Clot activators and anticoagulant additives for blood collection. A critical review on behalf of COLABIOCLI WG-PRE-LATAM.

In the clinical laboratory, knowledge of and the correct use of clot activators and anticoagulant additives are critical to preserve and maintain samples in optimal conditions prior to analysis. In 2017, the Latin America Confederation of Clinical Biochemistry (COLABIOCLI) commissioned the Latin American Working Group for Preanalytical Phase (WG-PRE-LATAM) to study preanalytical variability and establish guidelines for preanalytical procedures to be applied by clinical laboratories and health care professionals. The aim of this critical review, on behalf of COLABIOCLI WG-PRE-LATAM, is to provide information to understand the mechanisms of the interactions and reactions that occur between blood and clot activators and anticoagulant additives inside evacuated tubes used for laboratory testing. Clot activators - glass, silica, kaolin, bentonite, and diatomaceous earth - work by surface dependent mechanism whereas extrinsic biomolecules - thrombin, snake venoms, ellagic acid, and thromboplastin - start in vitro coagulation when added to blood. Few manufacturers of evacuated tubes state the type and concentration of clot activators used in their products. With respect to anticoagulant additives, sodium citrate and oxalate complex free calcium and ethylenediaminetetraacetic acid chelates calcium. Heparin potentiates antithrombin and hirudin binds to active thrombin, inactivating the thrombin irreversibly. Blood collection tubes have improved continually over the years, from the glass tubes containing clot activators or anticoagulant additives that were prepared by laboratory personnel to the current standardized evacuated systems that permit more precise blood/additive ratios. Each clot activator and anticoagulant additive demonstrates specific functionality, and both manufacturers of tubes and laboratory professional strive to provide suitable interference-free sample matrices for laboratory testing. Both manufacturers of in vitro diagnostic devices and laboratory professionals need to understand all aspects of venous blood sampling so that they do not underestimate the impact of tube additives on laboratory testing.

Expression of MIF and TNFA in psoriatic arthritis: relationship with Th1/Th2/Th17 cytokine profiles and clinical variables.

Psoriatic arthritis (PsA) is an autoimmune inflammatory disease associated with psoriasis. The cause of this pathology is still unknown, but research suggests the diseases are caused by a deregulated cytokine production. MIF is a cytokine associated with immunomodulation of Th1, Th2, and Th17 cytokine profiles in inflammatory diseases. Based on this knowledge, the aim of this study was to determine the association of MIF and TNFA expression with Th1, Th2, and Th17 cytokine profiles in serum levels of PsA patients. A cross-sectional study was performed in 50 PsA patients and 30 control subjects (CS). The cytokine profiles were quantified by BioPlex MagPix system and the mRNA expression levels by real-time PCR. TNFA mRNA expression was 138.81-folds higher in PsA patients than CS (p < 0.001). Regarding MIF mRNA expression, no significant differences were observed; however, a positive correlation was identified between MIF mRNA expression and PsA time of evolution (r = - 0.53, p = 0.009). An increase of Th1 (IFNγ: PsA = 37.1 pg/mL vs. CS = 17 pg/mL, p < 0.05; TNFα: PsA = 24.6 pg/mL vs. CS = 9.8 pg/mL, p < 0.0001) and Th17 cytokine profiles (IL-17: PsA = 6.4 pg/mL vs. CS = 2.7 pg/mL, p < 0.05; IL-22: PsA = 8.4 pg/mL vs. CS = 1.8 pg/mL, p < 0.001), were found in PsA patients. Th2 cytokines were not significantly different in both groups. In conclusion, a high expression of TNFA mRNA, as well as an increase of Th1 and Th17 cytokine profiles evaluated by IFNγ, TNFα, IL-17, and IL-22 cytokines, was observed in PsA patients.