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Congenital and acquired disorders of coagulation
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Jeanne M Lusher, Roshni Kulkarni
The treatment of APS is based on clinical manifestations. While thrombosis is a common manifestation, some patients may present with bleeding episodes due to hypoprothrombinaemia.71,73 Asymptomatic patients with APS may need no treatment except during periods of prolonged immobilization. Patients with thrombosis and/or APS-associated fetal loss are candidates for antithrombotic therapy with LMWH or unfractionated heparin. Long-term oral anticoagulants and low-dose aspirin are often recommended for prevention of recurrent thrombosis. Monitoring of anticoagulation therapy by APTT is difficult and unreliable – hence, heparin assays by automated methodology, as well as prothrombin-proconvertin time and chromogenic FX assays are recommended. Besides anticoagulant therapy, immune-suppression with intravenous immunoglobulin (IVIG), corticosteroids, or cyclophosphamide are sometimes utilized to decrease antibody levels in symptomatic patients.
The Hematologic System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Another clotting factor frequently absent or deficient in the circulation, prothrombin, is formed by the liver and requires vitamin K as an intermediary in its production. A deficiency of vitamin K, liver disease, or a hereditary defect, therefore, can cause hypoprothrombinemia, resulting in increased bleeding.
Lupus Anticoagulants: Characteristics, Methods of Laboratory Detection and Some Clinical Associations
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Thomas Exner, Douglas Triplett
Finally, occasional patients with LA display a true deficiency of prothrombin. This is usually apparent from a prolonged prothrombin time which “corrects” on mixing with normal plasma.74 The hypoprothrombinemia may result from the binding of circulating prothrombin to an antibody in vivo and the rapid removal of this complex from circulation. Recently, it has been shown that up to 70% of patients with LA may display an altered immunoelectrophoretic mobility of their prothrombin possibly due to complexation with such an antibody.5,76 Possibly the antibody recognizes the phospholipid-binding domain of prothrombin directly76 or its complex with phospholipids present in vivo.
Helicobacter pylori antibiotic eradication coupled with a chemically defined diet in INS-GAS mice triggers dysbiosis and vitamin K deficiency resulting in gastric hemorrhage
Published in Gut Microbes, 2020
Lisa Quinn, Alexander Sheh, Jessie L Ellis, Donald E Smith, Sarah L Booth, Xueyan Fu, Sureshkumar Muthupalani, Zhongming Ge, Dylan A Puglisi, Timothy C Wang, Tamas A Gonda, Hilda Holcombe, James G Fox
MKn composition was markedly different in antibiotic-treated groups where there was a 13.8% decrease in MK6 abundance and a 12.1% increase in MK11 abundance (Figure 4(c–f)). As an increase of similar magnitude in MK11 was observed in healthy mice on chow diet (Figure 4(f)), we focused on the large decrease in MK6 in antibiotic-treated mice on AAD diets. While bacterially derived MKn alone may not be sufficient to improve all blood coagulation metrics,51 Akiyama et al. were able to show differences in liver absorption and coagulation activity based on the number of prenyl units of MKn in a rat model of hypoprothrombinemia.49 In this model, hypoprothrombinemia was induced via a vitamin K-deficient diet and warfarin, leading to undetectable MKn levels in both plasma and liver. MK1-14, as well as MD, was administered orally or intravenously to hypoprothrombinemic rats. MK4, MK5, and MK6 increased hepatic MKn levels and markedly improved hypoprothrombinemia. MK7 and MK8 slightly improved coagulation activity, but the remaining MKn, including MK11, provided no improvement in coagulation activity.49
Congenital prothrombin defects: they are not only associated with bleeding but also with thrombosis: a new classification is needed
Published in Hematology, 2018
Antonio Girolami, Silvia Ferrari, Elisabetta Cosi, Bruno Girolami, Anna Maria Lombardi
Prothrombin deficiency is one of the rarest coagulation disorders with a prevalence of about 1:1.500.000 [1–3]. The defect is usually classified in Type I in which there is a concomitant decrease of prothrombin activity and antigen and in Type II in which prothrombin activity is low, whereas antigen is normal or near normal. The first type is also known as ‘True’ deficiency or hypoprothrombinemia, whereas the latter is known as dysprothrombinemia. Association of hypoprothrombinemia with dysprothrombinemia (hypo-dysforms) has also been described. The same is true for the combination between two dysprothrombinemias (dys-dysforms) [1–3].
Cefoperazone-sulbactam and risk of coagulation disorders or bleeding: a retrospective cohort study
Published in Expert Opinion on Drug Safety, 2020
Wen Wang, Yanmei Liu, Chuan Yu, Jing Tan, Weiyi Xiong, Duo Dong, Sheyu Li, Rui Zhang, Jijie Li, Yu Wu, Zhiyong Zong, Na Su, Kang Zou, Guizhi Wu, Xin Sun
The proportion of PT prolongation among patients treated with antibiotics containing cefoperazone varied between studies (range: 4–68%). Strom et al. revealed PT prolongation by 5 s in 12.3% of patients, which is higher than the proportion observed in our results [11]. The probable explanation for this inconsistency may be due to different definitions of hypoprothrombinemia, and the heterogeneity of patients across studies. Sattler et al. reported that 64% and 24.4% of patients with renal failure [6] and cancer [26], respectively, developed hypoprothrombinemia.