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Journal articles on the topic 'White clot syndrome'

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Published: 4 June 2021

Last updated: 9 February 2022

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1

STANTON, PAUL E., JAMES R. EVANS, ARMAND A. LEFEMINE, NGHIA M. VO, GILBERT A. RANNICK, CALVIN V. MORGAN, PHILIP J. HINTON, and MARTHA READ. "White Clot Syndrome*." Southern Medical Journal 81, no. 5 (May 1988): 616–20. http://dx.doi.org/10.1097/00007611-198805000-00018.

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2

Miller, Peggy, and Sheryl Yardley. "WHITE CLOT SYNDROME." AJN, American Journal of Nursing 85, no. 10 (October 1985): 1051. http://dx.doi.org/10.1097/00000446-198510000-00003.

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3

Miller, Peggy, and Sheryl Yardley. "WHITE CLOT SYNDROME." AJN, American Journal of Nursing 85, no. 10 (October 1985): 1051. http://dx.doi.org/10.1097/00000446-198510000-00005.

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4

Chang, Jae C. "White clot syndrome." Postgraduate Medicine 87, no. 1 (January 1990): 293–98. http://dx.doi.org/10.1080/00325481.1990.11704541.

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5

Mallios, Alexandros, and William Jennings. "White Clot Syndrome." European Journal of Vascular and Endovascular Surgery 55, no. 3 (March 2018): 404. http://dx.doi.org/10.1016/j.ejvs.2017.09.007.

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6

Daubert, G. P. "The white clot syndrome." Journal of Clinical Pharmacy and Therapeutics 30, no. 6 (December 2005): 503. http://dx.doi.org/10.1111/j.1365-2710.2005.00675.x.

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7

Somers, D. L., C. Sotolongo, and J. A. Bertolatus. "White clot syndrome associated with renal failure." Journal of the American Society of Nephrology 4, no. 2 (August 1993): 137–41. http://dx.doi.org/10.1681/asn.v42137.

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In a minority of patients, heparin administration is associated with thrombocytopenia and this thrombocytopenia may be associated with thromboembolic events. Heparin-associated thromboembolism is described as heparin-associated thrombocytopenia and thrombosis or white clot syndrome. White clot syndrome is caused by antibodies to a heparin-platelet membrane complex. The diagnosis carries a high mortality and morbidity from limb thromboembolism. Treatment includes discontinuation of heparin, use of alternate anticoagulants, and aggressive treatment of thromboses. A case in which acute renal fail

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8

Kuhar, Peggy A., and Kathleen M. Hill. "White Clot Syndrome: When Heparin Goes Haywire." American Journal of Nursing 91, no. 3 (March 1991): 59. http://dx.doi.org/10.2307/3426548.

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9

Broughan, Thomas A., Kandice Kottke-Marchant, and David P. Vogt. "THE ???WHITE CLOT SYNDROME??? IN HEPATIC TRANSPLANTATION." Transplantation 61, no. 6 (March 1996): 982–84. http://dx.doi.org/10.1097/00007890-199603270-00027.

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10

Kuhar, Peggy A., and Kathleen M. Hill. "White Clot Syndrome: When Heparin Goes Haywire." AJN, American Journal of Nursing 91, no. 3 (March 1991): 59–60. http://dx.doi.org/10.1097/00000446-199103000-00019.

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11

Batra, Munish K., Michael D. Adolph, James C. Thornton, Aspi M. Byramjee, Alan O. Oliver, and Helmut Schreiber. "Antithrombin III Deficiency and White Clot Syndrome." Vascular Surgery 30, no. 1 (January 1996): 37–44. http://dx.doi.org/10.1177/153857449603000107.

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12

Köppel, C., D. Barckow, and H. Riess. "Severe white-clot syndrome after unfractionated heparin." Intensive Care Medicine 17, no. 3 (March 1991): 185. http://dx.doi.org/10.1007/bf01704726.

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13

Shelly, M. P., R. V. Majer, C. Perkins, T. Pierce, and M. S. Nielsen. "White clot syndrome and continuous arteriovenous haemofiltration." Intensive Care Medicine 16, no. 5 (May 1990): 334–35. http://dx.doi.org/10.1007/bf01706362.

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14

AbuRahma, Ali F., James P. Boland, and Todd Witsberger. "Diagnostic and therapeutic strategies of white clot syndrome." American Journal of Surgery 162, no. 2 (August 1991): 175–79. http://dx.doi.org/10.1016/0002-9610(91)90183-e.

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15

Adebonojo, Samuel A., George Nova, and Ishwar N. Visweshwar. "White Clot Syndrome-Heparin-Induced Platelet Aggregation: A Case Report." Annals of Saudi Medicine 11, no. 6 (November 1991): 698–700. http://dx.doi.org/10.5144/0256-4947.1991.698.

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16

Melanson, Scott W., Barry Silver, and Michael B. Heller. "Deep vein thrombosis, pulmonary embolism, and the white clot syndrome." American Journal of Emergency Medicine 14, no. 6 (October 1996): 558–60. http://dx.doi.org/10.1016/s0735-6757(96)90098-4.

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17

Desmet, G., A. Louwagie, A. Criel, M. Hidayat, and A. Van Hoof. "Heparin-Induced Thrombocytopenia With Disseminated Intravascular Coagulation And White Clot Syndrome A Case Report." Acta Clinica Belgica 43, no. 6 (January 1988): 419–22. http://dx.doi.org/10.1080/17843286.1988.11717969.

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18

Pfeiffer, G., J. Eberhardt, and R. Hamann. "White-clot-syndrome in heparin-induced thrombocytopenia type II with cross reactivity to danaparoid." Gefässchirurgie 5, no. 2 (May 12, 2000): 125–29. http://dx.doi.org/10.1007/s007720050192.

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19

Kleinschmidt, S., T. Ziegenfuß, U. Seyfert, and A. Greinacher. "Septisch-toxisches Herz-Kreislauf-Versagen als Folge einer Heparin-induzierten Thrombozytopenie mit „White-Clot-Syndrome”." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 28, no. 01 (February 1993): 58–60. http://dx.doi.org/10.1055/s-2007-998879.

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20

Claeys, L. G. Y. "Multiple Postoperative Thromboembolic Events and Fatal Pulmonary Embolism : the White Clot Syndrome. A Case Report." Acta Chirurgica Belgica 101, no. 3 (June 1, 2001): 139–40. http://dx.doi.org/10.1080/00015458.2001.12098604.

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21

Soetrisno, Coco Kokarkin. "NON-CLOTTING HAEMOLYMPH OF WSSV-INFECTED SHRIMP: IS IT A FACTOR IN INFECTION PROCESSES?" Indonesian Aquaculture Journal 4, no. 2 (December 31, 2009): 109. http://dx.doi.org/10.15578/iaj.4.2.2009.109-119.

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White spot syndrome virus is recognized as the most prominent pathogen of penaeid shrimp and has been affecting this shrimp farming industry around the world. The virus may reduce the shrimp’s immune response and alter enzymatic and biochemical composition of tissues. Similar to other environmental stressed or other pathogeninfected shrimp, in late stages of WSSV infection, shrimp will fail to clot the haemolymph, so any minor injury will lead to increased haemolyph loss. A series of experiments to determine the effect of non-clotting haemolymph on WSSV infection were carried out in controlled

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22

Celińska-Löwenhoff, Magdalena, Teresa Iwaniec, Agnieszka Padjas, Jacek Musiał, and Anetta Undas. "Altered fibrin clot structure/function in patients with antiphospholipid syndrome: association with thrombotic manifestation." Thrombosis and Haemostasis 112, no. 08 (2014): 287–96. http://dx.doi.org/10.1160/th13-11-0980.

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SummaryWe tested the hypothesis that plasma fibrin clot structure/function is unfavourably altered in patients with antiphospholipid syndrome (APS). Ex vivo plasma clot permeability, turbidity and susceptibility to lysis were determined in 126 consecutive patients with APS enrolled five months or more since thrombotic event vs 105 controls. Patients with both primary and secondary APS were characterised by 11% lower clot permeability (p<0.001), 4.8% shorter lag phase (p<0.001), 10% longer clot lysis time (p<0.001), and 4.7% higher maximum level of D-dimer released from clots (p=0.02)

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23

Fernandez-Bello, Ihosvany, Raul Justo Sanz, Elena Monzón Manzano, Francisco García Río, Carolina Cubillos, Cristina Balbás-García, Teresa Álvarez-Roman, et al. "Platelet Dysfunction and Cellular Microparticles May be Involved in the Hipercoagulable State Observed in Obstructive Sleep Apnea Syndrome." Blood 132, Supplement 1 (November 29, 2018): 5048. http://dx.doi.org/10.1182/blood-2018-99-116018.

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Abstract Introduction: Obstructive sleep apnea syndrome (OSA) is a common disorder characterized by repetitive episodes of nocturnal breathing cessation due to upper airway collapse that cause intermittent hypoxia. Because of this, there is an increase in oxidative stress, endothelial damage and mortality associated with the incidence of thrombotic events. The evaluation of platelet function by flow cytometry (FCM) and hemostatic capacity through global hemostasis tests have been successfully used in the study of the prothrombotic state associated to numerous diseases. We anticipate that these

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24

Johnston, Ian, Vincent M. Hayes, Douglas B. Cines, and Mortimer Poncz. "A Targeted Photochemical Microfluidic Vascular Injury Model for in Vitro Thrombosis Studies: Usage in Heparin-Induced Thrombocytopenia (HIT)." Blood 126, no. 23 (December 3, 2015): 212. http://dx.doi.org/10.1182/blood.v126.23.212.212.

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Abstract Replicating the complexities of the human blood vessel include the establishment of a 3-D confluency of viable endothelial cells (ECs) on an appropriate matrix, use of human whole blood or specific components of blood, varied shear stresses, and the induction of a localized and controlled injury within the observable field to understand and intervene in hemostatic events. This array of complexities have made vascular modeling an important unmet challenge. Such a model would enhance our understanding of the pathogenesis of diverse coagulation disorders, such as the prothrombotic disord

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25

Waller, Amanda P., Katelyn J. Wolfgang, and Bryce A. Kerlin. "The Hypofibrinolytic Defect of Nephrotic Syndrome Is Directly Proportional to Fibrin Network Density." Blood 132, Supplement 1 (November 29, 2018): 1218. http://dx.doi.org/10.1182/blood-2018-99-119947.

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Abstract Introduction Nephrotic syndrome (NS) is characterized by massive proteinuria (secondary to podocyte injury), hypoalbuminemia, and edema. Importantly, NS is associated with a complex acquired hypercoagulopathy and a high incidence (~25%) of life-threatening thrombotic complications. Both hypercoagulopathy and hypofibrinolysis are described contributors to NS-related VTE risk. However, the mechanisms underlying the latter are poorly understood. We previously showed NS disease severity is directly proportional to both hypercoagulopathy and fibrinolytic resistance There is evidence that f

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26

Tyukachev, V. E., D. A. Oks, and A. A. Butylkin. "A case of successful systemic thrombolysis in massive thromboembolia of pulmonary artery against the background of pregnancy." Patologiya krovoobrashcheniya i kardiokhirurgiya 21, no. 3 (November 22, 2017): 95. http://dx.doi.org/10.21688/1681-3472-2017-3-95-99.

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<p>We present a clinical case of successful systemic thrombolysis in a pregnant patient with massive pulmonary embolism. A 29-year old patient at 28 weeks of pregnancy was hospitalized 2 hours after sudden suffocation in a presyncopal state and hypotension of 90/50 mm Hg. ECG showed the signs of overload of right heart chambers in the form of a typical S1-Q3-T3 (McGinn–White) syndrome, as well as the Kosuge sign. Echocardiography verified pulmonary 3 Grade hypertension (81 mm Hg), enlargement of the right atrium and ventricle, 3 Grade tricuspid regurgitation and paradoxical movement of t

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27

Baranova, Anastasya A., Ilya G. Pochinka, Leonid G. Strongin, Ksenia N. Jurkova, and Maya I. Dvornikova. "Clinical correlates of thrombodynamics in men with metabolic syndrome: the impact of insulin resistance." Problems of Endocrinology 62, no. 5 (September 22, 2016): 24–25. http://dx.doi.org/10.14341/probl201662524-25.

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Background. Hypercoagulation is one of the cardiovascular risk factors in patients with metabolic syndrome (MS). It results from various factors including hyperhomocysteinemia, endothelial dysfunction, non-enzymatic glycation of proteins etc.The aim of this study was to assess clinical correlates of thrombodynamics in insulin resistant and non insulin resistant men with metabolic syndrome.Methods. We investigated 79 patients with MS diagnosed in accordance with IDF criteria (2009). The main group consisted of 44 men with MS including insulin resistance. The control group consisted of 35 men wi

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28

Pchelin, Ivan Y., Natalia V. Hudiakova, and Alexander N. Shishkin. "Clinical correlates of thrombodynamics in men with metabolic syndrome: the impact of insulin resistance." Problems of Endocrinology 62, no. 5 (September 22, 2016): 25–26. http://dx.doi.org/10.14341/probl201662525-26.

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Background. Hypercoagulation is one of the cardiovascular risk factors in patients with metabolic syndrome (MS). It results from various factors including hyperhomocysteinemia, endothelial dysfunction, non-enzymatic glycation of proteins etc.The aim of this study was to assess clinical correlates of thrombodynamics in insulin resistant and non insulin resistant men with metabolic syndrome.Methods. We investigated 79 patients with MS diagnosed in accordance with IDF criteria (2009). The main group consisted of 44 men with MS including insulin resistance. The control group consisted of 35 men wi

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29

Steffel, J., and T. F. Lüscher. "Individualized antithrombotic therapy." Hämostaseologie 36, no. 01 (2016): 26–32. http://dx.doi.org/10.5482/hamo-14-12-0080.

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SummaryClot formation in the circulation is a physiological mechanism preventing bleeding at sites of loss of vascular integrity. Clot formation may also occur intravascularly under pathological conditions, e. g. leading to myocardial infarction, stroke, and critical limb ischaemia. Clot formation involves activation of the coagulation cascade and of platelets eventually leading to an occlusive clot. In the venous circulation, clots are rich in erythrocytes and fibrin, while in the arterial circulation platelets predominate. Accordingly, drugs have been developed to interfere with the activati

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30

Cayla, Guillaume, Pierre Sie, Johanne Silvain, Delphine Brugier, Jean-Pierre Cambou, Daniel Thomas, Ana Pena, et al. "Short-term effects of the smoke-free legislation on haemostasis and systemic inflammation due to second hand smoke exposure." Thrombosis and Haemostasis 105, no. 06 (2011): 1024–31. http://dx.doi.org/10.1160/th11-02-0062.

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SummaryIt was the objective of this study to assess the effect of the implementation of the smoke-free legislation on haemostasis and systemic inflammation in second-hand smoking (SHS)-exposed healthy volunteers. Fibrin-rich clot properties, platelet reactivity and inflammatory biomarkers were measured before and four months following the implementation of the smoke-free legislation in gender and age-matched healthy volunteers exposed (n=23, exposed) and unexposed (n=23, controls) to occupational SHS. The primary objective was to compare fibrin-rich clot stiffness before and after implementati

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31

Vorobev, Alexander Viktorovich, Alexander Davidovich Makatsaria, Andrey Mikhailovich Chabrov, and Alexander Anatol’evich Savchenko. "Pathogenesis of Trousseau’s syndrome." Journal of obstetrics and women's diseases 64, no. 4 (September 15, 2015): 85–94. http://dx.doi.org/10.17816/jowd64485-94.

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Malignancies and thrombosis have common pathogenetic features that was shown by A. Trousseau in 1865. There is now no doubt that the cancer patients occur much more frequently thromboembolism, and migratory venous thrombosis is a manifestation of paraneoplastic syndrome in cancer patients. In general, any manifestation of thrombohemorrhagic complications in cancer patients called Trousseau’s syndrome. While thrombotic complications such as venous thromboembolism are most frequent in cancer patients, may also experience severe bleeding symptoms due to systemic coagulopathies, including dissemin

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Hamarshi, Majdi, Tasma Harindhanavudhi, Maha Abu Kishk, Ammar Hamad, and Joseph Pyle. "Lymphoplasmacytic Lymphoma with IgA Gammopathy, Case Report and Review of Literature." Blood 110, no. 11 (November 16, 2007): 4409. http://dx.doi.org/10.1182/blood.v110.11.4409.4409.

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Abstract The Second International Workshop on Waldenstrom’s macroglobulinemia Consensus Panel has recommended diagnostic criteria that have been modified by the Mayo Clinic and large cohort studies 1–5. Essential to the criteria: IgM monoclonal gammopathy regardless of the size of the M protein, 10% or greater bone marrow infiltration by small lymphocytes that exhibit plasmacytoid or plasma cell differentiation with an intertrabecular pattern, and typical immunophenotype. We present a 72 year old WM who is free of any past medical history, presented with worsening ataxic gait for four months,

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Fitzmaurice, David, Kate Fletcher, Sheila Greenfield, Sue Jowett, Alison Ward, Carl Heneghan, Eve Knight, et al. "Prevention and treatment of venous thromboembolism in hospital and the community: a research programme including the ExACT RCT." Programme Grants for Applied Research 8, no. 5 (May 2020): 1–104. http://dx.doi.org/10.3310/pgfar08050.

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Background Deep-vein thrombosis and pulmonary embolism, collectively known as venous thromboembolism when clots are formed in the venous circulation, are common disorders that are often unprovoked (i.e. there is no obvious reason for the clot occurring). Some people, after having an unprovoked clot, are at a high risk of developing another, or at risk of developing a secondary clot, most importantly in the lungs. Furthermore, in the long term, some patients will develop circulation problems known as post-thrombotic syndrome. The aim of this programme was to improve the understanding of both th

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Seredavkina, N., T. Reshetnyak, T. Lisitsyna, and A. Lila. "AB0305 IS THERE HYPERCOAGULATION IN PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME AND BEHCET’S DISEASE?" Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1178.2–1179. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1319.

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Background:Whereas antiphospholipid syndrome (APS) is a non-inflammatory vasculopathy and is associated with thrombosis in 98% of cases, Behcet’s disease (BD) is a systemic vasculitis of unknown etiology, characterized by vascular damage of any calibre. Both venous and arterial thromboses occur in 45% of BD patients and are associated not with hypercoagulable disease but with inflammatory changes in the vascular wall mediated by hypersecretion of pro-inflammatory cytokines and endothelial cells dysfunction. Thrombodynamics (TD) is a new global test for diagnosing plasma haemostasis disorders,

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35

Yeh, C., B. Camilotti, H. Hanif, R. Mohindra, C. Sun, P. Kim, S. Lin, and M. Sholzberg. "P001: Proof-of-principle in a large animal pilot: cardiac arrest may be associated with acute, transient coagulopathy that may drive post-cardiac arrest syndrome." CJEM 22, S1 (May 2020): S64—S65. http://dx.doi.org/10.1017/cem.2020.209.

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Introduction: Many cardiac arrest survivors die later due to hemorrhage or thromboembolism, thought to be caused by acquired coagulopathy in post-cardiac arrest syndrome (PCAS) from shock and reperfusion injury. Understanding PCAS is a priority identified by the AHA for the prevention of complications in cardiac arrest survivors. Shock dysregulates both coagulation and fibrinolysis. The key effector enzyme thrombin (Th), is responsible for both up- and down-regulating coagulation and fibrinolysis. Measuring early Th activity may allow for predicting PCAS coagulopathy, and early medical interve

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36

Sedney, Cara L., Brenton R. Coger, and Julian E. Bailes. "Posterior Fossa Subdural Hematoma Resulting in Locked-in Syndrome: Case Report." Neurosurgery 69, no. 2 (March 30, 2011): E497—E500. http://dx.doi.org/10.1227/neu.0b013e318218cf85.

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Abstract BACKGROUND AND IMPORTANCE: Locked-in syndrome (LIS) is a well-known and devastating clinical entity, of which stroke is the most common cause; the distant second, trauma, usually results in LIS from basilar artery dissection. Our case report describes a posterior fossa subdural hematoma causing LIS, likely by direct compression of neural structures, which is a unique etiology and prognosis compared with other causes. CLINICAL PRESENTATION: A 34-year-old female experienced a posterior fossa subdural hematoma. She was taken emergently for evacuation, and on postoperative examination was

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Swanepoel, Albe C., Amcois Visagie, and Etheresia Pretorius. "Synthetic Hormones and Clot Formation." Microscopy and Microanalysis 22, no. 4 (August 2016): 878–86. http://dx.doi.org/10.1017/s1431927616011478.

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AbstractCombined oral contraceptives (COCs), colloquially referred to as “the pill,” have been regarded as a medical breakthrough, as they have improved the lives of countless women, from simplifying family planning to the treatment of acne, endometriosis, polycystic ovarian syndrome, and dysmenorrhea. Unfortunately, COC usage has been associated with an increased occurrence of venous thrombosis and therefore a systemic hypercoagulable state in susceptible females. Here we discuss the health risks of COC usage and use viscoelastic and morphological techniques to investigate the effect of diffe

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38

Ringer, Coral N., Rebecca J. Engberg, Kristen E. Carlin, Kellie J. Micheletti, Dianna L. Shankland, and Robert M. DiBlasi. "Assessment of mask efficiency for preventing transmission of airborne illness through aerosols and water vapor." Gates Open Research 5 (July 20, 2021): 105. http://dx.doi.org/10.12688/gatesopenres.13318.1.

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Background: Currently the Center for Disease Control has advised the use of face coverings to prevent transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to those who are unvaccinated. This study seeks to evaluate if cloth masks have increased efficiency with the addition of a filter material. Methods: An adult airway and test lung model were exposed to nebulized ‘coarse’ aerosol droplets (0.5-11 µm) and humidified ‘fine’ water vapor particles (0.03-0.05 µm). Aerosol was quantified based on particles deposited on the face, airway and lung model. Tracheal humidity level

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Odani, Kentaro, Junya Abe, Yoshiaki Tsuyuki, Soshi Yanagita, Kazuya Shiogama, Mitsuhiro Tachibana, and Yutaka Tsutsumi. "Acute Coronary Syndrome in Acute Myeloid Leukemia with Maturation Accompanying Megakaryocytic Differentiation." Case Reports in Pathology 2020 (September 21, 2020): 1–7. http://dx.doi.org/10.1155/2020/8886298.

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An autopsy case (85-year-old Japanese male) of myeloperoxidase- (MPO-) positive acute myeloid leukemia with maturation (M1) accompanying megakaryocytic differentiation is presented. The patient manifested acute coronary syndrome. Even after emergent percutaneous coronary intervention, his performance status remained poor, so no chemotherapy against leukemia was given. The final white blood cell count reached 291,700/μL, and the platelet count was elevated to 510,000/μL. No cytogenetic studies were performed. He died at the 25th day of hospitalization. Autopsy revealed marked leukemic infiltrat

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Dobesh, Paul P., and Julie H. Oestreich. "Novel Direct-Acting Anticoagulants for Risk Reduction in ACS." Journal of Pharmacy Practice 26, no. 4 (November 19, 2012): 358–66. http://dx.doi.org/10.1177/0897190012465954.

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Acute coronary syndrome (ACS) is a devastating adverse cardiovascular event with a massive burden on patient morbility and mortality, as well as the economy. Approximately 1.2 million people are hospitalized annually for ACS in the United States, with direct medical costs estimated at $150 billion in 2009. Rehospitalization is common, often as the result of recurrence of the initial event or complications of ACS or its therapy. Thrombosis is central to the pathogenesis of ACS. The current standard of care includes dual antiplatelet therapy, which reduces platelet activation and aggregation, in

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Kemerov, S. V., V. M. Vorobjev, M. R. Karpova, M. M. Solov᾿ev, and G. Tz Dambaev. "Prevention of pathological syndromes and post-morbidity rehabilitation of patients with heavy surgical infection on the basis of the complications development prediction index." Bulletin of Siberian Medicine 17, no. 3 (September 29, 2018): 70–79. http://dx.doi.org/10.20538/1682-0363-2018-3-70-79.

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Purpose of the study: working out an easy-to-use complication development index (CDI), designing a program for post morbidity rehabilitation of patients with surgical infection to improve the results of its treatment and reduce lethality.Materials and methods. A retrospective results analysis of treatment of 320 patients for purulent peritonitis and abdominal sepsis was carried out, including 268 patients (the comparison group) and 52 (the core group) with whom the complications development index was calculated. While studying this group of patients, the same protocol was used to prevent and t

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42

Johansen, Max E., Wenche Jy, Lawrence L. Horstman, Carlos Bidot, and Yeon S. Ahn. "Red Cell-Derived Microparticles (RMP) Correct or Improve Abnormal Coagulation Profiles in TEG in a Variety of Disorders of Different Pathology." Blood 118, no. 21 (November 18, 2011): 2277. http://dx.doi.org/10.1182/blood.v118.21.2277.2277.

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Abstract Abstract 2277 Introduction: Thromboelastography (TEG) reports several viscoelatstic changes during clot formation, giving useful information on multiple parameters, and can give information on effects of therapeutic measures. We previously demonstrated that RMP can improve clotting parameters in selected bleeding disorders, judging by TEG. In this report we characterize the abnormalities seen in TEG in several disease states, and how RMP can modify or correct the abnormal parameters. Methods: (i) The following patient groups were studied by TEG: Patients with ITP (n=10), other non imm

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Brooks, Marjory B., James L. Catalfamo, H. Alex Brown, Pavlina Ivanova, and Jamie Lovaglio. "A hereditary bleeding disorder of dogs caused by a lack of platelet procoagulant activity." Blood 99, no. 7 (April 1, 2002): 2434–41. http://dx.doi.org/10.1182/blood.v99.7.2434.

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We have discovered a novel canine hereditary bleeding disorder with the characteristic features of Scott syndrome, a rare defect of platelet procoagulant activity. Affected dogs were from a single, inbred colony and experienced clinical signs of epistaxis, hyphema, intramuscular hematoma, and prolonged bleeding with cutaneous bruising after surgery. The hemostatic abnormalities identified were restricted to tests of platelet procoagulant activity, whereas platelet count, platelet morphology under light microscopy, bleeding time, clot retraction, and platelet aggregation and secretion in respon

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Kotova, Yana N., Nadezhda A. Podoplelova, Sergey I. Obydennyy, Elizaveta A. Kostanova, Alexander A. Ryabykh, Aleksandra S. Demyanova, Maria I. Biriukova та ін. "Binding of Coagulation Factor XIII Zymogen to Activated Platelet Subpopulations: Roles of Integrin αIIbβ3 and Fibrinogen". Thrombosis and Haemostasis 119, № 06 (1 квітня 2019): 906–15. http://dx.doi.org/10.1055/s-0039-1683912.

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AbstractFactor XIIIa (fXIIIa) is a transglutaminase that plays a crucial role in fibrin clot stabilization and regulation of fibrinolysis. It is known to bind to procoagulant platelets. In contrast, the zymogen fXIII interaction with platelets is not well characterized. We investigated the interaction of zymogen fXIII with activated platelet subpopulations. Confocal microscopy and flow cytometry using fluorescently labelled factors and antibodies. Phosphatidylserine (PS)-positive activated platelets bound 700 to 800 molecules/cell of fXIII at 100 nM, while both PS-negative activated platelets

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Matusik, Pawel, Bartlomiej Guzik, Christian Weber, and Tomasz J. Guzik. "Do we know enough about the immune pathogenesis of acute coronary syndromes to improve clinical practice?" Thrombosis and Haemostasis 108, no. 09 (2012): 443–56. http://dx.doi.org/10.1160/th12-05-0341.

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SummaryMorbidities related to atherosclerosis, such as acute coronary syndromes (ACS) including unstable angina and myocardial infarction, remain leading causes of mortality. Unstable plaques are inflamed and infiltrated with macrophages and T lymphocytes. Activated dendritic cells interact with T cells, yielding predominantly Th1 responses involving interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α), while the role of interleukin 17 (IL-17) is questionable. The expansion of CD28nullCD4 or CD8 T cells as well as pattern recognition receptors activation (especially Toll-like rece

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Cacciapuoti, Federico. "Thrombophilias: therapeutic employment of direct oral anticoagulants in venous hypercoagulable states." Italian Journal of Medicine 14, no. 3 (September 17, 2020): 136–42. http://dx.doi.org/10.4081/itjm.2020.1296.

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Thrombophilia or hypercoagulable state is a predisposition to form clots. Thrombophilia can be inherited or acquired, and prevalently involves venous vessels. Inherited thrombophilia consists of congenital conditions, as methylenetetrahydrofolate reductase polymorphism, Factor V Leiden and prothrombin gene mutations, natural anticoagulant deficiencies, high level of factor VIII, or dysfibrinogenemia. These congenital disorders can be responsible for venous thromboembolism, particularly deep venous thrombosis, pulmonary embolism, and, less frequently, mesenteric veins thrombosis, kidneys’ veins

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Chen, PP, M. Wu, and BH Hahn. "Some antiphospholipid antibodies bind to various serine proteases in hemostasis and tip the balance toward hypercoagulant states." Lupus 19, no. 4 (March 30, 2010): 365–69. http://dx.doi.org/10.1177/0961203310361488.

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The body has an elaborate system that maintains blood circulation and rapidly stops bleeding when vessels are damaged. Abnormalities that disrupt this balance may lead to thrombosis. While β2-glycoprotein I is generally accepted as the major antigen for antiphospholipid antibodies in the antiphospholipid syndrome, our accumulated studies show that some antiphospholipid antibodies bind homologous enzymatic domains of several serine proteases involved in hemostasis and fibrinolysis. Functionally, some of the protease-reactive antiphospholipid antibodies hinder anticoagulant regulation and resolu

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Kunk, Paul, B. Gail Macik, and Melissa Rice. "Non-Warfarin Oral Anticoagulants in Anti-Phospholipid Syndrome." Blood 126, no. 23 (December 3, 2015): 1133. http://dx.doi.org/10.1182/blood.v126.23.1133.1133.

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Abstract Introduction: Anti-Phospholipid Syndrome (APS) is a serious and deadly disorder leading to a significant risk of thrombi, requiring lifelong therapeutic anticoagulation. Traditionally, the vitamin K antagonist (VKA) warfarin has been considered standard of care in this patient population. However, the VKAs require frequent laboratory monitoring, have a narrow therapeutic window, numerous drug interactions and dietary restrictions. Due to these factors, many patients suffer recurrent thrombi and/or major bleeding, warranting therapy modification or switching to parenteral anticoagulant

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Santiago, Marc Reinald G., and Natividad A. Almazan. "Gradenigo Syndrome." Philippine Journal of Otolaryngology-Head and Neck Surgery 23, no. 2 (December 27, 2008): 46–48. http://dx.doi.org/10.32412/pjohns.v23i2.747.

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Chronic suppurative otitis media (CSOM) has a potential for intratemporal complications. Gradenigo syndrome, lateral sinus thrombosis and cavernous sinus thrombosis must be considered when patients present with ear discharge, headache, fever and lateral rectus palsy. Computed Tomography and Magnetic Resonance Imaging are essential in confirming the diagnosis but do not substitute for a good clinical eye in establishing the diagnosis and initiating proper treatment. CASE A 17 year old male with an 11-year history of otorrhea on the right ear was admitted because of on-and-off diffus

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Del Pozzo, Jill, Erica F. Weiss, Diana Bronshteyn, David M. Masur, John J. McGinley, and Ronda F. Facchini. "A-57 The Neuropsychological Impact of Antiphospholipid Antibody Syndrome: A Case Study." Archives of Clinical Neuropsychology 36, no. 6 (August 30, 2021): 1099. http://dx.doi.org/10.1093/arclin/acab062.75.

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Abstract Objective Antiphospholipid Antibody Syndrome (APS), also known as Hughes Syndrome, is an autoimmune condition linked to various adverse medical and neurological outcomes affecting 5 in 100,000. APS results from antibodies (aPL) that attack blood proteins that bind to phospholipids (e.g., 2-glycoprotein I and prothrombin), which can cause blood flow problems, increased risk of blood clots, and recurrent vascular thrombotic events. Research suggests APS may lead to various neurologic/medical issues including memory loss, visual disturbances, and dementia. Method Neuropsychological evalu

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