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The twentieth century
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
Heparin was found to be an antithrombin, an antiprothrombin, and an antithromboplastin, and proved to be the most important, the safest, and the most certain of the anticoagulant drugs. A ready antidote existed in the form of a 1% solution of protamine sulfate. Unlike the dicumarol type of anticoagulants, the heparin molecule was too large to cross the placenta and was safe to use in pregnancy. The use of heparin in vitro to prevent blood from clotting led to its use to prevent venous thrombosis.
Management of recurrent second-trimester missed abortion
Published in Minakshi Rohilla, Recurrent Pregnancy Loss and Adverse Natal Outcomes, 2020
Ideally, aspirin is started preconceptionally because of its probable favorable effect on implantation. Heparin is started after confirming intrauterine pregnancy. A baseline platelet count should be assessed prior to starting treatment. Low molecular weight heparin may be preferred over unfractionated heparin since it is easier to administer. The dose of heparin depends on the patient's history and aPL profile.
Anticoagulation
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Louis M. Fink, Nicole A. Massoll, Alex A. Pappas
Although heparin has a relatively short T1/2 (11/2 hr), more rapid reversal may be necessary after ECC or in cases where a heparin overdose has occurred. Heparin can be neutralized by protamine sulfate. For acute heparin reversal, the usual therapeutic dose is 1.3 mg of protamine sulfate for each 100 U of UFH in the patient’s plasma (26,27). The dose of protamine necessary for reversal of LMWH varies with the specific preparations of LMWH. The amount of protamine necessary for heparin reversal can be determined by adding varying amounts of protamine to the thrombin time assay, by titration of the ACT with varying protamine concentrations, or by using the Xa inhibition assay (to determine the plasma heparin concentration).
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
Heparin as a therapeutic anticoagulant is linked to a 10 − 15% risk of significant bleeding (305). Factors that may increase bleeding risk include old age, recent trauma or surgery, cardiopulmonary resuscitation, longer hospital stay, and decreased white blood cell/platelet counts (306). These risk factors are common among patients with COVID-19. Heparin-induced thrombocytopenia (HIT), a rare complication of heparin therapy, is estimated to occur in 0.2–3% of patients (307). The adverse HIT reaction results from the development of antibodies against platelet factor 4, which triggers thrombocytopenia. Repurposing of heparin and its derivatives as first-line therapeutics against SARS-CoV-2 is promising; however, this clinical approach needs an in-depth evaluation (308).
Pullulan based derivatives: synthesis, enhanced physicochemical properties, and applications
Published in Drug Delivery, 2022
Surendra Agrawal, Divya Budhwani, Pravina Gurjar, Darshan Telange, Vijay Lambole
Anticoagulants are used to stop the thickening of the blood and the formation of clots. Heparin is one of the popular anticoagulants. Pullulan derivatization via sulfation has been done with the aim to develop an alternative to heparin. Sulfated pullulan can be obtained by the reaction of pullulan and sulfur trioxide–pyridine complex in DMF (dimethylformamide) at 75 °C and 95 °C for 3–8 h. Sulfate pullulan can also be obtained from pullulan reaction with SO3-DMF (N,N-dimethyl formamide) complex, but due to SO3–DMF complex, resultant pullulan becomes more reactive and less viscous; therefore, SO3–Py (pyridine) complex is more preferred to achieve stable and viscous derivative. Pullulan sulfate C-6 is the most preferential position for sulfation, followed by C-3, while C-4 remained mostly unsulfated (Mähner et al., 2001). It was reported that pullulan sulfate prevents coagulation by interfering with several stages of coagulation (Alban et al., 2002).
Treatment of severe COVID-19: an evolving paradigm
Published in Expert Opinion on Pharmacotherapy, 2022
The therapeutic approach for patient severe COVID-19 involves a combination of medications: the systemic corticosteroid dexamethasone improves mortality for the treatment of severe COVID-19, while the antiviral remdesivir may have modest but shows no statistically significant benefit in mortality or other clinical outcomes in patients with severe disease [21–23]. Prophylactic anticoagulation with heparin is now recommended to prevent blood clots because therapeutic anticoagulation did not improve survival [24,25]. Other immunomodulators, such as baricitinib and tocilizumab, are also recommended for some hospitalized patients (Table 1). This multifactorial approach has consistently shown benefit, but mortality from severe COVID-19 remains unacceptably high and better treatment options are urgently needed [14,26,27].