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PubMed1985

Monocyte thromboplastin (tissue factor): complementary effect of lymphocytes upon its generation by endotoxin-stimulated monkey (Macaca fuscata) cells.

Monkey (Macaca fuscata) mononuclear leukocytes were stimulated to produce thromboplastin (tissue factor) upon exposure to lipopolysaccharide, LPS. The stimulation was dose-related in the concentration range of 10(-5) to 10(-1) micrograms/ml of LPS. Lipid A portion of the LPS molecule was essential to induce the leukocyte ability for tissue factor generation. Thus, a lipid-lipid interaction between LPS and the cells is a plausible trigger for eliciting the ability. Approximately 50% of the tissue factor thus produced appeared to be located on the cell surface, at which the coagulation cascade is probably initiated via the activation of factor VII. Among monkey mononuclear cell populations, monocytes were responsible for LPS-induced tissue factor production. Lymphocytes amplified the basal ability of monocytes to produce the factor by two-fold at physiological lymphocyte-monocyte ratios of 8:1 to 10:1. This indicates a complementary effect of lymphocytes upon the LPS-mediated monocyte ability. The medium supernatant from LPS-stimulated lymphocytes affected the monocyte competence while the stimulated lymphocytes did not. This result suggests that a soluble product of lymphocytes, i.e., lymphokine-like mediator, but not the cellular entity, participates in LPS-induced tissue factor production of monocytes.

Animals↗
PubMed2004

Prolonged activated partial thromboplastin time in pregnancy: a brief report.

BACKGROUND: Limited data are available regarding causes of prolonged activated partial thromboplastin time (aPTT) in otherwise normal pregnancies. We retrospectively evaluated clinical data of pregnant women in whom an elevated aPTT was noted on routine prenatal testing. Our intent was to identify various causes of prolonged aPTT and to evaluate whether the pregnancies were adversely affected. METHODS: A retrospective review of medical records of 36 pregnant patients with a prolonged aPTT as the sole abnormal coagulation test seen in the outpatient department of a tertiary care hospital over a period of 4 years. RESULTS: Patients' median age was 26 (range, 19-41) years and median duration of gestation period was 19 (range, 8-38) weeks. Fifteen patients were primigravida. Of 36 patients, repeated aPTT values were normal in 24 (67%) patients, whereas 12 (33%) patients had persistently elevated aPTT values. Factor XI deficiency was found in 5 patients, lupus anticoagulant in 3 patients, elevated anticardiolipin antibody in 2 patients, and low von Willebrand Factor level in 1 patient. Overall, 23 patients delivered. No patients experienced excessive bleeding or thromboembolism. CONCLUSION: Factor XI deficiency and antiphospholipid antibody were 2 major abnormalities identified in patients with prolonged aPTT. These coagulopathies were not associated with excessive bleeding or thromboembolism. Repeat normal aPTT in approximately 2 thirds of patients suggests that proper sample collection and processing are important for coagulation assays to avoid erroneous clotting times.

Adult↗
PubMed1995

Aprotinin prolongs whole blood activated partial thromboplastin time but not whole blood prothrombin time in patients undergoing cardiac surgery.

Aprotinin is being used increasingly to limit cardiopulmonary bypass (CPB)-induced coagulation derangements. Since whole blood prothrombin time (PT) and activated partial thromboplastin time (APTT) assays are beneficial in the treatment of bleeding after CPB, we studied the potential effect of aprotinin on these whole blood assays. Blood specimens from 151 cardiac surgical patients were obtained in two phases: prior to heparin administration, before CPB, and subsequent to heparin neutralization after CPB. After collection, blood specimens were divided into two aliquots and mixed with either normal saline (NS) or aprotinin (A, 200 or 400 Kallikrein inhibiting units (KIU)/mL). Whole blood specimens were used to measure whole blood PT and APTT using CoaguChek Plus instruments. Whole blood PT results were similar between normal saline. (NS)- and aprotinin-spiked specimens before CPB (A, 12.9 +/- 1.5s; NS, 12.8 +/- 1.5s; P = 0.76) and after CPB (A, 17.5 +/- 2.4s; NS, 17.7 +/- 2.4s; P = 0.58). In contrast, whole blood APTT results were prolonged in aprotinin-spiked specimens prior to CPB (A, 63.3 +/- 32.2s; NS, 38.6 +/- 16.3s; P < 0.0001) and after CPB (A, 65.9 +/- 23.7s; NS, 45.7 +/- 14.4s; P < 0.0001). A dose-dependent prolongation of whole blood APTT by aprotinin was demonstrated by a greater mean difference in APTT (P = 0.0001) between specimens spiked with NS or 200 KIU (17.5 +/- 12.2s) vs 400 KIU (27.8 +/- 21.5s) of aprotinin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

On-site prothrombin time, activated partial thromboplastin time, and platelet count. A comparison between whole blood and laboratory assays with coagulation factor analysis in patients presenting for cardiac surgery.

BACKGROUND: Although available hemostasis assays from institutional laboratories permit an analytical approach to diagnosis and treatment of coagulation disorders following cardiopulmonary bypass, their clinical utility has been limited by delays in obtaining results. The development of instrumentation for on-site testing allows rapid return of results. This study was designed to compare whole blood (WB) results obtained from on-site coagulation assays with values provided by our institutional laboratory (LAB). METHODS: After Institutional Human Studies Committee approval, 362 patients presenting for cardiac surgery requiring cardiopulmonary bypass were enrolled in this study. Prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet count (PLT) assays were performed in both WB and LAB systems. PT, aPTT, and PLT measurements were compared between WB and LAB assays using blood specimens obtained from at least two time points for each patient. Normal range values for both PT and aPTT methods were determined by using measurements from a normal reference population. Coagulation factor levels were measured in a subset of patients to characterize the response of PT and aPTT assays to individual and multiple factor levels. To employ Bayes' theorem and calculate predictive indexes (e.g., sensitivity, specificity), the disease or factor deficiency was determined using factor levels. Predictive indexes were used to evaluate the ability of PT and aPTT assays to identify factor deficiency. RESULTS: PLT counts were similar between systems. Linear regression and bias analysis demonstrated similar results for WB and LAB PT and discordant results for aPTT measurements. Both PT assays had a similar normal range, whereas a wider distribution of results was evident for the WB aPTT normal range. Although statistically greater slopes for factor:aPTT regressions were observed for the WB system, WB aPTT correlated better with factor V and with factor V, VIII, and XII levels (multivariate linear regression). Diagnostic performance for factor levels less than 0.3 and 0.4 U/ml was similar for both WB and laboratory PT and aPTT assays. WB and LAB PT and aPTT assays performed similarly in detecting factor deficiency in the period after cardiopulmonary bypass. CONCLUSIONS: WB PT and PLT values correlate well with those obtained from the LAB. The discrepancy between measurement systems in aPTT values is probably a reflection of both different normal ranges and responsiveness to factor deficiency. These WB assays provide coagulation results that can accurately identify patients with quantitative deficiencies in platelets and coagulation factors.

Adult↗
PubMed2000

Assessment of activated partial thromboplastin time and factor IX in subjects attending an anticoagulation clinic.

Very low factor IX (FIX) levels in patients during oral anticoagulant (OA) treatment, due to mutations in the FIX gene, with prolonged activated partial thromboplastin time (aPTT) and associated with bleeding complications have recently been described. We measured aPTT in 595 OA patients while being within therapeutic ranges. Patients were divided into increasing international normalized ratio (INR) classes, and FIX determined in those belonging to the first and fifth quintiles of the aPTT distribution in each INR class. Results obtained in patients of all the first aPTT quintiles were compared with those of all the fifth quintiles. While INR was not different (2.79 versus 2.77 INR), aPTT was longer (1.65 versus 1.21 ratio; P < 0.0001) and FIX lower (0.29 versus 0.44 IU/ml; P < 0.0001) in patients of the fifth quintiles. Only one patient had a markedly reduced FIX (0.03 IU/ml). Bleeding rate was 4.8 and 6.2% patient-years (not significant) in patients of the first and fifth quintiles, respectively. We therefore found that FIX levels vary greatly in spite of similar achieved anticoagulation intensity; very low FIX is, however, a rare condition. In conclusion, screening for the recently identified mutations in FIX gene does not seem justified, and identifying patients with disproportionately prolonged aPTT, to detect those with particularly low FIX levels, is difficult because of the effect of the achieved anticoagulation intensity. Therefore, aPTT measurement is indicated only in patients with increased bleeding during OA.

Adolescent↗
PubMed2001

In vitro factor XI activation mechanism according to an optimized model of activated partial thromboplastin time test.

Whether the in vitro activation of factor XI in plasma is mediated by thrombin or by auto-activation remains a controversial question. In this context, we have simulated theoretical activated partial thromboplastin time (aPTT) by means of a program based on a body of 22 essential elementary reactions implemented with rate constants quoted in current literature. To meet self-consistency in input data issued from varying sources, the results were optimized using the simplex treatment. The performance of the model was systematically evaluated considering the extent of the deviations observed between predicted aPTT and laboratory measurements conducted on normal and factor VIII, IX, XI and XII single-factor deficient plasma. The influence of the auto-activation or thrombin-mediated activation of factor XI on these aPTTs was tested separately after insertion of these reactions in the model. According to the best fits, a mechanism accounting for an auto-activation reaction of activated factor XI rather than a positive feedback reaction mediated by thrombin seemed more likely. Based on this conclusion, a chart of self-consistent rate constant values accounting for the intrinsic pathway of coagulation under static conditions is proposed.

Blood Coagulation↗
PubMed2001

The activated partial thromboplastin time in early diagnosis of myocardial infarction.

Intracoronary thrombosis is fundamental to the pathogenesis of acute myocardial infarction (MI), yet few studies have examined the diagnostic value of routine coagulability markers, such as the activated partial thromboplastin time (aPTT), in patients with chest pain. We hypothesized that the initiation of thrombosis early in MI would shorten the aPTT, and conducted a retrospective cohort study of patients admitted with a diagnosis of chest pain through the emergency department of one community hospital between 1 January and 30 August 1998. Patients were diagnosed as MI positive or negative based on World Health Organization (WHO) criteria. The aPTT obtained on arrival (prior to anticoagulation therapy) was retrieved from the electronic medical record. Of 120 eligible patients (49% female, mean age 63.7 years), 27 (23%) were diagnosed with MI. Patients with an aPTT control (RR = 2.83, 95% confidence interval 1.15 to 6.96, P = 0.013). A shortened aPTT (<or= control) on presentation in patients with chest pain is associated with increased risk of acute MI. This information is available before other serum markers of MI, and may facilitate early treatment decisions. Further study is warranted.

Aged↗
PubMed2001

Disagreement between bedside and laboratory activated partial thromboplastin time and international normalized ratio for various novel anticoagulants.

During studies on warfarin, heparin and various anticoagulants with novel mechanisms of action, the activated partial thromboplastin time (aPTT) and the (apparent) international normalized ratio (INR) from a bedside monitor (Coagucheck Plus(R)) were compared with laboratory assay results. Data were compared using the Bland and Altman method of comparison where systematic differences result in significant slopes of the regression line. During heparin treatment, the bedside monitor largely underestimated the aPTT (slope = -0.80). During treatment with the direct thrombin inhibitor napsagatran (slope = 0.99), the pentasaccharides Org31540/SR90107A (slope = 0.77) and SanOrg34006 (slope = 0.35), and warfarin (slope = 0.60), the bedside monitor underestimated the aPTT at lower aPTT levels, while at higher aPTT levels it overestimated the laboratory values. The bedside monitor slightly overestimated the INR during treatment with warfarin (slope = 0.33). Apparent INR was largely overestimated during treatment with Org31540/SR90107A (slope = 1.38), SanOrg34006 (slope = 0.97), Napsagatran (slope = 1.23), and recombinant tissue factor pathway inhibitor (slope = 1.48, P < 0.001 for all regression lines). These results indicate that a substantial disagreement in aPTT or (apparent) INR exists between the bedside monitor and laboratory assay during treatment with the studied 'classic' and novel anticoagulants. The amount of disagreement depended on the anticoagulant given.

Anticoagulants↗
PubMed2002

Human plasma fibrinogen measurement derived from activated partial thromboplastin time clot formation.

Prothrombin time-derived measurement of fibrinogen (PTd) has already been described. Activated partial thromboplastin time-derived measurement of fibrinogen (aPTTd) has not yet been clearly defined. Using an MDA II coagulometer (Organon Teknika, Durham, North Carolina, USA), we have therefore compared fibrinogen levels determined with Clauss, PTd, and aPTTd assays and an enzyme immunoassay (EIA) in 172 samples. Of these, 47 were from pre-operative controls, 18 from patients with liver disease, 28 from patients with hyperfibrinogenaemia, 33 from patients treated with vitamin K antagonists, 22 from patients treated with unfractionated heparin and 24 from haemophilic patients. Within the normal range, interassay and intra-assay variations were comparable. For control samples, PTd, aPTTd and Clauss assays were well correlated, without any systematic error. EIA was also correlated but values were slightly higher (mean of difference = 0.24). Pathological samples showed an overestimation of fibrinogen when using PTd measurements in patients treated with vitamin K antagonists, as well as when using aPTTd measurements in patients presenting with factor VIII and factor IX deficiencies. These results indicate that, despite expected financial savings, aPTTd fibrinogen measurements should not be used without restriction. PTd and aPTTd fibrinogen determinations are provided without any additional cost. Their comparison with Clauss fibrinogen results may constitute a validation tool or have additional diagnostic utility (e.g. identifying polymerization abnormalities in case of dissimilar results).

Adult↗
PubMed2002

Thrombolytic fibrin specificity influences activated partial thromboplastin time prolongation in vitro.

Despite limited comparative data, guidelines suggest the same concomitant unfractionated heparin (UFH) dose for all fibrin-specific thrombolytic agents in acute myocardial infarction. Since a supratherapeutic activated partial thromboplastin time (aPTT) correlates with adverse outcomes, clarifying effects of various agents on aPTT are needed. The present in vitro study evaluated the influence of alteplase (rt-PA), reteplase (r-PA), and tenecteplase (TNK) on aPTT prolongation. Blood samples from healthy volunteers (n = 12) were treated with equipotent concentrations of rt-PA, r-PA, and TNK, with and without UFH. Samples of each treatment group were incubated at 37 degrees C; aPTT and fibrinogen activity were measured after 4 h. Mean aPTT values for rt-PA alone and r-PA alone were prolonged versus those of TNK alone (P = 0.001 for both). Combined with UFH, rt-PA and r-PA increased the aPTT versus UFH alone (P < 0.05 for both). Interestingly, TNK + UFH reduced the aPTT versus UFH alone (P < 0.001). A negative correlation existed between fibrinogen activity and aPTT for all treatments, except TNK alone. The present investigation illustrates that an agent with maximal fibrin specificity (TNK) has minimal effect on the aPTT, while agents with less fibrin specificity are more likely to prolong the aPTT, with and without UFH present.

Adult↗
PubMed2003

Comparison of four commercially available activated partial thromboplastin time reagents using a semi-automated coagulometer.

Large numbers of activated partial thromboplastin time (aPTT) reagents are sold in the market. The phospholipid content and its source, nature and the amount of activators are highly varied in different aPTT reagents. The present study was undertaken to evaluate which of the four aPTT reagents commonly used is suitable as an all-purpose reagent for a modest haemostasis laboratory. Four aPTT reagents (reagent A, Platelin LS; reagent B, Silimat; reagent C, Actin FSL; reagent D, CK Prest) were tested against 75 different plasmas obtained from normal patients as well as from patients with different haemostatic problems. All the tests were conducted by one of us (S.S.) in duplicates. Different aPTT reagents missed different proportions of mild factor VIII and factor IX deficiency (36.4, 18.2, 4.6 and 13.6% for reagents A, B, C and D, respectively) and showed abnormal results with normal plasmas (i.e. more than 5 s prolongation) (29.2, 25, 8.3 and 12.5% for reagents A, B, C and D, respectively). All the reagents faithfully picked up moderate and severe factor VIII and factor IX deficiency. There was no difference among the four aPTT reagents regarding their ability to prolong aPTT to therapeutic dosage of heparin or in their ability to give comparable factor VIII or factor IX levels in one-stage aPTT-based assays. There were differences in aPTT reagents in their ability to pick up mild deficiency of coagulation factor VIII and factor IX. Some reagents showed abnormal aPTT results in mild cases of factor VIII and factor IX deficiency without producing a large number of falsely prolonged aPTT with normal plasma.

Automation↗
PubMed2003

Management of lepirudin therapy for a patient with antiphospholipid antibody syndrome using the whole blood ecarin clot time and activated partial thromboplastin time.

A patient with antiphospholipid antibody syndrome (APS) and a history of heparin-induced thrombocytopenia required lepirudin therapy. The patient had an abnormal baseline activated partial thromboplastin time (aPTT), complicating management of his therapy. We investigated whether an alternative monitoring system, using a dry reagent technology [Thrombolytic Assessment System (TAS)], could be used to monitor the patient's whole blood ecarin clot time (ECT) and aPTT. Baseline values for the ECT and aPTT were normal with this system. During a continuous infusion of lepirudin, the patient's whole blood ECT was maintained between a desired range of 150-200 s for 73% of the time. Similarly, his whole blood aPTT was maintained between 60 and 80 s for 80% of the time. In contrast, the patient's plasma-based aPTT by standard methods was consistently > 150 s. The patient underwent surgical procedures without complications. To further investigate the finding that the patient's antibody did not affect the aPTT with this system, we performed the ECT and the aPTT assays on the TAS Analyzer with plasma samples from 10 patients with APS and abnormal aPTTs. All 10 samples had plasma ECT values within the normal range. Four patients had normalization of the aPTT, suggesting that a subset of patients with APS may benefit from the TAS aPTT assay when monitoring heparin or other anticoagulation therapy.

Anticoagulants↗
PubMed2004

Effects of vitamin K antagonist phenprocoumon on activated partial thromboplastin time measurement of direct thrombin inhibitors.

The activated partial thromboplastin time (aPTT) is currently the most common test used to measure the anticoagulation intensity of heparins and direct thrombin inhibitors (DTIs). Vitamin K antagonists variably affect aPTT reagents. Interactions between heparin and DTIs occur during concurrent therapy. Three DTIs (lepirudin, argatroban, melagatran) and one unfractionated heparin (liquemin) were added to normal plasma (NP) samples (n = 23) and to vitamin K antagonist plasma (VKAP) samples (n = 23) of patients treated with phenprocoumon. Lepirudin and argatroban were added at concentrations from 300 to 3000 ng/ml, melagatran from 30 to 1000 ng/ml, and unfractionated heparin from 0.016 to 0.48 IU/ml. Wave parameters of clotting time and aPTT ratio curves were evaluated by multivariate analysis for inhibitors, aPTT reagents and NP and VKAP samples. Normal ranges resulting from NP samples were 34.5 +/- 1.0 s with Pathromtin SL and 33.9 +/- 0.8 s with Platelin LS. Normal ranges using VKAP were 52.8 +/- 2.6 s (Pathromtin SL) and 44.2 +/- 1.1 s (Platelin LS) (P < 0.0001). Variance analysis showed that inhibitors, plasmas (NP versus VKAP) and reagents influenced the wave characteristics of aPTT (s) (P < 0.0001) and aPTT ratios (P < 0.0001). Distinct statistical differences between aPTT reagents on one hand and normal versus vitamin K antagonist plasma on the other hand make a comparison of reported aPTT results difficult, especially during overlapping therapy with vitamin K antagonists.

Anticoagulants↗
PubMed2004

Drotrecogin alfa activated (recombinant human activated protein C) in combination with heparin or melagatran: effects on prothrombin time and activated partial thromboplastin time.

Recombinant human activated protein C (rhAPC) has recently been demonstrated to be a promising candidate to improve the outcome for patients with severe sepsis. Plasma-derived activated protein C and unfractionated heparin (UH) exert anticoagulant synergy due to mechanisms that simultaneously decrease thrombin generation. Melagatran, a new direct thrombin inhibitor, does not bind to plasma proteins or requires antithrombin as a cofactor. The latter is often consumed in patients with severe sepsis. We investigated the anticoagulant efficiency in combined administration of rhAPC and UH or melagatran in terms of prolongation of the standard clotting assays activated partial thromboplastin time (aPTT) and prothrombin time (PT) in pooled plasma samples in vitro. RhAPC dose-dependently prolonged the aPTT but not the PT. The ability of UH and melagatran to prolong the aPTT was significantly enhanced in combination with rhAPC. The combined administration of rhAPC and melagatran, but not UH, resulted in additive prolongation of the PT. In control measurements the capability of rhAPC to suppress prothrombin fragment 1.2 generation dose-dependently increased in combination with heparin and melagatran. Our study demonstrates the respective effects of rhAPC, UH, melagatran and further different additive effects in combined administration of rhAPC and UH or melagatran on the prolongation of the aPTT and PT clotting assays usually used to monitor anticoagulant treatment.

Azetidines↗
PubMed1995

Effect of heparin on whole blood activated partial thromboplastin time using a portable, whole blood coagulation monitor.

OBJECTIVES: To evaluate the responsiveness of whole blood activated partial thromboplastin time (aPTT) to varying heparin doses in vitro and to examine the ex vivo relationship of whole blood aPTT to plasma heparin concentration. DESIGN: Prospective, controlled laboratory study. SETTING: Surgical suites and laboratory at a tertiary center. PATIENTS: Surgical patients and volunteers at a tertiary center were eligible for inclusion in this study. In vitro evaluation was performed using specimens obtained from each of five, healthy volunteers. Ex vivo evaluation was performed using specimens obtained from 30 cardiac surgical patients before and after systemic administration of heparin for extracorporeal circulation. INTERVENTIONS: Blood specimens were obtained from volunteers and added to syringes containing varying amounts of unfractionated porcine heparin for in vitro evaluation. For ex vivo evaluation, blood specimens were obtained from patients before and after systemic administration of 20 U/kg of heparin. MEASUREMENTS AND MAIN RESULTS: For the in vitro evaluation, specimens were divided into two aliquots after mixing with varying amounts of unfractionated porcine heparin. One aliquot was used to measure whole blood aPTT using a whole blood coagulation monitor immediately after blood collection and 3 mins later, and a second aliquot was used to determine plasma aPTT with a conventional, laboratory-based assay. Linear regression analysis demonstrated a high correlation (r = .94; r2 = .88) between aPTT assay systems and bias analysis demonstrated a mean aPTT measurement difference of 1.6 secs with +/- 2 SD limits of -15 to +18.2 secs. As indicated by comparable regression slopes, the in vitro aPTT responsiveness to increasing heparin concentration was similar with the two assay systems among individual subjects. Whole blood aPTT measurements after 3 mins of blood specimen storage were similar to immediate measurements. For ex vivo evaluation, blood specimens obtained from patients before and after systemic administration of heparin were divided into two aliquots. One aliquot was used to measure whole blood aPTT in duplicate and a second aliquot was used to measure plasma heparin concentration with an antifactor X active chromogenic assay. A high correlation (r = .89; r2 = .79) between whole blood aPTT and plasma heparin concentration was observed. CONCLUSIONS: Heparin responsiveness of whole blood aPTT, measured with a portable whole blood coagulation monitor, is similar to that of conventional laboratory aPTT over a clinically relevant range of heparin concentrations in vitro and ex vivo. On-site whole blood aPTT measurements should be useful in clinical situations requiring rapid aPTT results.

Blood Coagulation↗
PubMed1982

Bleeding in patients with activated partial thromboplastin time inhibitors.

We present a case in which an activated partial thromboplastin time (aPTT) inhibitor may have significantly contributed to prolonged bleeding in a patient and review five similar cases. The possibility of an aPTT inhibitor should be considered in the evaluation of patients with unexplained prolongation of PTT and PT. Such patients may develop significant bleeding even in the absence of other hematologic abnormalities.

Blood Coagulation↗
PubMed1996

Testing for Passovoy defect in children with prolonged activated partial thromboplastin time (APTT)

PURPOSE: To investigate the value of testing for Passovoy defect using the commercially available Passovoy trait plasma (PTP) in children with prolonged activated partial thromboplastin time (APTT). PATIENTS AND METHODS: We studied 13 children with prolonged APTT that corrected in a 1:1 mix with normal human plasma but not with PTP. In most children, a thorough laboratory investigation of the intrinsic pathway factors and von Willebrand factor was performed. RESULTS: Five patients had bleeding manifestations and eight were asymptomatic. Measurement of von Willebrand factor and intrinsic pathway factors revealed abnormal values in eight patients (low von Willebrand activity in six patients, low factor XII in one patient, and the presence of lupus anticoagulant in one patient). CONCLUSION: Our data suggest inability to diagnose Passovoy defect based on a mixing study. This study also raises the question of whether Passovoy defect exists as a distinct coagulation disorder.

Adolescent↗