Coagulation is a dynamic process and the understanding of the blood coagulation system has evolved over the recent years in anaesthetic practice. Although the traditional classification of the coagulation system into extrinsic and intrinsic pathway is still valid, the newer insights into coagulation provide more authentic description of the same. Normal coagulation pathway represents a balance between the pro coagulant pathway that is responsible for clot formation and the mechanisms that inhibit the same beyond the injury site. Imbalance of the coagulation system may occur in the perioperative period or during critical illness, which may be secondary to numerous factors leading to a tendency of either thrombosis or bleeding. A systematic search of literature on PubMed with MeSH terms 'coagulation system, haemostasis and anaesthesia revealed twenty eight related clinical trials and review articles in last 10 years. Since the balance of the coagulation system may tilt towards bleeding and thrombosis in many situations, it is mandatory for the clinicians to understand physiologic basis of haemostasis in order to diagnose and manage the abnormalities of the coagulation process and to interpret the diagnostic tests done for the same.

Overview of the coagulation system

Fibrinolysis and the control of blood coagulation.

epidurals, mask ventilation, and endotracheal tube insertion. Appendix E contains suggested readings, peer-reviewed publications mostly covering large epidemiologic studies and reviews. The index covers 8 pages and is very detailed, making the book useful for quick consultation. Given the need for brevity and inclusiveness, this little book provides a broad overview of our specialty and covers most of what a nonanesthesiologist should know about what we do.

Hemostasis and Thrombosis—Basic Principles and Clinical Practice

Background
Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or functional mutations in other genes that are still unknown. We sought to identify and characterize a hitherto unknown type of HAE with normal C1-INH and without mutation in the F12 gene.

Methods
The study comprised analysis of whole-exome sequencing, Sanger sequencing, and clinical data of patients.

Results
We detected a mutation in the plasminogen (PLG) gene in patients with HAEnCI. The mutation c.9886A>G was located in exon 9 leading to the missense mutation p.Lys330Glu (K330E) in the kringle 3 domain of the PLG protein. The mutation was identified by next-generation sequencing in 14 patients with HAEnCI belonging to 4 of 7 families. Family studies revealed that this type of HAE was transmitted as an autosomal dominant trait. The PLG gene mutation was present in all studied symptomatic patients and was also found in 9 of 38 index patients from 38 further families with HAEnCI. Most patients had swelling of face/lips (78.3%) and tongue (78.3%). A total of 331 of all 3.795 tongue swellings (8.7%) were associated with dyspnea, voice changes, and imminent asphyxiation. Two women died by asphyxiation due to a tongue swelling.

Conclusions
Hereditary angioedema with a mutation in the PLG gene is a novel type of HAE. It is associated with a high risk of tongue swellings.

Hereditary angioedema with a mutation in the plasminogen gene

Plasmin, one of the most potent and reactive serine proteases, is involved in various physiological processes, including embryo development, thrombolysis, wound healing and cancer progression. The proteolytic activity of plasmin is tightly regulated through activation of its precursor, plasminogen, only at specific times and in defined locales as well as through inhibition of active plasmin by its abundant natural inhibitors. By exploiting the plasminogen activating system and overexpressing distinct components of the plasminogen activation cascade, such as pro-uPA, uPAR and plasminogen receptors, malignant cells can enhance the generation of plasmin which in turn, modifies the tumor microenvironment to sustain cancer progression. While plasmin-mediated degradation and modification of extracellular matrix proteins, release of growth factors and cytokines from the stroma as well as activation of several matrix metalloproteinase zymogens, all have been a focus of cancer research studies for decades, the ability of plasmin to cleave transmembrane molecules and thereby to generate functionally important cleaved products which induce outside-in signal transduction, has just begun to receive sufficient attention. Herein, we highlight this relatively understudied, but important function of the plasmin enzyme as it is generated de novo at the interface between cross-talking cancer and host cells.

/pdf/cell-surface-remodeling-by-plasmin-a-new-function-for-an-old-2ve2mhsrnt.pdf

Cell surface remodeling by plasmin: a new function for an old enzyme.

Summary.  Plasminogen deficiency has emerged as a well‐recognized disorder in which reduced levels of plasminogen lead to the development of pseudo membranes on mucosal surfaces, with subsequent end‐organ damage of the affected tissue. Ligneous conjunctivitis is the most recognizable, well‐documented, and common presentation of the clinical syndromes associated with plasminogen deficiency, although numerous other organs have been reported to be affected. Interestingly, while plasminogen deficiency was initially believed to be related to development of venous thromboembolic disease, more recent data suggest that decreased plasminogen levels may not, in and of themselves, increase the risk of thrombosis. Two types of plasminogen deficiency have been described in the literature. Type I represents a quantitative deficiency and type II a qualitative deficiency. It appears that hypoplasminogenaemia (type I deficiency) is the type most associated with pseudomembrane disease. A variety of genetic mutations has been identified recently and is reported to lead to these disorders. These defects have been identified in diverse populations, with no specific ethnic predilection. However, this disorder may have increased prevalence in areas and communities where consanguinity is more common. Despite the fact that the characteristic lesions are now better recognized and plasminogen levels are accurately and easily measured, adequate treatment of the clinical manifestations of this disorder is lacking. For ligneous conjunctivitis, a plasminogen concentrate formulated into an ophthalmologic preparation has been found to be an effective local therapy. Unfortunately, no plasminogen concentrate is currently available commercially for either systemic or local therapy.

Plasminogen deficiency: PLASMINOGEN DEFICIENCY

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Plasminogen deficiency: PLASMINOGEN DEFICIENCY