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At least 37 records · Page 2Linked to original sources
PubMed2001

Anti-PF4-heparin immunoglobulin G is the major class of heparin-induced thrombocytopenia antibody: findings of an enzyme-linked immunofiltration assay using membrane-bound hPF4-heparin.

An enzyme-linked immunofiltration assay (ELIFA) was developed for detecting anti-human platelet factor 4 (hPF4)-heparin antibody in sera of patients with heparin-induced thrombocytopenia (HIT). The immunofiltration assay was developed to capture HIT antibody by hPF4-heparin complex adsorbed onto a positively charged nylon membrane, as an alternative to plastic bound hPF4. Of 75 sera with a positive serotonin-release assay (SRA), anti-PF4-heparin of the immunoglobulin (Ig)G class was detected in 72 (96%) sera. With SRA-negative sera from thrombocytopenic patients treated with heparin, anti-hPF4-heparin IgG and IgA were detected in 16% (n = 126) and 14% (n = 74) of sera respectively; 6% (n = 71) of SRA-negative sera contained both IgG and IgA anti-hPF4-heparin antibodies. The detection of anti-hPF4-heparin IgG in all HIT sera supports the assay of anti-PF4-heparin IgG as being a sensitive screening test for HIT. Alternatively, the absence of anti-hPF4-heparin IgA cannot be used as a test for excluding HIT, as it was detected in only 48% of SRA-positive HIT sera. However, it may be used to support the diagnosis of HIT, when HIT IgG is weak. This study emphasized the need to use different immobilizing media for the capture of anti-PF4-heparin antibody.

Antibodies↗
PubMed1986

Heparin-associated thrombocytopenia: a prospective comparison of bovine lung heparin, manufactured by a new process, and porcine intestinal heparin.

Heparin-associated thrombocytopenia has been reported most commonly with bovine lung preparations. We prospectively evaluated the incidence of thrombocytopenia in 43 patients receiving intravenous continuous infusions of either bovine lung heparin, manufactured by a new process, or a standard porcine intestinal mucosa heparin for a minimum of five days in a double-blind, randomized fashion. The decision to continue heparin therapy beyond five days was made by the patient's primary physician. All patients had documented acute thromboembolic disease, pretherapy platelet counts greater than 150 000/mm3, and no evidence of prior coagulation disturbance. No patients had undergone cardiopulmonary bypass or hemodialysis within seven days previous to the initiation of heparin therapy. Thrombocytopenia was defined as a decline in platelet count from the normal range of 150 000-350 000/mm3 to less than 100 000/mm3. Thrombocytopenia occurred in one patient (4.6 percent) receiving bovine lung heparin on day nine of therapy and in no patients (0 percent) receiving porcine intestinal mucosa heparin. Adverse reactions occurred in nine patients (42.9 percent) receiving porcine intestinal heparin and five patients (22.7 percent) receiving bovine lung heparin. This difference was not statistically significant. The results of this study indicate that the incidence of thrombocytopenia is low (less than five percent) with both bovine lung heparin, manufactured by a new process, and porcine intestinal mucosa heparin when therapy is limited to short therapeutic courses (less than 1 week).

Aged↗
PubMedDate not supplied

Subcutaneous low-molecular-weight heparin versus standard heparin and the prevention of thromboembolism in medical inpatients. The Heparin Study in Internal Medicine Group.

In a multicenter, double-blind clinical trial in 1,968 inpatients 1 daily subcutaneous administration of LMW heparin plus 2 placebo injections or 3 x 5,000 IU unfractionated (UF) heparin was given for 10 (8-11) days. The primary end point was the incidence of proximal deep-vein thrombosis or pulmonary embolism. Patients were assessed during the study period for development of proximal deep-vein thrombosis by compression sonography at days 1 and 10 and for pulmonary embolism by scintigraphy in symptomatic patients. Aim of the study was to demonstrate the equivalence of both treatment regimens. A total of 1,968 patients were randomized to receive UF or LMW heparin. Of these, 378 patients were excluded during the study period, so that 780 patients on UF and 810 on LMW heparin were included in the efficacy analysis. Four primary end points were observed with UF and 6 with LMW heparin, demonstrating the equivalence of treatments (p = 0.012). Additionally, pulmonary embolism was suspected as the cause of death in 6 patients who died during the study (3 per treatment group). A higher frequency of death (n = 32) was observed in the LMW-heparin group (p = 0.02) particularly documented in a part of the centers. Safety analysis showed a higher frequency of local pruritus, local erythema and subcutaneous hematoma, a higher increase in plasma levels of triglycerides, total cholesterol, alanine aminotransferase and aspartate aminotransferase, and a decrease of antithrombin III in patients receiving UF heparin. A decrease in platelet count (values ranging between 40,000 and 80,000/microliter) was observed in 4 patients with UF and in none with LMW heparin. No severe thrombocytopenia was observed. Subcutaneous LMW heparin is as effective as UF heparin for prophylaxis of thromboembolism in bedridden, hospitalized medical patients.

Aged↗
PubMed1983

Structure-activity relationships of heparin. Independence of heparin charge density and antithrombin-binding domains in thrombin inhibition by antithrombin and heparin cofactor II.

To better understand how heparin structure affects its activity the relationships between the functional domains for inhibitor binding and charge density were investigated to determine how these domains affect heparin-mediated thrombin inhibition by two different heparin-dependent protease inhibitors, antithrombin (AT) and heparin cofactor II (HC II). A series of heparins, fractionated systematically by charge density, was further fractionated on antithrombin agarose to isolate more homogeneous subfractions that were either inactive or highly active with respect to thrombin inhibition by AT. With AT, the activities of the AT-active subfractions increased sharply with heparin charge density, while those with little or no affinity for AT were virtually inactive. In contrast, with HC II inhibitor, the activities of the heparins depended only upon their charge densities and were independent of AT affinity. At any given charge density, the heparin before fractionation by AT affinity and the fractions that were highly active and inactive with AT were all equally active with HC II. The two inhibitors also differed in their reactivity with heparan sulfate and dermatan sulfate. A charge-density effect with the subfractions having similar high affinity for AT demonstrates that charge density represents a heparin functional domain that is independent of the AT-binding domain. The behavior of the AT-inactive heparins, being fully active with HC II, demonstrates the functional domain necessary for AT binding is not needed to produce HC II activity.

Animals↗
PubMed1999

Comparison of low-molecular-weight heparin, administered primarily at home, with unfractionated heparin, administered in hospital, and subcutaneous heparin, administered at home for deep-vein thrombosis.

In this study, 294 patients with acute proximal DVT (deep venous thrombosis) were randomly assigned to receive intravenous standard heparin in the hospital (98 patients) or low-molecular-weight heparin (LMWH) (nadroparin 0.1 mL [equivalent to 100 AXa IU] per kg of body weight subcutaneously twice daily) administered primarily at home (outpatients) or alternatively in hospital (97 patients) or subcutaneous calcium heparin (SCHep) (99 patients, 0.5 mL bid) administered directly at home. The study design allowed outpatients taking LMWH heparin to go home immediately and hospitalized patients taking LMWH to be discharged early. Patients treated with standard heparin or LMWH received the oral anticoagulant starting on the second day, and heparin was discontinued when the therapeutic range (INR 2-3) had been reached. Anticoagulant treatment was maintained for 3 months. Patients treated with SCHep were injected twice daily for 3 months without oral anticoagulants. Patients were evaluated for inclusion and follow-up with color duplex scanning. Venography was not used. In case of suspected pulmonary embolism (PE) a ventilatory-perfusional lung scan was performed. Endpoints of the study were recurrent or extension of DVT, bleeding, the number of days spent in hospital, and costs of treatments. Of the 325 patients included, 294 completed the study. Dropouts totaled 31 (10.5%); six of the 325 included patients (1.8%) died from the related, neoplastic illness. Recurrence or extension of DVT was observed in 6.1% of patients in the LMWH group, in 6.2% in the standard heparin group, and in 7.1% in the SCHep group. Most recurrences (11/17) were in the first month in all groups. Bleedings were all minor, mostly during hospital stay. Hospital stay in patients treated with LMWH was 1.2+/-1.4 days in comparison with 5.4+/-1.2 in those treated with standard heparin. There was no hospital stay in the SCHep group. Average treatment costs in 3 months in the standard heparin group (US $2,760) were considered to be 100%; in comparison costs in the LMWH group was 28% of the standard heparin and 8% in the SCHep group. This study indicated that LMWH and SCHep can be used safely and effectively to treat patients with proximal DVT at home at a lower cost.

Ambulatory Care↗
PubMed2003

Acute pulmonary thromboembolism induced by prophylactic heparin use and a heparin-coated catheter: a case of heparin-induced thrombocytopenia and thrombosis syndrome.

Heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) is a potentially life-threatening side effect of heparin therapy, triggered by an immune response, and has been reported to be related not only to the therapeutic use of heparin but also to heparin-coated catheters. A 45-year-old woman with intrapelvic malignancy developed an acute pulmonary thromboembolism (PE) after hysterectomy despite prophylactic heparin use. Subsequent large doses of heparin for treatment of the PE exacerbated the thrombocytopenia and, moreover, a large thrombus formed around the heparin-coated central venous catheter. Anti-heparin-platelet factor 4 complex antibody and heparin-induced platelet aggregation assay were positive, so the diagnosis was HITTS, and heparin was replaced by argatroban after carrying out thrombectomy. This therapy was successful, and the patient made favorable progress.

Acute Disease↗
PubMed2001

[Heparin concentration and hemostatic alterations with low systemic heparinization during CPB using heparin-coated circuits].

Extracorporeal circulation with heparin coated circuits allows reduction of systemic heparin. The authors investigated the effects of this method on the hemostatic and fibrinolytic systems and heparin concentration simultaneously. Ten patients undergoing coronary artery bypass surgery were studied. The dose of heparin was 100 IU.kg-1, and the target activated clotting time (ACT) was more than 300 seconds. Blood samples were obtained at the following times; before and after giving heparin, 10 and 40 minutes after the start of extracorporeal circulation, after cross-clamp release, and after giving protamine, and heparin concentration, ACT, thrombin-antithrombin complex (TAT), plasmin alpha 2 plasmin inhibition complex (PIC), and D-dimer were measured. ACT was kept over 300 seconds without additional heparin administration. Heparin concentration was maintained at 1.0 IU.ml-1. However, after release of the aortic cross-clamp, TAT, PIC, D-dimer increased significantly. Despite reduced systemic heparinization, heparin concentration was maintained adequately. Thrombin generation and fibrinolytic activity showed no significant increase until the release of the aortic cross-clamp.

Adult↗
PubMed2005

Identification, diagnosis and treatment of heparin-induced thrombocytopenia and thrombosis: a registry of prolonged heparin use and thrombocytopenia among hospitalized patients with and without cardiovascular disease. The Complication After Thrombocytopenia Caused by Heparin (CATCH) Registry steering committee.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is estimated to occur in 1-5% of all patients receiving heparin, and 25-50% of such cases develop heparin-induced thrombocytopenia with thrombosis (HITT) A conservative estimate based only on cardiovascular patients suggests that in the United States approximately 100,000 patients develop thrombocytopenia, and 25-50,000 develop HITT annually. Both HIT and HITT are associated with high morbidity and mortality and represent substantial worldwide public health concerns. REGISTRY DESIGN: The objective of the Complication After Thrombocytopenia Caused by Heparin (CATCH) Registry is to identify the incidence of HIT and/or HITT in patients treated with systemic heparin (unfractionated or low molecular weight heparin) in contemporary practice. Additional objectives include to: (1) provide a comprehensive database of patients with suspected HIT or HITT, (2) monitor and define clinical events, including thrombocytopenia, thrombosis, and mortality among patients treated with prolonged (> 96 hours) heparin, (3) describe the incidence and outcomes of HIT and HITT in patients who are treated with heparin and who develop thrombocytopenia in the Coronary Care Unit setting, and (4) document and characterize current diagnostic and therapeutic strategies of suspected HIT. The unblinded registry will record approximately 5,000 patients at 60-80 US hospitals with either prolonged systemic heparin administration or thrombocytopenia and those with suspected HIT or HITT. Enrollment began in the first quarter 2003 and was completed at the end of 2004. IMPLICATIONS: The registry will provide valuable insights to the incidence and consequences of HIT and HITT that will enable improvements in diagnosis and treatment.

Cardiovascular Diseases↗
PubMed1985

The heparin-mobilisable pool of platelet factor 4: a comparison of intravenous and subcutaneous heparin and Kabi heparin fragment 2165.

Some clinical advantages are claimed for low molecular weight heparin so the mobilisation of platelet factor 4 (PF 4) from the endothelial pool by the heparins may be relevant. Unfractionated (UF) heparin has been compared with Kabi heparin fragment 2165. A single intravenous (i.v.) injection of 60 iu/kg heparin was compared with 5000 anti-Xa units of Kabi-2165. Less PF 4 was mobilised by Kabi-2165 and some apparently remained in the pool and was released when the pool was subsequently challenged by giving i.v. heparin. Subcutaneous (s.c.) injections of 5000 iu heparin twice daily were compared with 5000 anti-Xa units of Kabi-2165 once daily, each given for a week. The plasma PF 4 was never raised yet when finally challenged with i.v. heparin the pool was "empty" or refractory after the s.c. heparin but some PF 4 remained after the s.c. Kabi-2165. The two glycosaminoglycans (GAGs) had widely differing half-lives but the t/2 of the PF 4 mobilised by the two GAGs was similar even though the PF 4 is apparently bound to the GAG.

Adult↗
PubMed1995

Carboxyl-terminal truncation of leucine76 converts heparin-binding EGF-like growth factor from a heparin-enhancible to a heparin-suppressible growth factor.

Previous studies have indicated that heparin differentially regulates heparin-binding EGF-like growth factor (HB-EGF) and amphiregulin (AR) mitogenic activity. To further explore this phenomenon, these mitogens were compared under identical cell culture conditions in two different assays. The results of our present investigation demonstrated that AR-mediated mitogenic activity in the murine AKR-2B fibroblast-like cell line was inhibited by heparin, while HB-EGF activity was enhanced. However, the absolute effect of heparin appeared to be cell type specific since HB-EGF mitogenic activity was not dramatically affected by coincubation with heparin when tested on human dermal fibroblasts. Several studies have indicated that mutation of a conserved leucine in the carboxyl-terminal region of both EGF and transforming growth factor-alpha results in decreased affinity for EGF receptors. Since this leucine is present in the analogous position of HB-EGF, but absent in AR, we examined the effect of deleting this residue by carboxyl-terminal truncation of HB-EGF. Analysis of recombinant forms of HB-EGF demonstrated that HB-EGF can be converted to a heparin-inhibited growth factor if the putative mature form of the protein is truncated by two residues (leucine76 and proline77) at the carboxyl terminus. Further analysis demonstrated that only leucine76 appears to be required for heparin-dependent enhancement of HB-EGF-mediated mitogenic activity, indicating that this amino acid may play a pivotal role in controlling the response of HB-EGF to heparin or related glycosaminoglycan sulfates. Our results also suggest that expression of different HB-EGF forms in vivo could result in the production of HB-EGFs with divergent responses to sulfated glycosaminoglycans and proteoglycans.

Amino Acid Sequence↗
PubMed2000

Isoamyl nitrite depolymerized heparin as a universal calibrator for heparins and low molecular weight heparins.

Because the subcutaneous absorption of heparin depends on its molecular weight, high performance size exclusion chromatography methods, among others, have been developed for its determination. Because heparin consists of polymer chains of varying lengths, a large number of calibrators, 19 in our work, are required for these molecular weight analyses. Because the preparation of that many calibrants is both time-consuming and expensive, other methods requiring fewer calibrants are being sought. In pursuit of these aims, a heparinase-degraded heparin has been accepted as the first international reference preparation low molecular weight heparin for molecular weight calibration. We have previously proposed another calibrant, the Heparin Mass Calibrator. In this article, we introduce another calibrant, called the Heparin Molecular Mass Calibrant. It offers the advantage of a much wider availability because it is a commercial product. In addition to having a superior refractive index chromatography run profile, when used in combination with two Narrow Range Calibrators with molecular weights of 34.4 and 18.4 kDa, this new calibrant covers both the higher and the lower molecular weight ranges. Besides, ultraviolet detection is not needed for molecular weight calculations. Therefore, it is proposed that its feasibility as a universal reference calibrator for both heparins and low molecular weight heparins be considered.

Amyl Nitrite↗
PubMed1983

[Heparin and antiheparin in childhood. 3. Heparin level measurements and their importance in heparin monitoring].

Measurements of the heparin level were made under continuous anticoagulation in a total of 7 patients. For the purpose of monitoring heparin the coagulation time values were determined parallelly. Except a patient with a sepsis and a 7 days old newborn baby the desired prolongation for the partial thromboplastin time and the reaction time of thrombelastogram resulted from heparin titres lying within the range of 0.2-0.7 U/ml of plasma. Even after applying depot preparations there was a relatively good correspondance of heparin level curves and coagulation parameters. In childhood the partial thromboplastin time is primarily suitable for monitoring the heparin therapy. Heparin half-life times calculated during the transumbilical exchange transfusion in 7 children amounted to values ranging between 40-110 minutes. In addition to checking low dose heparinizing, measurements of the level are suitable for deriving dosage standards for neutralizing heparin effects by protamine sulfate.

Adolescent↗
PubMed1998

Heparin-induced thrombocytopenia: IgG binding to PF4-heparin complexes in the fluid phase and cross-reactivity with low molecular weight heparin and heparinoid.

Early diagnosis of heparin-induced thrombocytopenia (HIT) is essential to reduce morbidity and mortality. We report an enzyme immunoassay which detects the binding of HIT IgG to PF4-heparin in the fluid phase. Our fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because, unlike in an ELISA, a clearly defined amount of antigen is available for antibody binding. We were able to detect anti-PF4-heparin IgG in 26/28 (93%) HIT patients. We investigated cross-reactivity of anti-PF4-heparin antibodies with PF4 complexed to alternative heparin-like anticoagulants. Low molecular weight heparins cross-reacted with 23/26 (88%) of the sera from HIT patients while half of the HIT sera weakly cross-reacted with PF4-danaparoid (Orgaran). The thrombocytopenia and thrombosis of most of these patients resolved during danaparoid therapy, indicating that detection of low affinity antibodies to PF4-danaparoid by immunoassay may not be an absolute contraindication for danaparoid administration.

Anticoagulants↗
PubMed1994

At high heparin concentrations, protamine concentrations which reverse heparin anticoagulant effects are insufficient to reverse heparin anti-platelet effects.

Combined effects of heparin and protamine on plasma clot structure and platelet function were studied. Anticoagulant effects were monitored as changes in aPTT. Clot structure was defined in terms of fibrin fiber mass/length ratio (mu) and clot elastic modulus (EM). Platelet function was studied utilizing platelet aggregation and platelet force development (PFD) measurements. Heparin (1 U/ml) prolonged the aPTT from 30 to > 300 seconds, reduced PFD from 5,100 to 0 dynes, decreased mu (in batroxobin-induced gels) from 1.36 to 1.08 x 10(13) daltons/cm and decreased clot EM from 9,600 to 2000 dynes/cm2. Varying amounts of protamine reversed these effects: 16 micrograms/ml normalized the aPTT, 20 micrograms/ml normalized PFD, 32 micrograms/ml corrected mu, and 20 micrograms/ml returned EM to baseline. At high heparin concentrations (4 U/ml), protamine concentrations which corrected anticoagulant effects were inadequate to reverse antiplatelet effects. A protamine concentration of 40 micrograms/ml normalized the aPTT and mu, but 140 micrograms/ml of protamine was required to reverse heparin suppression of force development and clot elastic modulus. Excess protamine inhibited clotting and platelet function. In plasma containing 1 u heparin/ml, 140 micrograms protamine/ml reduced PFD by 83%, prolonged the aPTT by 63%, and reduced clot EM by 75%. In heparin free plasma, > 75 micrograms protamine/ml prolonged the aPTT. Thus, platelet function and clot structure are sensitive to protamine during heparin neutralization, and anti-platelet effects of heparin may persist when the aPTT is completely corrected. Excess protamine inhibits platelet function and compromises clot structure.

Blood Coagulation↗
PubMed1990

Monitoring heparin therapy: relationships between the activated partial thromboplastin time and heparin assays based on ex-vivo heparin samples.

Five different APTT-reagents, two amidolytic anti-IIa assays, one amidolytic anti-Xa assay, and one coagulometric anti-Xa/anti-IIa assay were used to assess the effect of heparin in patients treated for venous thromboembolic disease. Good correlations were observed between log-transformed APTTs determined with the various reagents (correlation coefficients: 0.92-0.96). Nevertheless there were important differences in the slopes of the lines of relationship between the APTT reagents. Good correlations were observed between the anti-Xa and anti-IIa assay results (correlation coefficients: 0.92-0.97). However, the amidolytic anti-Xa activity was significantly higher (p less than 0.001) than the two amidolytic anti-IIa activities. Less good correlations were observed between the log-transformed APTTs and the anti-Xa or anti-IIa activities (correlation coefficients: 0.64-0.78). The correlations were improved by transforming the APTT into APTT-ratio, i.e. the ratio of the patient's APTT to the same patient's APTT after removal of heparin from the plasma sample by means of ECTEOLA-cellulose treatment. The correlation coefficients of log (APTT-ratio) with anti-Xa or anti-IIa ranged from 0.76 to 0.87. For both APTT and amidolytic heparin assay, the response to in vitro heparin was different from the response to ex vivo heparin. Therefore, equivalent therapeutic ranges should be assessed by using ex vivo samples rather than in vitro heparin. Because of the response differences between the APTT reagents, it is not adequate to define a therapeutic range for heparin therapy without specification of the reagent.

Administration, Oral↗
PubMed1981

In vivo studies on the inhibition of coagulation by fractionated heparin and by a heparin analogue. II. Effects of a heparin analogue.

SSHA, a semi-synthetic heparin analogue, and sodium heparin from porcine intestinal mucosa were injected subcutaneously into six healthy volunteers over a period of three days in a cross-over trial. Before injection and 2, 4, 6, 8 hrs afterwards, the heparin-like activity was measured with the APTT, the anti-Xa clotting test and two chromogenic substrate assays. The results show that SSHA mediates both anti-Xa and antithrombin activities in vivo. A comparison between the effects of SSHA and heparin is problematical due to the heterogeneity of different heparin preparations. Low doses of the analogue (45 mg s.c.) induced proportionally higher and longer lasting anti-Xa activities than higher doses (90 mg s.c.). Repeated injections of SSHA twice daily led to increasing effects on two tests for heparin-like activity, whereas two other tests remained unchanged. Both drugs were tolerated equally well, side effects were not detected. Clinical studies are required to demonstrate whether SSHA is similar or superior to low-dose heparin for use in thrombosis prophylaxis.

Adult↗
PubMed1981

In vivo studies on the inhibition of coagulation by fractionated heparin and by a heparin analogue. I. Effects of heparin fractions.

High and low molecular weight heparin fractions obtained by gel filtration chromatography of sodium mucosal heparin were injected subcutaneously into six healthy volunteers and compared with the unfractionated substance in a cross-over trial. Equal doses of 5,000 U were administered twice daily over a period of three days and heparin activity was repeatedly controlled before and 2, 4, 8 hrs after injection by means of the APTT, the anti-Xa clotting test and a chromogenic substrate assay. In addition, the in vivo effect of subcutaneously administered fractionated heparin on platelet function was examined on three of the volunteers. The results show that s.c. injections of the low molecular weight fraction induced markedly higher anti-Xa activity than injections of the other preparations. At the same time, APTT results did not significantly differ. Unfractionated heparin and the high molecular weight fraction enhanced ADP-induced platelet aggregation and collagen-mediated MDA production, while the low molecular weight fraction hardly affected these assays, but potently inhibited thrombin-induced MDA production. All heparin preparations stimulated the release of platelet Factor 4 in plasma. During the three-day treatment periods, no side-effects and no significant changes in the response to heparin injections were detected.

Adult↗
PubMed1994

Feasibility study of heparin mass calibrator as a GPC calibrator for heparins and low molecular weight heparins.

The proposed European Pharmacopoeial (EP) method for molecular weight determination of low molecular weight heparins (LMWHs) has been shown to have a range which is too narrow to allow for the accurate molecular weight determinations of all LMWHs. We have recently shown that a chemically degraded benzyl ester of unfractionated heparin, ITH-3, is a better calibrator using this methodology. Data is presented here which indicates that this calibrator cannot only be used to determine the molecular weights of LMWHs but also of unfractionated heparins. Therefore, it is now renamed heparin mass calibrator or HMC because of this extension of range. Weight average molecular weight, number average molecular weight, peak molecular weight, and dispersity values were calculated using the HMC calibration and a reference narrow-range 19-calibrator method for various LMWHs and unfractionated heparins. Values for the parameters calculated using the HMC calibration were found not to be significantly different from those of the reference method until the molecular weight exceeded 15.0 kDa. In contrast, the molecular weight profile obtained with the proposed EP method was significantly different from the reference method for samples > 8.0 kDa. The range exhibited by the HMC calibrator should allow it to be used for both LMWHs and unfractionated heparins.

Chromatography, High Pressure Liquid↗