, biomarkers indicating increased endothelial cell activity/damage, and absence of thrombocytopenia were independent predictors of CVEs in this prospective study. Our results indicate that activation of the endothelium and the coagulation system are important features in SLE related CVD. Furthermore, we observed that the risk of CVEs seems to differ between subgroups of SLE patients.

Objective: Reference values are usually defined based on blood samples from healthy men or nonpregnant women. This is not optimal as many biological markers changes during pregnancy and adequate reference values are of importance for correct clinical decisions. There are only few studies on the variations of laboratory tests during normal pregnancies, especially during the first two trimesters. It is thus a need to establish such reference values., Design: Longitudinal study of laboratory markers in normal pregnancies., Setting: Uppsala University Hospital, Sweden., Population: Healthy pregnant females., Methods: We have studied 25 frequently used laboratory tests during 52 normal pregnancies. Each woman was sampled up to nine times and the samples were divided according to collection time into the following groups: gestational week 7-17; week 17-24; week 24- 28; week 28-31; week 31-34; week 34-38; predelivery (0-2 weeks before delivery) and postpartum (> 6 weeks after delivery). The 2.5 and 97.5 percentiles for these markers were calculated according to the recommendations of the International Federation of Clinical Chemistry on the statistical treatment of reference values., Results: Reference intervals are reported for plasma alanine aminotransferase, albumin, alkaline phosphatase, pancreas amylase, apolipoprotein A1, apolipoprotein B, aspartate aminotransferase, bilirubin, calcium, chloride, creatinine, cystatin C, ferritin, gamma-glutamyltransferase, iron, lactate dehydrogenase, magnesium, phosphate, potassium, sodium, transferrin, triglycerides, thyroid-stimulating hormone, urate and urea during these pregnancy periods., Conclusions: Most of the analytes change during normal pregnancy. It is thus of importance to use special reference values during pregnancy.

Objective: Maintaining an adequate blood glucose level is essential for neuron integrity. The increased energy demand imposed on the fetus by the birth process in combination with a limited glucose production capacity therefore threatens brain function. It is logical to presume that mechanisms increasing glucose mobilization as well as decreasing peripheral glucose utilization has evolved to preserve brain function, even after complicated deliveries., Design: We studied umbilical cord levels of hormones involved in acute glucose regulation as well as insulin-like growth factor-I (IGF-I), modulating factors insulin-like growth factor binding protein (IGFBP)-1 and -3 as well as interleukin-6 (IL-6) in 149 infants born after different degrees of birth stress. We measured glucose, insulin, IGF-I, IGFBP-1, IGFBP-3, glucagon, growth hormone (GH), prolactin, adrenocorticotropin (ACTH), cortisol and IL-6 in umbilical cord blood of infants born at term gestation after: A) elective Cesarean-section (n = 37), B) normal delivery (n = 87) or C) complicated delivery (n = 25). All infants were of normal birth weight for gestational age. Arterial pH and lactate as well as S-100B, a marker of neuronal damage, were used as stress variables., Results: With increasing fetal stress, we found significant and generally progressive elevations in glucose, IGFBP-1, IL-6, ACTH, cortisol, glucagon, GH, prolactin and lactate. This was accompanied by significant decreases of IGF-I, insulin and arterial pH. S-100B and IGFBP-3 levels did not differ between groups. IGFBP-1 showed a significant positive correlation to IL-6 and lactate and a significant negative correlation to both IGF-I and arterial pH., Conclusions: Increasing stress and energy demands during birth are accompanied by increasing fetal levels of glucose-mobilizing hormones in combination with depressed levels of insulin and IGF-I, despite increasing blood glucose. Furthermore, IGFBP-1 and IL-6 increase steeply, presumably aimed at diminishing insulin-like activity of IGF-I, thereby reducing peripheral glucose utilization. We believe that IGFBP-1 and IL-6 deserve evaluation as potential intrapartum indicators of fetuses at risk for asphyxia.

Renal dysfunction measured by serum creatinine is associated with increased cardiovascular morbidity and mortality. Plasma cystatin C has been shown in several studies to be superior to plasma creatinine for the estimation of glomerular filtration rate (GFR). The aim of the present study was to investigate the relationship between cystatin C and mortality in elderly men. Serum cystatin C was analyzed by nephelometry in a group of 77-year-old men (n=792) and correlated cystatin C levels with mortality during a follow-up period of 1-4 years. The cystatin C values were significantly correlated with overall mortality (p=0.013). Mortality was three times higher in the highest cystatin C quintile in relation to the lowest quintile.

Objective: To investigate the clinical potential of several markers of spinal cord ischemia in cerebrospinal fluid (CSF) and serum during aneurysm repair of the descending thoracic or thoracoabdominal aorta., Design: Observational study of consecutive patients. Nonblinded, nonrandomized., Setting: University hospital thoracic surgical unit., Participants: Eleven consecutive elective patients., Interventions: Distal extracorporeal circulation and maintenance of CSF pressure <10 mmHg until intrathecal catheter removal., Measurements and Main Results: CSF and serum levels of S100B (and its isoforms S100A1B and S100BB), neuronal-specific enolase (NSE), and the CSF levels of glial fibrillary acidic protein (GFAp) and lactate were determined. Two patients had postoperative neurologic deficit. One with a stroke showed a 540-fold increased GFAp, a 6-fold NSE, and S100B increase in CSF. One with paraplegia had a 270-fold increase in GFAp, a 2-fold increase in NSE, and 5-fold increased S100B in CSF. One patient without deficit increased GFAp 10-fold, NSE 4-fold, and S100B 23-fold in CSF. CSF lactate increased >50% in 6 of 9 patients without neurologic deficit. Serum S100B increased within 1 hour of surgery in all patients without any concomitant increase in CSF. S100A1B was about 70% of total S100B in both serum and CSF in patients with or without neurologic defects. S100B in CSF increased 3-fold in 3 of 9 asymptomatic patients., Conclusions: In patients with neurologic deficit, GFAp in CSF showed the most pronounced increase. Biochemical markers in CSF may increase without neurologic symptoms. There is a significant increase in serum S100B from surgical trauma alone without any increase in CSF.

C-reactive protein (CRP) is a protein produced mainly in the liver upon stimulation by interleukin-6. CRP is part of the acute phase response to inflammation and plasma concentrations rise 100-1000 times in patients with for example bacterial infections. High sensitive methods have made it possible to measure and compare low CRP levels in plasma. Prospective studies have shown that increased but comparatively low plasma CRP concentrations are associated with future coronary heart disease (CHD) in healthy individuals and in patients with known CHD. Further support for an important role for CRP comes from in vitro studies that have suggested that the CRP protein is intimately and actively involved in the atherosclerotic process. This has stimulated the interest for clinical evaluation and treatment of increased plasma CRP levels.