Study indicates a genetic test may show which chemotherapy patients are at risk for serious blood clots

Chemotherapy is known to carry a risk of venous thromboembolism in cancer patients, a particularly common risk in frequent cancers like breast cancer. But a genetic test may predict which of these patients are most likely to develop such serious blood clots, researchers report.

VTE is preventable through prophylaxis treatment with heparin, an anticoagulant. But because a side effect is less controllable bleeding, the drug is not routinely recommended to patients undergoing chemotherapy.

Researchers examined 4,261 Swedish women diagnosed with primary invasive breast cancer between 2001 and 2008. Risk stratification was based on chemotherapy use and genetic susceptibility, which was determined by a risk score assessing nine genes involved in VTE. Patients ranked in the highest 5 percent were classified as having a high genetic susceptibility.

Patients were followed for a median of 7.6 years, and 276 experienced a VTE during that time.

Read more:
Blood Clot Risk in Breast Cancer Patients Seen via Gene Test

Source: Breast cancer news

Platelet Activation and Factors for Clot Formation

Great animation of coagulation process

View in YouTube
Platelet Activation and Factors for Clot Formation


Source: YouTube

Quality Improvement in the Coagulation Laboratory

Reducing the Number of Insufficient Blood Draw Specimens for Coagulation Testing

To report the efforts of our laboratory to reduce quantity-not-sufficient (QNS) specimens via several methods and to directly measure the effect of expired collection tubes on the amount of blood that can be drawn.

A study tracked the number of QNS venous-blood specimens per month received by our coagulation laboratory from March 2008 to December 2012. Interventions involved communications that informed nurses and phlebotomists how to avoid drawing QNS specimens and floor sweeps, in which laboratory staff searched for and removed expired vacuum-based blood-collection tubes (VBCTs) from inpatient hospital floors. Also, we assessed 11 healthy donors to determine the amount of blood that could be drawn into expired VBCTs.

During the study period, the rate of QNS specimens dropped from a mean of 0.7% to 0.3%. In expired VBCTs collected from healthy donors, we observed a statistically significant difference in the amount of blood drawn into nonexpired vs expired VBCTs (P <.001). Also, there was a negative relationship between the number of months that the VBCT had been expired and the amount of blood that could be drawn into the VBCTs (P <.001). For every month that VBCTs were expired, the amount of blood drawn decreased by approximately 1.8 mm (0.1 mL), using linear regression analysis.

This study strongly suggests that expired VBCTs consistently and progressively yield QNS specimens. Methods to reduce blood draws from expired VBCTs may include communications promoting proper blood draw technique, floor sweeps to remove expired VBCTs, and improved inventory management.

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Quality Improvement in the Coagulation Laboratory

Source: Medscape

Blood Clot

Amazing image of blood clot.

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Scinerds: Blood Clot NIH: National Heart, Lung,...

Source: Tumblr via Scientific Illustration

Activated protein C

The homeostatic blood protease, activated protein C (APC), can function as an antithrombotic on the basis of inactivation of clotting factors Va and VIIIa; a cytoprotective on the basis of endothelial barrier stabilization and anti-inflammatory and antiapoptotic actions; and a regenerative on the basis of stimulation of neurogenesis, angiogenesis, and wound healing. Pharmacologic therapies using recombinant human and murine APCs indicate that APC provides effective acute or chronic therapies for a strikingly diverse range of preclinical injury models. APC reduces the damage caused by the following: ischemia/reperfusion in brain, heart, and kidney; pulmonary, kidney, and gastrointestinal inflammation; sepsis; Ebola virus; diabetes; and total lethal body radiation. For these beneficial effects, APC alters cell signaling networks and gene expression profiles by activating protease-activated receptors 1 and 3. APC’s activation of these G protein–coupled receptors differs completely from thrombin’s activation mechanism due to biased signaling via either G proteins or β-arrestin-2. To reduce APC-associated bleeding risk, APC variants were engineered to lack >90% anticoagulant activity but retain normal cell signaling. Such a neuroprotective variant, 3K3A-APC (Lys191-193Ala), has advanced to clinical trials for ischemic stroke. A rich data set of preclinical knowledge provides a solid foundation for potential translation of APC variants to future novel therapies.

Read more:
Activated protein C: biased for translation

 Read more: Blood Journal

Coagulation Cascade Animation Video

Awesome animation of the physiology of Hemostasis


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Coagulation Cascade Animation - Physiology of Hemostasis

Source: YouTube

Clot Capture

A blood clot (gray) ensnares many different types of cells.

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Image of the Day: Clot Capture 

Source: The Scientist Magazine

As the clot thickens

Supporting coagulation

Source: Facebook via Lab Humor

Sodium Citrate Tubes Versus CTAD

In today's laboratory, we strive to take as little blood from a patient as possible and also trying to decrease our costs. In current Sodium Citrate tubes the stability time is only 1 hour from collection to running, unless you remove the plasma, which will allow stability for 2 hours. The CTAD tube would give a 4 hour stability time on the Anti-factor Xa test. But could it be used for our other coagulation testing, such as Protimes, APTT, Fibrinogen and D Dimer?

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The CTAD Tube Dilemma

Source: Advance

APTT vs Anti-factor Xa

Anticoagulation therapy and laboratory monitoring methods are rapidly evolving. Drug monitoring should provide a very useful and clinically effective means of determining an optimal dose regimen for each individual. The ideal assay for monitoring unfractionated heparin remains a subject of debate. However, one cannot ignore the drawbacks of the current and widely used method, the APTT. The anti-factor Xa assay has been gaining momentum recently, and is continuing to do so because of its advantages over APTT. There are studies that have demonstrated that anti-factor Xa actually saves the hospital money; and more importantly, is a valuable tool for optimal patient care management.This is through less patient testing and monitoring needed; consequently, fewer dose adjustments are done. Therefore, the patient is stabilized quicker and released from the hospital earlier.

Read more:
Laboratory Methods of Heparin Monitoring, Part 3

Activated Partial Thromboplastin Time [APTT]

The APTT in contrast to the PT, measures the activity of the intrinsic and common pathways of coagulation. The division of the clotting cascade into the intrinsic, extrinsic and common pathways has little in vivo validity but remains a useful concept for interpreting the results of laboratory investigations. The term 'thromboplastin' in this test refers to the formation of a complex formed from various plasma clotting factors which converts prothrombin to thrombin and the subsequent formation of the fibrin clot. The term 'Activated Partial Thromboplastin Time (APTT)' derives from the original form of the test (devised in 1953) in which only the phospholipid concentration of the test was controlled (as opposed to the phospholipid and the surface activator concentrations) and the name 'partial thromboplastin' was applied at the time to phospholipid preparations which accelerated clotting but did not correct the prolonged clotting times of haemophilic plasma. Essentially the term 'partial' means phospholipid is present but no Tissue Factor.

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Activated Partial Thromboplastin Time [APTT]

Source: Practical Haemostasis

Synthetic Platelet-like Particles

A new class of synthetic platelet-like particles could augment natural blood clotting for the emergency treatment of traumatic injuries – and potentially offer doctors a new option for curbing surgical bleeding and addressing certain blood clotting disorders without the need for transfusions of natural platelets.

The clotting particles, which are based on soft and deformable hydrogel materials, are triggered by the same factor that initiates the body’s own clotting processes. Testing done in animal models and in a simulated circulatory system suggest that the particles are effective at slowing bleeding and can safely circulate in the bloodstream. The particles have been tested with human blood, but have not undergone clinical trials in humans.

Read more:
Platelet-like particles augment natural blood clotting for treating trauma

Source: Georgia Tech

INR Failure

It´s never a good day when your INR is the same than your haemoglobin.


Hb = 13,5 g/dL, INR.....

The Platelet Party

Blood cloth. They are stuck :)

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The Awkward Yeti

Source: The Awkward Yeti
Image credits: Nick Seluk

Pre-analytical Variables in Coagulation Testing

The use of modern laboratory instrumentation with high levels of test reliability and appropriate quality assurance measures will lead to very few analytical errors within hemostasis testing. Nevertheless, incorrect or inappropriate test results are still reported, often due to events outside the control of the laboratories performing the tests. This is due primarily to pre-analytical events associated with sample collection and processing, as well as post-analytical events related to the reporting and interpretation of test results. This review focuses on the pre-analytical phase, highlighting contributory elements and providing suggestions on how problems can be minimized or prevented, thereby improving the likelihood that reported test results actually represent the true clinical status of the patient rather than that of an inappropriate sample. This review should be of value to both laboratory personnel and clinicians because an appreciation of these issues will enable the optimal clinical management of patients.

Read more:
Pre-analytical Variables in Coagulation Testing Associated With Diagnostic Errors in Hemostasis

Source: Lab Medicine
Image credits: Renegedhealth

Heparin-Induced Thrombocytopenia

Patients receive blood thinners (anticoagulants) to treat or prevent blood clots. The most commonly used intravenous anticoagulant is heparin. This Cardiology Patient Page focuses on heparin-induced thrombocytopenia (HIT), a complication of heparin therapy. This complication of heparin is often confusing because in HIT, heparin does the opposite of what it is supposed to do:,It forms rather than prevents new blood clots.

Ordinarily, heparin prevents clotting and does not affect the platelets, components of the blood that help form blood clots. Triggered by the immune system in response to heparin, HIT causes a low platelet count (thrombocytopenia).  Two distinct types of HIT can occur: nonimmune and immune-mediated. Nonimmune HIT, which occurs most frequently, is characterized by a mild decrease in the platelet count and is not harmful. The second type, immune-mediated HIT, occurs much less frequently but is dangerous. Immune-mediated HIT causes much lower platelet counts. Paradoxically, despite a very low platelet count, patients who suffer from HIT are at risk for major clotting problems.

Read more:
Heparin-Induced Thrombocytopenia

Source: Circulation
Image credits: Kanchana Chansung

A Practical Guide to Laboratory Haemostasis

Practical-Haemostasis.com site is designed to teach practical laboratory haemostasis and was written for laboratory staff, doctors in training and anyone who has an interest in haemostasis. It stems from a series of seminars that have run in Cambridge for some years and from numerous requests for practical data interpretation exercises in haemostasis. The site will allow you work through various tests and to undertake a number of data-interpretation questions with the answers provided and an explanation as to how these answers were derived. We have included comprehensive data on the interpretation of the various tests and we hope, useful comments. The site is not designed to discuss the management of clinical problems.

Read more:
Practical-Haemostasis.com

Open:
Interavctive site map (in the image)

 Source: practical-haemostasis.com

Biomedical scientist discovers method to increase survival in sepsis

Sepsis, the body's response to severe infections, kills more people than breast cancer, prostate cancer and HIV/AIDS combined. On average, 30 percent of those diagnosed with sepsis die. A new study conducted by Jamey Marth, director of UC Santa Barbara's Center for Nanomedicine and professor of the Sanford-Burnham Medical Research Institute, reports a new method to increase survival in sepsis. The results appear today in the Proceedings of the National Academy of Sciences.

Building on earlier work in which Marth's team revealed the biological purpose of the Ashwell-Morell receptor (AMR) in the liver, the new discovery not only describes the AMR's protective mechanism, but also outlines a way to leverage it for therapeutic use. Sepsis often triggers widespread blood coagulation and thrombosis, which can lead to organ failure and death.

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Biomedical scientist discovers method to increase survival in sepsis




















Source: Science Daily
Image credits: UCSB

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Mystery in blot clotting disorder solved

Scientists claim to have finally solved the bloodcurdling mystery, a key breakthrough which has implications for the treatment of bleeding disorders.
A team at Harvard University has in fact uncovered the fundamental feedback mechanism that the body uses to regulate the clotting of blood, by applying cutting-edge techniques in single-molecule manipulation.

Read more:
Mystery in blot clotting disorder solved

Source: Science Daily
Image credits WebMD

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The Basics of Prothrombin Time

Prothrombin time was described by Quick in 1935. It is the time taken by re-calcified plasma to clot in the presence of tissue procoagulant extract known as thromboplastin. It asses the efficiency of the extrinsic coagulation system. The test depends on activation of factor X by factor VII by tissue factor.

The details of the method are beyond the scope of this text. The outline is as follows. Thromboplastin is added to plasma that has been separated from blood collected in sodium citrate and allowed time to mix. To this mixture calcium chloride is added. The time taken for the plasma to clot is the prothrombin time. The end point (clotting) may be determined manually or using automated (optical or magnetic) methods.

Read more:
Prothrombin Time 

Source: All about blood
Image credits: All about blood

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