Immune Thrombocytopenic Purpura as a Hemorrhagic Versus Thrombotic Disease: An Updated Insight into Pathophysiological Mechanisms.

Immune thrombocytopenic purpura (ITP) is a blood disorder characterized by a low platelet count of (less than 100 × 109/L). ITP is an organ-specific autoimmune disease in which the platelets and their precursors become targets of a dysfunctional immune system. This interaction leads to a decrease in platelet number and, subsequently, to a bleeding disorder that can become clinically significant with hemorrhages in skin, on the mucous membrane, or even intracranial hemorrhagic events. If ITP was initially considered a hemorrhagic disease, more recent studies suggest that ITP has an increased risk of thrombosis. In this review, we provide current insights into the primary ITP physiopathology and their consequences, with special consideration on hemorrhagic and thrombotic events. The autoimmune response in ITP involves both the innate and adaptive immune systems, comprising both humoral and cell-mediated immune responses. Thrombosis in ITP is related to the pathophysiology of the disease (young hyperactive platelets, platelets microparticles, rebalanced hemostasis, complement activation, endothelial activation, antiphospholipid antibodies, and inhibition of natural anticoagulants), ITP treatment, and other comorbidities that altogether contribute to the occurrence of thrombosis. Physicians need to be vigilant in the early diagnosis of thrombotic events and then institute proper treatment (antiaggregant, anticoagulant) along with ITP-targeted therapy. In this review, we provide current insights into the primary ITP physiopathology and their consequences, with special consideration on hemorrhagic and thrombotic events. The accumulated evidence has identified multiple pathophysiological mechanisms with specific genetic predispositions, particularly associated with environmental conditions.

The Pulmonary Venous Return from Normal to Pathological-Clinical Correlations and Review of Literature.

Pulmonary veins carry oxygenated blood from lungs to the left atrium of the heart. The anatomy of the pulmonary veins is variable with some anatomic variants. In clinical practice the difference between the normal anatomy of pulmonary veins with its variants and abnormal anatomy is very important for clinicians. Variants of pulmonary veins may occur in number, diameter and normal venous return. We present a case report and a review of the literature with the pulmonary venous return that deviates from the usual anatomical configuration and ranges from normal variant drainage to anomalous pulmonary-systemic communication. Initially, it was considered as an anatomical variant of the pulmonary venous return associated with the persistence of the left superior vena cava. Upon detailed exploration it was established that it was an anomaly of the pulmonary venous return which led in time to the installation of its complications. Diagnosis can be difficult, sometimes missed, or only made late in adulthood when complications were installed. Knowledge of variant anatomy and anomalous pulmonary venous return play a crucial role in the diagnostically challenging patient.

Medical Staff Training - Quality Initiative to Reduce Errors in the Pre-Preanalytical Phase.

BACKGROUND: Numerous studies indicate that most error sources in hemostasis laboratories occur during the pre preanalytical phase through biological product sampling. OBJECTIVES: The purpose of this study was documentation, monitoring, and reduction of preanalytical errors through operator training. METHODS: For a period of 4 months in the "St. SpiridonË® Hospital from Iasi, 978 specimens were identified with non-conformities, due to the following causes: insufficiently-collected, hemolyzed- and coagulated samples. Data collection was conducted in two stages: before and after training of medical staff in clinical departments, upon improving the coagulation specimen sampling practices. RESULTS: The study pointed out that subsequent to training, a reduction of the coagulated samples has been registered as follows: in medical departments from 33.33% to 16.78%, in surgery from 27.20% to 17.02%, ICU (intensive care units) from 10.63% to 8.74%, and slightly in EU (emergency) from 10.63% to 8.74%. Moreover, we noticed that the incidence of hemolyzed samples increased in clinical sections, as follows: EU from 4.50% to 14.89%, medical departments from 3.42% to 9.21%, surgery from 1.44% to 6.38%, and 4.50% to 14.89% for ICU. The insufficiently sampled volume persisted during the study in almost all sections: surgery from 1.80% to 4.96%, medical from 2.52% to 4.96%, EU from 1.80% to 3.78% with a slight decrease in ICU from 1.26% to 1.18%. CONCLUSIONS: Nurses traditionally represent the core of quality medical services. Peer education is effective and implementation and compliance of sample collection procedure rules ultimately providing patient safety.

Chronometric vs. Structural Hypercoagulability.

Prolonged tourniquet stasis induced by venepuncture can lead to the release of the plasma of cell lysis products, as well as tissue factor (TF), impairing the quality of coagulation test results. The accidental presence of TF in vitro can trigger the coagulation mechanism, generating a false decrease in prothrombin time (PT). Background and Objectives: Identification of short PT tests below the normal reference value that could suggest a situation of hypercoagulability. The study aimed to compare the results of the shortened PT tests at their first determination with the eventual correction following duplication of the analysis from the same sample. Materials and methods: Identification of the shortened PT tests has been carried out for a period of 4 months, upon 544 coagulation samples referred to the Hematology department of Sf. Spiridon County Clinical Emergency Hospital from Iasi, Romania. Results: Out of the 544 samples of which the results indicated a state of hypercoagulability, by repeating the determination from the same sample, for 200 (36.76%) PT tests (p = 0.001) the value was corrected, falling within the normal reference range. For 344 (63.24%) tests, the results suggested a situation of hypercoagulability. Conclusions: In order to guarantee the highest quality of the laboratory services, a proper interpretation and report of the patients' results must be congruent and harmoniously associated to the actual clinical condition of the patient. Duplication of the PT determination from the same sample would exclude situations of false hypercoagulability and would provide significant improvement for the patient's safety.

Interferences between Clot in the Erythrocyte Sediment and Hemostasis Exploration.

BACKGROUND: The selection and rejection of non-conforming coagulation specimens is essential in safeguarding quality management in hemostasis laboratories that provide routine testing for bleeding and thrombotic disorders. In order to increase quality, it is important to reduce pre-analytical errors that generally account for 60 - 70% of total laboratory failure. The accidental presence of clots in vitro, in the pre-analytical phase of the coagulation, is a reason for coagulation specimen rejection, given that the reliability of test results can be adversely compromised. This study aimed to ascertain the effect of clots identified in the post-analytical phase within the blood sample sediments upon standard laboratory tests such as PT (prothrombin time) and APTT (activated partial thromboplastin time). METHODS: From a total of 24,670 coagulation specimens gathered and prospectively collected and analyzed at the Haematology Laboratory of the Ë®Sf. SpiridonË® Emergency County Hospital Iasi, Romania, during four months, 671 were identified with clot. Of the coagulated samples, 153 (22.80%) were considered for this study, including those specimens pinpointed with sediment clot through a post-analytical new reverification procedure. RESULTS: The comparative study of the PT and APTT results obtained based on the samples identified with sediment clots in relation to the actual results recorded after the repetition of the sampling, pointed out 43.93% false results for PT1 test, with a significant difference between the variances of the values at the two evaluated moments (t = 2.961, p = 0.0037). The pattern was congruent in the case of the APTT test as well, exhibiting 69.04% false results, for which the variances of values at the two evaluated moments displayed significant differences (t = 2.208, p = 0.0306). In both of the cases significantly lower mean values were noted in the second determination of PT (PT1: 33.1 ± 39.6 vs. PT2: 25.8 ± 30.5) and APTT (APTT1: 42.8 ± 42.7 vs. APTT2: 38.1 ± 26.1. Results are important as they highlight the actual interference between the clot in the erythrocyte sediment and the evaluation of the patient's hemostasis. CONCLUSIONS: Our results confirm that the presence of clots in the erythrocyte sediment, with no identification prior to centrifugation, significantly affect the PT and APTT analysis, their accurate results being critical for the proper diagnosis and monitoring of anticoagulant therapy.

Blood Clot Identification Procedures in Clinical Laboratory Sampling.

BACKGROUND: Monitoring of anticoagulation therapy is based on screening tests: prothrombin time (PT) and activated partial thromboplastin time (APTT). The accidental presence of a clot in the coagulation samples determines a false prolongation of PT by fibrinogen (FI) consumption and the false or delayed prolongation of APTT, depending on FI consumption or activation. The purpose of this study is to document from the present data re-garding procedures used to exclude the accidental presence of clot in the sample. METHODS: For a more efficient approach, we conducted a study based on research from the main databases that included original and peer-reviewed studies. RESULTS: We have reported studies in which pre-analytical procedures have been recommended and studies that have also presented post-analytical protocols. A correlation between the efficiency of the procedures in terms of additional laboratory costs has been performed, as well. CONCLUSIONS: Focusing on patient safety, it remains a continuous challenge for each laboratory to be able to establish its own pre-analytical and post-analytical procedure for highlighting accidental clot presence, thus ensuring provision of results with maximum confidence to the clinicians.

Apolipoproteins A and B and PCSK9: Nontraditional Cardiovascular Risk Factors in Chronic Kidney Disease and in End-Stage Renal Disease.

PURPOSE: Nontraditional cardiovascular risk factors as apolipoprotein A (ApoA), apolipoprotein B (ApoB), and the proprotein convertase subtilisin/kexin type 9 (PCSK9) increase the prevalence of cardiovascular mortality in chronic kidney disease (CKD) or in end-stage renal disease (ESRD) through quantitative alterations. This review is aimed at establishing the biomarker (ApoA, ApoB, and PCSK9) level variations in uremic patients, to identify the studies showing the association between these biomarkers and the development of cardiovascular events and to depict the therapeutic options to reduce cardiovascular risk in CKD and ESRD patients. METHODS: We searched the electronic database of PubMed, Scopus, EBSCO, and Cochrane CENTRAL for studies evaluating apolipoproteins and PCSK9 in CKD and ESRD. Randomized controlled trials, observational studies (including case-control, prospective or retrospective cohort), and reviews/meta-analysis were included if reference was made to those keys and cardiovascular outcomes in CKD/ESRD. RESULTS: 18 studies met inclusion criteria. Serum ApoA-I has been significantly associated with the development of new cardiovascular event and with cardiovascular mortality in ESRD patients. ApoA-IV level was independently associated with maximum carotid intima-media thickness (cIMT) and was a predictor for sudden cardiac death. The ApoB/ApoA-I ratio represents a strong predictor for coronary artery calcifications, cardiovascular mortality, and myocardial infarction in CKD/ESRD. Plasma levels of PCSK9 were not associated with cardiovascular events in CKD patients. CONCLUSIONS: Although the "dyslipidemic status" in CKD/ESRD is not clearly depicted, due to different research findings, ApoA-I, ApoA-IV, and ApoB/ApoA-I ratio could be predictors of cardiovascular risk. Serum PCSK9 levels were not associated with the cardiovascular events in patients with CKD/ESRD. Probably in the future, the treatment of dyslipidemia in CKD/ESRD will be aimed at discovering new effective therapies on the action of these biomarkers.