Showing posts with label levonox. Show all posts
Showing posts with label levonox. Show all posts

Saturday, April 5, 2008

103 - low molecular weight heparins


In medicine, low-molecular-weight heparin (LMWH) is a class of medication used as an anticoagulant in diseases that feature thrombosis, as well as for prophylaxis in situations that lead to a high risk of thrombosis.[1]

Heparin is a naturally-occurring polysaccharide that inhibits coagulation, the process whereby thrombosis occurs (see Heparin: Mechanisms of action). Natural heparin consists of molecular chains of varying lengths, or molecular weights. Chains of molecular weight from 5000 to over 40,000 Daltons, making up polydisperse pharmaceutical-grade heparin.[2]

Heparin derived from natural sources, mainly porcine intestine or bovine lung, can be administered therapeutically to prevent thrombosis (see anticoagulation). However, the effects of natural, or unfractionated heparin can be difficult to predict. After a standard dose of unfractionated heparin, coagulation parameters must be monitored very closely to prevent over- or under-anticoagulation.

Low-molecular-weight heparins (LMWHs), in contrast, consist of only short chains of polysaccharide. LMWHs are defined as heparin salts having an average molecular weight of less than 8000 Da and for which at least 60% of all chains have a molecular weight less than 8000 Da. These are obtained by various methods of fractionation or depolymerisation of polymeric heparin. They have a potency of greater than 70 units/mg of anti-factor Xa activity and a ratio of anti-factor Xa activity to anti-thrombin activity of >1.5.[3]

Low-molecular-weight heparin products

The anhydromannose in IdoA(2S)-anhydromannose can be reduced to an anhydromannitol

Various methods of heparin depolymerisation are used in the manufacture of low-molecular-weight heparin.[4] These are listed below:

  • Oxidative depolymerisation with hydrogen peroxide. Used in the manufacture of ardeparin (Normiflo®)
  • Deaminative cleavage with isoamyl nitrite. Used in the manufacture of certoparin (Sandoparin®)
  • Alkaline beta-eliminative cleavage of the benzyl ester of heparin. Used in the manufacture of enoxaparin (Lovenox® and Clexane®)
  • Oxidative depolymerisation with Cu2+ and hydrogen peroxide. Used in the manufacture of parnaparin (Fluxum®)
  • Beta-eliminative cleavage by the heparinase enzyme. Used in the manufacture of tinzaparin (Innohep® and Logiparin®)
  • Deaminative cleavage with nitrous acid. Used in the manufacture of dalteparin (Fragmin®), reviparin (Clivarin®) and nadroparin (Fraxiparin®)

Deaminative cleavage with nitrous acid results in the formation of an unnatural anhydromannose residue at the reducing terminal of the oligosaccharides produced. This can subsequently be converted to anhydromannitol using a suitable reducing agent as shown to the left.

UA(2S)-GlcNS(6S)

Likewise both chemical and enzymatic beta-elimination result in the formation of an unnatural unsaturated uronate residue(UA) at the non-reducing terminal, as shown to the left.

Differences between low molecular weight heparin products

Comparisons between LMWHs prepared by similar processes vary. For example, a comparison of Dalteparin and Nadroparin suggests they are more similar than products produced by different processes. However comparison of enoxaparin and tinzaparin shows they are very different from each other with respect to chemical, physical, and biological properties.

As might be expected, products prepared by distinctly-different processes are dissimilar in physical, chemical, and biological properties.

see references.[5][6][7][8][9][10].

Differences from unfractionated heparin

Its differences with unfractioned heparin include:

  • Average molecular weight: heparin is about 20000 Da and LMWH is about 3000 Da
  • Once-daily dosing, rather than a continuous infusion of unfractionated heparin
  • No need for monitoring of the APTT coagulation parameter
  • Possibly a smaller risk of bleeding
  • Smaller risk of osteoporosis in long-term use
  • Smaller risk of heparin-induced thrombocytopenia, a feared side-effect of heparin.
  • The anticoagulant effects of heparin are typically reversible with protamine sulfate, while the effect on LMWH is limited
  • Has less of an effect on thrombin compared to heparin, but maintains the same effect on Factor Xa.

Clinical uses

Because it can be given subcutaneously and does not require APTT monitoring, LMWH permits outpatient treatment of conditions such as deep vein thrombosis or pulmonary embolism that previously mandated inpatient hospitalization for unfractionated heparin administration

The use of LMWH needs to be monitored closely in patients at extremes of weight or in-patients with renal dysfunction. An anti-factor Xa activity may be useful for monitoring anticoagulation. Given its renal clearance, LMWH may not be feasible in patients that have end-stage renal disease.

Use in venothromboembolic disease associated with cancer

The CLOT study, published in 2003, showed that, in patients with malignancy and acute venous thromboembolism, dalteparin was more effective than coumarin in reducing the risk of recurrent embolic events.[11]

References

  1. ^ Weitz JI (1997). "Low-molecular-weight heparins". N Engl J Med 337 (10): 688-98. PMID 9278467.
  2. ^ Linhardt, R.J. Gunay, N. S. (1999). "Production and chemical processing of low molecular weight heparins". Sem. Thromb. Hem. 25 (3): 5-16.
  3. ^ European Pharmacopedia Commission (1991). "{{{title}}}". Pharmeuropa 3: 161-165.
  4. ^ Linhardt, R.J. Gunay, N. S. (1999). "Production and chemical processing of low molecular weight heparins". Sem. Thromb. Hem. 25 (3): 5-16.
  5. ^ Green, D. Hirsh, J. Heit, J. et al (1991). "Low molecular weight heparin: A critical analysis of clinical trials". Pharmacol. Rev. 2: 45-50.
  6. ^ Barrowcliffe, T. W. (1995). "Low molecular weight heparin(s)". Br. J. Haematol. 90: 1-7.
  7. ^ Donayre C. E. (1996). "Current use of low molecular weight heparins". Semin. Vascul. Surg. 9: 362-371.
  8. ^ Hunt, D. (1998). "Low molecular weight heparins in clinical practice". Southern Medical J. 91: 2-10.
  9. ^ Fareed, J. Jeske, W. Hoppensteadt, D. Clarizio, R. Walenga, J. M. (1998). "Low molecular weight heparins: Pharmacologic profile and product differentiation". Am. J. Cardiol. 82: 3L-10L.
  10. ^ Ramos-Sánchez MC, Barrio-Arredondo MT, De Andrés Santos AI, Martín-Gil J, Martín-Gil F.J. (1995). "Thermal analysis of aqueous solutions of heparins". Thermochim Acta 262: 109-115.
  11. ^ Lee AY, Levine MN, Baker RI, Bowden C, Kakkar AK, Prins M, Rickles FR, Julian JA, Haley S, Kovacs MJ, Gent M (2003). "Low-molecular-weight heparin versus a coumarin for the prevention of recurrent venous thromboembolism in patients with cancer". N Engl J Med 349 (2): 146-53. PMID 12853587.

101 - acute coronary syndrome

A spectrum of myocardial ischemic disorders characterized by atherothrombotic plaque disruption which results in unstable angina, Non–ST-elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI)

Acute myocardial ischemia is chest pain due to insufficient blood supply to the heart muscle that results from coronary artery disease (also called coronary heart disease).

Patients who have symptoms of acute myocardial ischemia and who are made to undergo electrocardiogram (ECG or EKG) may or may not have an ST elevation. (An ECG provides a graph of the heartbeat. Portions of the graph are labeled P, Q, R, S and T. An ST elevation describes a rise in a particular portion of this graph.) Most patients who have ST-segment elevation will ultimately develop a Q-wave acute myocardial infarction (heart attack). (The Q-wave describes another part of an ECG graph.) Patients who have ischemic discomfort without an ST-segment elevation are having either unstable angina, or a non-ST-segment elevation myocardial infarction that usually leads to a non-Q-wave myocardial infarction.

Acute coronary syndrome thus covers the spectrum of clinical conditions ranging from unstable angina to non-Q-wave myocardial infarction and Q-wave myocardial infarction. These life-threatening disorders are a major cause of emergency medical care and hospitalization in the United States. Coronary heart disease is the leading cause of death in the United States. Unstable angina and non-ST-segment elevation myocardial infarction are very common manifestations of this disease.

The drugs used for the treatment of ACS

Anticoagulants: delay/prevent clot formation and extension (Heparin, LMWH)

  • Unfractionated Heparin (UFH) : Widely used antithrombotic agent but has the disadvantages of Heparin Induced Thrombocytopenia (HIT)
  • Low-Molecular-Weight Heparin (LMWH) : Fraction of standard (UFH) heparin, effective subcutaneous administration. Egs. enoxaparin, dalteparin, reviparin, nadroparin, fraxiparin.

LUPENOX (Enoxaparin 20, 40, 60mg PFS). Lupenox is in-licensed from Italfarmaco,Italy.

Antiplatelet drugs: interfere with platelet activity (ASA, CLOPIDOGREL, GP IIb/IIIa Inhibitors)

  • Aspirin (ASA) : Prevents platelet aggregation by blocking TxA2
  • Clopidogrel / Ticlopidine : Inhibit ADP-dependent activation of GP IIb/IIIa complex. Useful in patients hypersensitive to ASA or predisposed to GI bleeding. Also used in combination with ASA in the management of ACS.
  • Abciximab, Eptifibatide, Tirofiban : Inhibits the GP IIb/IIIa inhibitors and thus prevents platelets from binding to each other
  • Cilostazol - An add-on to other antiplatelet agents, helps in the management of Intermittent Claudication and also in prevention of Restenosis

CLOPITAB (Clopidogrel 75mg)

CLOPITAB-A (Clopidogrel 75mg + Aspirin 75/150mg)

TIROFUSE (Tirofiban 5mg/100ml I.V injection)

CILODOC (Cilostazol 50,100mg)

Thrombolytic agents: (Plasminogen Activators) dissolve existing thrombi (tPA, Streptokinase). A number of ongoing large randomized trials are attempting to determine whether the combination of fibrinolytic therapy with low-molecular-weight heparin or a glycoprotein IIb/IIIa antagonist enhances coronary reperfusion and reduces mortality and late reocclusion.

l Streptokinase - The most widely used thrombolytic agent and can now be made using recombinant DNA technology

l Alteplase, Reteplase and Tenecteplase – Offers more powerful results in dissolving the thrombus. In combination with Enoxaparin reduces early ischemic events

Isosorbide-5-mononitrate: An anti-anginal agent which helps balance the oxygen demand and supply in patients suffering from Angina.

ISONORM (Isosorbide-5-mononitrate 10, 20, 30mg SR)

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