Hematology: basic principles and practice
TL;DR: The sixth edition of Hoffman and co-authors' valuable textbook, which could well be the one to buy if you need one for your office desk or for the junior staff room, offers an authoritative narrative on the biology, diagnosis and therapy of a wide range of hematological disorders.
Abstract: Long gone are the days when a single author, such as Max Wintrobe or James Jandl, could single-handedly write a textbook embracing all that was known of contemporary hematology. Hoffman and co-authors have just published the sixth edition of their valuable textbook. They have recruited more than 300 authors, mostly from the United States, for individual chapters and produced a truly comprehensive compendium. They presumably offer an authoritative narrative on the biology, diagnosis and therapy of a wide range of hematological disorders. I say presumably because it was, forgivably I hope, way beyond my capacity to read the book cover-to-cover. Those few chapters that I did read, on topics close to my heart, were clearly written by experts, some of whom I knew personally, and all were informative and essentially error-free. The cited references, some listed under the heading ‘Suggested Further Reading’, were generally limited to 30, a feature I liked, but the full list was in many cases accessible online for the aficionado. The high quality of the diagrams, all of which seem to have been prepared especially for this book, deserves special commendation. Textbooks presumably made big profits for publishing houses in the past. Whether that is true today is less certain. The speed with which new knowledge is obtained in the 21st century and the pace of change of clinical practice do raise the question of whether a publishing house can really keep up and sell sequential copies of a popular textbook. And how precisely does one use the book which in this case weighs 5 kg? The answer, if there is one, must lie in electronic updating, an area where this book seems to excel. Once having bought the book, the reader can log into a dedicated website and obtain a complete list of references for a given chapter and update information on the topic of his/her interest. At a time when textbooks could be an endangered species, this could well be the one to buy if you need one for your office desk or for the junior staff room.
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TL;DR: Platelets provide a procoagulant surface facilitating amplification of cancer‐related coagulation, and can be recruited to shroud tumor cells, thereby shielding them from immune responses, and facilitate cancer growth and dissemination.
568 citations
TL;DR: An appreciation of the precise relationship between complement activation and thrombosis may facilitate the development of novel therapeutics, as well as improve the clinical management of patients withThrombotic conditions that are characterized by complement-associated inflammatory responses.
Abstract: The parallel expression of activation products of the coagulation, fibrinolysis, and complement systems has long been observed in both clinical and experimental settings. Several interconnections between the individual components of these cascades have also been described, and the list of shared regulators is expanding. The co-existence and interplay of hemostatic and inflammatory mediators in the same microenvironment typically ensures a successful host immune defense in compromised barrier settings. However, dysregulation of the cascade activities or functions of inhibitors in one or both systems can result in clinical manifestations of disease, such as sepsis, systemic lupus erythematosus, or ischemia–reperfusion injury, with critical thrombotic and/or inflammatory complications. An appreciation of the precise relationship between complement activation and thrombosis may facilitate the development of novel therapeutics, as well as improve the clinical management of patients with thrombotic conditions that are characterized by complement-associated inflammatory responses.
379 citations
Cites background from "Hematology: basic principles and pr..."
...It is now well established that hemostasis involves a combination of processes supporting blood clotting (coagulation) in sites at which the vascular integrity has been compromised and a subsequent dissolution of blood clots (fibrinolysis) [12]....
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TL;DR: Promotion of pathogen transmission by bioactive molecules in tick saliva was described as saliva-assisted transmission (SAT), and SAT candidates comprise compounds with anti-haemostatic, anti-inflammatory and immunomodulatory functions, but the molecular mechanisms by which they mediate pathogen Transmission are largely unknown.
Abstract: Ticks require blood meal to complete development and reproduction. Multifunctional tick salivary glands play a pivotal role in tick feeding and transmission of pathogens. Tick salivary molecules injected into the host modulate host defence responses to the benefit of the feeding ticks. To colonize tick organs, tick-borne microorganisms must overcome several barriers, i.e., tick gut membrane, tick immunity, and moulting. Tick-borne pathogens co-evolved with their vectors and hosts and developed molecular adaptations to avoid adverse effects of tick and host defences. Large gaps exist in the knowledge of survival strategies of tick-borne microorganisms and on the molecular mechanisms of tick-host-pathogen interactions. Prior to transmission to a host, the microorganisms penetrate and multiply in tick salivary glands. As soon as the tick is attached to a host, gene expression and production of salivary molecules is upregulated, primarily to facilitate feeding and avoid tick rejection by the host. Pathogens exploit tick salivary molecules for their survival and multiplication in the vector and transmission to and establishment in the hosts. Promotion of pathogen transmission by bioactive molecules in tick saliva was described as saliva-assisted transmission (SAT). SAT candidates comprise compounds with anti-haemostatic, anti-inflammatory and immunomodulatory functions, but the molecular mechanisms by which they mediate pathogen transmission are largely unknown. To date only a few tick salivary molecules associated with specific pathogen transmission have been identified and their functions partially elucidated. Advanced molecular techniques are applied in studying tick-host-pathogen interactions and provide information on expression of vector and pathogen genes during pathogen acquisition, establishment and transmission. Understanding the molecular events on the tick-host-pathogen interface may lead to development of new strategies to control tick-borne diseases.
261 citations
Cites background from "Hematology: basic principles and pr..."
...…a complex and efficient mechanism that controls blood loss after vascular injury through a series of physiological events leading to termination of blood loss from damaged blood vessels (vasoconstriction), formation of a platelet plug, fibrin clot formation and fibrinolysis (Hoffman et al., 2009)....
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TL;DR: Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders, and parenteral replacement therapy should be started soon after the vitamin deficiency has been established.
Abstract: Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and, less often, optic nerve atrophy. The spinal cord manifestation, subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity confined to posterior or posterior and lateral columns in the cervical and thoracic spinal cord. Isolated peripheral neuropathy is less frequent, but likely overlooked. Vitamin B12 deficiency has been correlated negatively with cognitive functioning in healthy elderly subjects. Symptoms include slow mentation, memory impairment, attention deficits and dementia. Optic neuropathy occurs occasionally in adult patient. It is characterized by symmetric, painless and progressive visual loss. Parenteral replacement therapy should be started soon after the vitamin deficiency has been established.
232 citations
TL;DR: Future hemostatic research in nephrotic syndrome should focus on identifying cohorts at highest risk for thrombosis through the use of clinical markers and biomarkers as well as searching for molecular targets to correct the prothrombotic pathophysiology of this disease.
Abstract: After infections, thromboembolism is considered by many experts to be the most significant life-threatening complication of nephrotic syndrome. The purpose of this review is to summarize the epidemiology, clinical and molecular pathophysiology, and management of this complication. Children (2.8%) are less likely than adults (26.7%) with nephrotic syndrome to develop thromboembolism. However, infants and children aged >12 years are at much greater risk. Membranous histologic changes increase thromboembolic risk at all ages; in particular, adults with membranous nephropathy have the highest reported risk (37.0%) and children with membranous histology have a rate (25%) that approaches the overall adult rate. There are striking, but variable, pathologic alterations of molecular hemostasis associated with nephrotic syndrome. No clear molecular therapeutic targets have been identified, but most studies show that the major pathologic changes involve antithrombin, fibrinogen, and factors V and VIII. There is inadequate evidence to support routine prophylactic therapy. Therapy includes anticoagulation in all cases, with thrombolysis reserved for those with the most severe thromboembolic disease. Future hemostatic research in nephrotic syndrome should focus on identifying cohorts at highest risk for thrombosis through the use of clinical markers and biomarkers as well as searching for molecular targets to correct the prothrombotic pathophysiology of this disease.
231 citations