Evaluation of the diagnostic performance of fibrin monomer in disseminated intravascular coagulation.
ABSTRACT Fibrin-related markers (FRM) such as fibrin monomer (FM) and D-dimer (DD) are considered useful biological markers for the diagnosis of disseminated intravascular coagulation (DIC). However, no studies on the diagnostic performance of different FRMs have been published in Korea. The aim of this study was to evaluate the diagnostic performance of FM for DIC in comparison with DD.
The reference limit of FM was determined based on plasma sample data obtained from 210 control individuals. To evaluate diagnostic performance, FM data from the plasma samples of 139 patients with DIC-associated diseases were obtained for DIC scoring. FM was measured by immunoturbidimetry using STA-LIATEST FM (Diagnostica Stago, France). Patients were classified according to the DIC score as non-DIC, non-overt DIC, or overt DIC. ROC curve analyses were performed.
The reference limit in the control individuals was determined to be 7.80 µg/mL. Patients with DIC-associated diseases were categorized as non-DIC (N=43), non-overt DIC (N=80), and overt DIC (N=16). ROC curve analyses showed that the diagnostic performance of FM was comparable to DD in both non-overt DIC and overt DIC (P=0.596 and 0.553, respectively). In addition, FM had higher sensitivity, specificity, positive predictive value, and negative predictive value than DD for differentiating overt DIC from non-DIC.
This study demonstrated that the diagnostic performance of FM for DIC was comparable to DD. FM might be more sensitive and more specific than DD in the diagnosis of overt DIC, but not non-overt DIC.
- [show abstract] [hide abstract]
ABSTRACT: The diagnosis of disseminated intravascular coagulation (DIC) should encompass both clinical and laboratory information. The International Society for Thrombosis and Haemostasis (ISTH) DIC scoring system provides objective measurement of DIC. Where DIC is present the scoring system correlates with key clinical observations and outcomes. It is important to repeat the tests to monitor the dynamically changing scenario based on laboratory results and clinical observations. The cornerstone of the treatment of DIC is treatment of the underlying condition. Transfusion of platelets or plasma (components) in patients with DIC should not primarily be based on laboratory results and should in general be reserved for patients who present with bleeding. In patients with DIC and bleeding or at high risk of bleeding (e.g. postoperative patients or patients due to undergo an invasive procedure) and a platelet count of <50 x 10(9)/l transfusion of platelets should be considered. In non-bleeding patients with DIC, prophylactic platelet transfusion is not given unless it is perceived that there is a high risk of bleeding. In bleeding patients with DIC and prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), administration of fresh frozen plasma (FFP) may be useful. It should not be instituted based on laboratory tests alone but should be considered in those with active bleeding and in those requiring an invasive procedure. There is no evidence that infusion of plasma stimulates the ongoing activation of coagulation. If transfusion of FFP is not possible in patients with bleeding because of fluid overload, consider using factor concentrates such as prothrombin complex concentrate, recognising that these will only partially correct the defect because they contain only selected factors, whereas in DIC there is a global deficiency of coagulation factors. Severe hypofibrinogenaemia (<1 g/l) that persists despite FFP replacement may be treated with fibrinogen concentrate or cryoprecipitate. In cases of DIC where thrombosis predominates, such as arterial or venous thromboembolism, severe purpura fulminans associated with acral ischemia or vascular skin infarction, therapeutic doses of heparin should be considered. In these patients where there is perceived to be a co-existing high risk of bleeding there may be benefits in using continuous infusion unfractionated heparin (UFH) due to its short half-life and reversibility. Weight adjusted doses (e.g. 10 mu/kg/h) may be used without the intention of prolonging the APTT ratio to 1.5-2.5 times the control. Monitoring the APTT in these cases may be complicated and clinical observation for signs of bleeding is important. In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended. Consider treating patients with severe sepsis and DIC with recombinant human activated protein C (continuous infusion, 24 microg/kg/h for 4 d). Patients at high risk of bleeding should not be given recombinant human activated protein C. Current manufacturers guidance advises against using this product in patients with platelet counts of <30 x 10(9)/l. In the event of invasive procedures, administration of recombinant human activated protein C should be discontinued shortly before the intervention (elimination half-life approximately 20 min) and may be resumed a few hours later, dependent on the clinical situation. In the absence of further prospective evidence from randomised controlled trials confirming a beneficial effect of antithrombin concentrate on clinically relevant endpoints in patients with DIC and not receiving heparin, administration of antithrombin cannot be recommended. In general, patients with DIC should not be treated with antifibrinolytic agents. Patients with DIC that is characterised by a primary hyperfibrinolytic state and who present with severe bleeding could be treated with lysine analogues, such as tranexamic acid (e.g. 1 g every 8 h).British Journal of Haematology 02/2009; 145(1):24-33. · 4.94 Impact Factor
- Journal of Thrombosis and Haemostasis 04/2007; 5(3):604-6. · 6.08 Impact Factor
- Thrombosis and Haemostasis 12/2001; 86(5):1327-30. · 6.09 Impact Factor
Evaluation of the Diagnostic Performance of Fibrin Monomer in
Disseminated Intravascular Coagulation
Kyoung-Jin Park, M.D., Eui-Hoon Kwon, M.T., Hee-Jin Kim, M.D., and Sun-Hee Kim, M.D.
Department of Laboratory Medicine & Genetics, Samsung Medical Center, Sungkyunkwan University School Medicine, Seoul, Korea
Background: Fibrin-related markers (FRM) such as fibrin monomer (FM) and D-dimer (DD) are considered useful biological mark-
ers for the diagnosis of disseminated intravascular coagulation (DIC). However, no studies on the diagnostic performance of differ-
ent FRMs have been published in Korea. The aim of this study was to evaluate the diagnostic performance of FM for DIC in com-
parison with DD.
Methods: The reference limit of FM was determined based on plasma sample data obtained from 210 control individuals. To evalu-
ate diagnostic performance, FM data from the plasma samples of 139 patients with DIC-associated diseases were obtained for DIC
scoring. FM was measured by immunoturbidimetry using STA-LIATEST FM (Diagnostica Stago, France). Patients were classified ac-
cording to the DIC score as non-DIC, non-overt DIC, or overt DIC. ROC curve analyses were performed.
Results: The reference limit in the control individuals was determined to be 7.80 µg/mL. Patients with DIC-associated diseases were
categorized as non-DIC (N=43), non-overt DIC (N=80), and overt DIC (N=16). ROC curve analyses showed that the diagnostic per-
formance of FM was comparable to DD in both non-overt DIC and overt DIC (P=0.596 and 0.553, respectively). In addition, FM had
higher sensitivity, specificity, positive predictive value, and negative predictive value than DD for differentiating overt DIC from
Conclusions: This study demonstrated that the diagnostic performance of FM for DIC was comparable to DD. FM might be more
sensitive and more specific than DD in the diagnosis of overt DIC, but not non-overt DIC.
Key Words: Area under the curve (AUC), Disseminated intravascular coagulation (DIC), D-dimer (DD), Fibrin monomer (FM), Fibrin-
related marker (FRM), ROC
Received: December 27, 2010
Revision received: April 7, 2011
Accepted: May 12, 2011
Corresponding author: Hee-Jin Kim, M.D.
Department of Laboratory Medicine & Genetics, Samsung Medical Center,
Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu,
Seoul 135-710, Korea
Tel: +82-2-3410-2710, Fax: +82-2-3410-2719, Email: email@example.com
Manuscript No: KJLM-10-180
ISSN 1598-6535 © The Korean Society for Laboratory Medicine.
This is an Open Access article distributed under the terms of the Creative Commons Attribution
Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits
unrestricted non-commercial use, distribution, and reproduction in any medium, provided
the original work is properly cited.
Korean J Lab Med 2011;31:143-147
Diagnostic Hematology KJLM
Disseminated intravascular coagulation (DIC) is a syste-
mic thrombohemorrhagic disorder that is associated with
hyperactivation of coagulation and secondary fibrinolysis .
It is characterized by organ failure resulting from microvas-
cular thrombosis, and bleeding resulting from the consump-
tion of platelets and coagulation factors. Until recently, there
was no single laboratory test to confirm the diagnosis of
DIC. However, a combination of tests in patients with DIC-
associated disease might be helpful in the diagnosis of the
disorder. A scoring system was introduced for the diagnosis
of overt DIC by the International Society of Thrombosis and
Hemostasis (ISTH) in 2001 [1-3]. A score of 5 or greater in-
dicates a diagnosis of overt DIC [2, 3]. The components of
the scoring system include a decreased platelet count, pro-
longation of prothrombin time (PT), increased fibrin-related
markers (FRMs), and decreased fibrinogen [1-3].
FRMs include D-dimer (DD), fibrin degradation product
(FDP), and fibrin monomer (FM). DD is produced by sec-
ondary fibrinolysis of cross-bound fibrin in the post-throm-
botic state. In contrast, FM is produced by the release of fi-
brinopeptide A from fibrinogen by thrombin in a hyperco-
agulable state. Therefore, DD could be considered a post-
thrombotic marker while FM could be considered an im-
pending thrombotic marker [4, 5]. Although some studies
showed advantages of FM over DD for the diagnosis or
Park K-J, et al. • Diagnostic Performance of FM in DIC
prognostication of DIC [5-8], data for evaluating the diag-
nostic performance of different types of FRMs is limited. In
addition, there were no defined cut-offs of FRMs for the di-
agnosis of DIC. For this reason, the present study was per-
formed to evaluate the diagnostic performance of FM for
DIC in comparison with DD.
MATERIALS AND METHODS
To establish a reference limit for FM, plasma samples from
210 control subjects were obtained. They were adult individ-
uals who visited our institute for routine health check-ups
and they had normal results in blood tests, including coagu-
lation screening tests. Those with autoimmune diseases,
chronic liver diseases, or thrombosis, and those on medica-
tion were excluded.
To evaluate the diagnostic performance of FRMs for DIC
scoring, FM data from plasma samples were obtained from
139 patients with DIC-associated diseases. According to the
DIC scoring system [1-3, 9] (Table 1), the patients were
classified into 3 groups as follows: Group 1 without DIC
(overt DIC score and non-overt DIC score was zero), Group
2 with non-overt DIC (overt DIC score range, 1-4 points
and non-overt DIC score was 1 point or higher), and Group
3 with overt DIC (overt DIC score was 5 points or higher).
2. Laboratory analyses
All blood samples for coagulation tests were collected
into tubes containing 3.2% sodium citrate and were proces-
sed within 4 hours after collection. Aliquots of plasma sam-
ples were prepared and frozen until the determination of
FM. Coagulation tests for DIC scoring were performed us-
ing the following reagents (STA-NEOPLASTINE CI PLUS
for PT, STA-PTT for activated partial thromboplastin time
[aPTT], STA-FIBRINOGEN for fibrinogen, STA-STA-
CHROM AT III for antithrombin [AT], STA-STACHROM
PROTEIN C for protein C [PC], STA-DEFICIENT V and
VII for coagulation factor V and VII, respectively, STA-LI-
ATEST D-DI for DD, and STA-LIATEST for FM). FDP was
measured semi-quantitatively by latex agglutination (FDP
PLASMA), and DD and FM were measured by immuno-
turbidimetric assays. All analyses were performed on a
STA-R Evolution coagulation instrument (Diagnostica St-
ago, Asnieres, France).
3. Statistical analysis
To determine the reference limit of FM in the control po-
pulation, we first checked for the normality of the data us-
ing the D’Agostino-Pearson test and eliminated outliers us-
ing the D/R ratio rule by Dixon. Hemostatic parameters
among the 3 groups were compared by 1-way ANOVA or
the Kruskal-Wallis test. The correlation between the DIC
score and the levels of FRMs was analyzed, and ROC curve
analysis was performed to compare the diagnostic perfor-
mance. According to the cut-offs of FRMs from the ROC
curve, sensitivity, specificity, positive predictive value (PPV),
negative predictive value (NPV), and the odds ratio were
calculated. A P value of less than 0.05 was considered statis-
tically significant. All statistical analyses were performed
using MedCalc software (Mariakerke, Belgium).
1. Reference limit of FM
The plasma levels of FM in the 210 control subjects ranged
from 1.64 to 9.66 µg/mL (median, 4.03 µg/mL). The data did
not follow a Gaussian distribution. Therefore, the cut-off
level was determined to be 7.80 µg/mL using the right-side
2. Comparison of hemostatic parameters for the diagnosis
of DIC in 3 groups
Among the 139 study patients, 43 were classified into
Group 1 (without DIC), 80 into Group 2 (with non-overt
DIC), and 16 patients into Group 3 (with overt DIC). Ma-
lignancies (35%), vascular diseases (29%), and infections
(20%) accounted for the majority of underlying diseases in
all patients. There were no differences among 3 groups in
the distribution of underlying diseases. All hemostatic pa-
rameters differed significantly among the 3 groups (Table 2).
The values of each parameter in Group 3 were significantly
Table 1. Scoring system for the diagnosis of disseminated intravascular co-
agulation [1-3, 9, 10]
No (0), Yes (2) Associated diseases
Platelet count (×103/µL)
Protein C activity (80-161%)*
Factor V activity (81-160%)*
Factor VII activity (68-149%)*
>100 (0), 50-100 (1), <50 (2) >100 (0), <100 (1)
<17 (0), 17-20 (1), >20 (2)
>100 (0), <100 (1)
Normal (0), <5 (1), >5 (2)
<17 (0), >17 (1)
>100 (-1), <100 (1)
NL (0), Inc (1)
NL (-1), Dec (1)
NL (-1), Dec (1)
NL (-1), Dec (1)
NL (-1), Dec (1)
*Local reference intervals; †Score for each parameter is in parentheses.
Abbreviations: NL, normal; Dec, decrease; Inc, increase.
Park K-J, et al. • Diagnostic Performance of FM in DIC
higher than in Group 2, and those in Group 2 were signifi-
cantly higher than in Group 1. The median values of DD in
Group 1, Group 2, and Group 3 were 2.08 µg/mL, 3.19 µg/
mL, and 8.76 µg/mL, respectively (Fig. 1A; P<0.001). The
median values of FM in Group 1, Group 2, and Group 3
were 5.95 µg/mL, 9.65 µg/mL, and 86.61 µg/mL, respec-
tively (Fig. 1B; P<0.001). There was a statistically signifi-
cant correlation between the levels of both FM and DD and
the DIC score (r=0.3975, P<0.0001 for FM, and r=0.4280,
P<0.0001 for DD). DD and FM were also significantly cor-
related in Group 1 and Group 2 (r=0.5556, P<0.0001 in
Groups 1 and 2 combined; r=0.6487, P<0.0001 in Group 1;
and r=0.5519, P<0.0001 in Group 2). However, there was
no significant correlation between DD and FM in Group 3
(with overt DIC; P=0.104). Two patients in Group 3 show-
ed extremely low levels of DD (0.56 µg/mL and 1.9 µg/mL),
while they had relatively high levels of FM (10.6 µg/mL and
61.33 µg/mL, respectively).
3. ROC curve analysis
On ROC curve analyses, the diagnostic performance of
FM and DD were similar in all 3 groups (Fig. 2, P=0.596 in
Group 2, and P=0.553 in Group 3). To discriminate Group
3 from Group 1, the values with the largest area under the
curve (AUC) were set as the cut-offs for DD and FM (3.92
µg/mL and 9.95 µg/mL, respectively). Below these cut-offs,
FM had a higher sensitivity, specificity, PPV, and NPV than
DD for differentiating overt DIC from non-DIC (Table 3).
To discriminate Group 2 from Group 1, the cut-offs for DD
and FM were 2.2 µg/mL and 7.80 µg/mL, respectively. DD
had a higher sensitivity, NPV, and odds ratio than FM for
differentiating non-overt DIC from non-DIC (Table 3).
Table 3. Cut-off values for fibrin-related markers
Cut-off Sensitivity Specificity PPV
I. Group 1 vs. Group 3 (Non-DIC vs. Overt DIC)
DD (µg/dL)3.92* 81.20
FM (µg/dL)9.95* 93.75
II. Group 1 vs. Group 2 (Non-DIC vs. Non-overt DIC)
DD (µg/dL)2.20* 70.00
NPV Odds ratio (95% CI)
29.09 66.67 20.67 (4.11-103.80)
55.56 91.18 12.92 (3.16-52.77)
70.00 53.49 2.68 (1.25-5.78)
73.30 42.902.06 (0.97-4.41)
*Values with the largest area under the curve (AUC); †Upper reference limit of FM.
Abbreviations: PPV, positive predictive value; NPV, negative predictive value; CI, con-
fidence interval; DIC, disseminated intravascular coagulation; DD, D-dimer; FM, fibrin
Table 2. Comparison of coagulation parameters among the 3 groups
Group 1 (N=43) Group 2 (N=80) Group 3 (N=16)
220.0 (184-258) 75.5 (44-117)
Factor V (%)
Factor VII (%) 116 (88.25-129.75) 61.5 (47-82)
Protein C (%) 102 (89-116.25)
16.3 (14.7-17.8) 22.2 (20.2-26.5)
5.95 (4.27-10.76) 9.65 (5.32-54.63) 86.61 (43.64-145.99) <0.001†
100 (92-109.5) 71.0 (49.5-83.5) 45.5 (30.0-60.5)
80 (64.5-110.5) 66.5 (46.5-87.5) 25.5 (7.5-36)
3.19 (1.62-8.41) 8.76 (4.45-35.96) <0.001*
32 (22-44.5)53.5 (39-67)
*By Kruskal-Wallis test; †By 1-way analysis of variance.
The data shown are the median (25p-75p).
Abbreviations: DD, D-dimer; FM, fibrin monomer; AT, antithrombin.
Fig. 1. Box plots of the plasma concentration of D-dimer (DD) (A) and fibrin monomer (FM) (B) in the 3 Groups. Data are expressed as median ±2SD. The statisti-
cal significance between the 2 groups was determined by 1-way analysis of variance.
Group 1 Group 2 Group 3
Fibrin monomer (μg/mL)
Group 1 Group 2 Group 3
Park K-J, et al. • Diagnostic Performance of FM in DIC
Hypercoagulation and secondary fibrinolysis are the ma-
jor pathologic mechanisms in DIC. Laboratory data based
on the clinical condition might be critical for the diagnosis
of DIC. Among the coagulation markers (PT, platelets, fi-
brinogen, FRM) in the DIC scoring system, FRMs such as
FM and DD best reflect the underlying pathology of DIC.
Because the measurement of FRMs has not been standard-
ized, local cut-off values remain to be defined for the appli-
cation of the ISTH DIC scoring system. For the diagnosis of
DIC, DD was very sensitive but not specific. However, little
is known about the diagnostic performance of FM in Ko-
rean patients with DIC.
The present study established a reference limit for FM in
healthy individuals and evaluated the diagnostic perfor-
mance of FM in patients with DIC-associated diseases. We
established the cut-off for FM in 210 healthy individuals as
7.80 µg/mL. The measurement of FM is based on immuno-
turbidimetry, which might be affected by interference from
hemolysis, bilirubinemia, and lipidemia. We excluded sam-
ples with abnormal routine laboratory findings. Okajima et
al.  reported that the level of FM in 116 healthy volun-
teers was less than 6.6 µg/mL using an ELISA method. Ha-
mano et al.  defined 6.1 µg/mL of FM as the clinical
baseline using a latex immunoturbidimetric assay.
In our study, a comparison of the ROC curves of FM and
DD showed that FM was comparable to DD as a marker for
the diagnosis of both non-overt DIC and overt DIC. Previ-
ous studies showed some controversial data [6, 12]. Accord-
ing to Dempfle et al. , FM was better indicator than DD
for the early diagnosis of DIC and its prognosis. In contrast,
large prospective studies by multiple institutions showed
that FM was not a useful marker for the differentiation of
“pre-DIC” from “not-DIC” . By the ISTH, “pre-DIC”
was defined as the state within a week before the onset of
DIC, while “non-overt DIC” was defined as the state with
hemostatic dysfunction that is compensated . We hypoth-
esized that FM might be a more useful marker for detection
of the early phase of non-overt DIC with compensation. The
level of FM in Group 2 with non-overt DIC was significantly
higher than that in Group 1 without DIC, and was lower
than that in Group 3 with overt DIC. Differences in DD
were also observed among the 3 Groups. However, compari-
son of ROC curves for FM and DD in the diagnosis of non-
overt DIC showed that FM was not a better indicator than
DD. Theoretically, FM would be produced earlier than DD
in a hypercoagulable state, while DD would be produced af-
ter thrombosis and fibrinolysis. Therefore, increased levels
of FM without an increase in DD might enhance the diag-
nostic power of FM. In the present study, there were 2 cases
showing an increase in FM with no increase in DD despite
the diagnosis of overt DIC. This suggested that for the diag-
nosis of overt DIC, FM is more sensitive than DD; however,
there was no difference between the ROC curves of DD and
FM. Assuming that the presence of heparin might influence
thrombin, which in turn might influence the formation of
FM, we investigated the history of anticoagulation, and did
not find any differences among the 3 Groups.
In the present study, we defined cut-offs for the FRMs
Fig. 2. ROC curves of D-dimer (DD) and fibrin monomer (FM) for the diagnosis of disseminated intravascular coagulation (DIC); (A) In Group 2 (non-overt DIC), the
area under the curve (AUC) of DD and FM were 0.638 and 0.610, respectively (P=0.596). (B) In Group 3 (overt DIC), the AUC of DD and FM were 0.819 and 0.858,
0 20 40 60 80 100
0 20 40 60 80 100
Park K-J, et al. • Diagnostic Performance of FM in DIC
based on the values with the largest AUC in ROC curves
and the reference limit in the control population. Using the
suggested cut-offs, FM showed lower sensitivity than DD in
patients with non-overt DIC, and higher sensitivity in pa-
tients with overt DIC. DD might be obtained from both in-
travascular coagulation and extravascular sources such as
trauma and local inflammation, while FM might result
from only intravascular sources . Therefore, FM might
have higher sensitivity for the diagnosis of overt DIC.
The present study had some limitations. First, the number
of the patients was very small, especially the number of pa-
tients with overt DIC. The magnitude of FM elevation
might be influenced by other factors such as medications or
the nature of underlying diseases. Therefore, some patients
with non-overt DIC had levels of FM that were more ele-
vated than in patients with overt-DIC. Second, we could not
investigate the levels of FM at the state of pre-DIC in the
present study. By definition, pre-DIC might reflect the early
phase of DIC more than non-overt DIC. Lastly, we would
like discuss the clinical utility of AT, PC, and factor V and
factor VII for non-overt DIC included in this study. The
clinical utility of these biomarkers in non-overt DIC is still
under investigation [2, 3, 9, 13, 14]. In addition, these tests
are typically not available as stat tests, as is the case at the
authors’ institution, which also limits their clinical utility.
In summary, we investigated the reference limit of FM in
healthy adults and evaluated the diagnostic performance of
FM in terms of the sensitivity, specificity, PPV, NPV, and
AUC for the diagnosis of DIC. FM had performance com-
parable to DD for the diagnosis of DIC.
Authors’ Disclosures of Potential Conflicts of Interest
No potential conflict of interest relevant to this article was
Reagents for the measurement of FM were provided free of
charge by the manufacturers.
1. Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diag-
nosis and management of disseminated intravascular coagulation.
British Committee for Standards in Haematology. Br J Haematol
2. Toh CH and Hoots WK. The scoring system of the Scientific and
Standardisation Committee on Disseminated Intravascular Coag-
ulation of the International Society on Thrombosis and Haemo-
stasis: a 5-year overview. J Thromb Haemost 2007;5:604-6.
3. Taylor FB Jr, Toh CH, Hoots WK, Wada H, Levi M. Towards defi-
nition, clinical and laboratory criteria, and a scoring system for
disseminated intravascular coagulation. Thromb Haemost 2001;
4. Wada H and Sakuragawa N. Are fibrin-related markers useful for
the diagnosis of thrombosis? Semin Thromb Hemost 2008;34:33-8.
5. Wada H, Sase T, Matsumoto T, Kushiya F, Sakakura M, Mori Y, et
al. Increased soluble fibrin in plasma of patients with disseminated
intravascular coagulation. Clin Appl Thromb Hemost 2003;9:233-
6. Dempfle CE, Wurst M, Smolinski M, Lorenz S, Osika A, Olenik D,
et al. Use of soluble fibrin antigen instead of D-dimer as fibrin-re-
lated marker may enhance the prognostic power of the ISTH overt
DIC score. Thromb Haemost 2004;91:812-8.
7. Ieko M, Nakabayashi T, Tarumi T, Naito S, Yoshida M, Kanazawa
K, et al. Soluble fibrin monomer degradation products as a poten-
tially useful marker for hypercoagulable states with accelerated fi-
brinolysis. Clin Chim Acta 2007;386:38-45.
8. Wada H, Wakita Y, Nakase T, Shimura M, Hiyoyama K, Nagaya S,
et al. Increased plasma-soluble fibrin monomer levels in patients
with disseminated intravascular coagulation. Am J Hematol 1996;
9. Toh CH and Downey C. Performance and prognostic importance
of a new clinical and laboratory scoring system for identifying
non-overt disseminated intravascular coagulation. Blood Coagul
10. Okajima K, Uchiba M, Murakami K, Okabe H, Takatsuki K. De-
termination of plasma soluble fibrin using a new ELISA method
in patients with disseminated intravascular coagulation. Am J He-
11. Hamano A, Umeda M, Ueno Y, Tanaka S, Mimuro J, Sakata Y. La-
tex immunoturbidimetric assay for soluble fibrin complex. Clin
12. Okamoto K, Wada H, Hatada T, Uchiyama T, Kawasugi K, Ma-
yumi T, et al. Frequency and hemostatic abnormalities in pre-DIC
patients. Thromb Res 2010;126:74-8.
13. Egi M, Morimatsu H, Wiedermann CJ, Tani M, Kanazawa T, Su-
zuki S, et al. Non-overt disseminated intravascular coagulation
scoring for critically ill patients: the impact of antithrombin levels.
Thromb Haemost 2009;101:696-705.
14. Oh D, Jang MJ, Lee SJ, Chong SY, Kang MS, Wada H. Evaluation of
modified non-overt DIC criteria on the prediction of poor outcome
in patients with sepsis. Thromb Res 2010;126:18-23.