Reviewer's report 
 An Unusual Case of an Ulcerative Colitis Flare resulting in disseminated intravascular Title: 
coagulopathy and a bladder hematoma: A Case Report 
 1  12 July 2004 Version: Date: 
 Adriaan A van Bodegraven Reviewer: 
Reviewer's report: 
General 
This is an interesting case, providing information of an unusal clinical course of UC due to (excessive) coagulation activation ------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can 
be reached) Data concerning the DIC-panel are rather sparse: what is the course of the fibrinogen concentration. 
Are their any variables concerning plasmin generation (more than DDimers) available? This is 
especially important because the course of DIC was rather acute (Serial repeat lab showed dropping 
Hb and platelets, whereas initial Fg concentration was normal). The rise of D-Dimer alone may be 
due to an exacerbation of UC, as has been shown by several authors. 'A thorough hematologic work-up of the patient did not reveal..'is stated in the discussion, but not in 
the results. What has been measured precisely and what were the values/findings? 
------------------------------------------------------------------------------- Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author can be trusted to correct) 
Data on pre-admission drugs are sparse (ASA, Cipro, Lansoprazole, 6-MP and steroids): what was 
the dosage and duration of the drug usage and what was the indication? Subsequently, a few words 
concerning the therapeutic intervention at the hospital may be given. Why was this regimen/strategy 
chosen, and why did the patient respond to IV steroids whereas such an apparently ineffective, 
abundant immunosuppressive drug strategy was prescribed before? 
Minor errors in language eg ('shistocytes', 'associated' without 'with' in the discussion section)and syntaxis (a fibrin clot consistent with a submucosal hematoma) can be found. Some vital references are missing; eg Bernstein CN, Blanchard JF, Houston DS, Wajda A. The 
incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory 
bowel disease: a population-based cohort study. Thromb Haemost 2001;85:430-4 (------------------------------------------------------------------------------- Discretionary Revisions (which the author can choose to ignore) 
The authors may extend their discussion with regard to the pathogenesis of DIC in the course of UC. 
Eg, do microparticles (generated from activated platelets) play a etiological role? Is this patient prone 
due to the drug or due to his age? 
Moreover, they may suggest that DIC is a rather difficult diagnosis to prove, and may be missed in 
patients, especially when not expected, which is in my opinion an important message of this case report. 
 Accept after minor essential revisions What next?: 
 An article whose findings are important to those with closely related research Level of interest: 
interests 
 Needs some language corrections before being published Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
None 
Reviewer's report 
 An Unusual Case of an Ulcerative Colitis Flare resulting in disseminated intravascular Title: 
coagulopathy and a bladder hematoma: A Case Report 
 1  12 July 2004 Version: Date: 
 Adriaan A van Bodegraven Reviewer: 
Reviewer's report: 
General 
This is an interesting case, providing information of an unusal clinical course of UC due to (excessive) coagulation activation ------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can 
be reached) Data concerning the DIC-panel are rather sparse: what is the course of the fibrinogen concentration. 
Are their any variables concerning plasmin generation (more than DDimers) available? This is 
especially important because the course of DIC was rather acute (Serial repeat lab showed dropping 
Hb and platelets, whereas initial Fg concentration was normal). The rise of D-Dimer alone may be 
due to an exacerbation of UC, as has been shown by several authors. 'A thorough hematologic work-up of the patient did not reveal..'is stated in the discussion, but not in 
the results. What has been measured precisely and what were the values/findings? 
------------------------------------------------------------------------------- Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author can be trusted to correct) 
Data on pre-admission drugs are sparse (ASA, Cipro, Lansoprazole, 6-MP and steroids): what was 
the dosage and duration of the drug usage and what was the indication? Subsequently, a few words 
concerning the therapeutic intervention at the hospital may be given. Why was this regimen/strategy 
chosen, and why did the patient respond to IV steroids whereas such an apparently ineffective, 
abundant immunosuppressive drug strategy was prescribed before? 
Minor errors in language eg ('shistocytes', 'associated' without 'with' in the discussion section)and syntaxis (a fibrin clot consistent with a submucosal hematoma) can be found. Some vital references are missing; eg Bernstein CN, Blanchard JF, Houston DS, Wajda A. The 
incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory 
bowel disease: a population-based cohort study. Thromb Haemost 2001;85:430-4 (------------------------------------------------------------------------------- Discretionary Revisions (which the author can choose to ignore) 
The authors may extend their discussion with regard to the pathogenesis of DIC in the course of UC. 
Eg, do microparticles (generated from activated platelets) play a etiological role? Is this patient prone 
due to the drug or due to his age? 
Moreover, they may suggest that DIC is a rather difficult diagnosis to prove, and may be missed in 
patients, especially when not expected, which is in my opinion an important message of this case report. 
 Accept after minor essential revisions What next?: 
 An article whose findings are important to those with closely related research Level of interest: 
interests 
 Needs some language corrections before being published Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
None 
Please review this paper.
user
Reviewer's report 
 An Unusual Case of an Ulcerative Colitis Flare resulting in disseminated intravascular Title: 
coagulopathy and a bladder hematoma: A Case Report 
 1  12 July 2004 Version: Date: 
 Adriaan A van Bodegraven Reviewer: 
Reviewer's report: 
General 
This is an interesting case, providing information of an unusal clinical course of UC due to (excessive) coagulation activation ------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can 
be reached) Data concerning the DIC-panel are rather sparse: what is the course of the fibrinogen concentration. 
Are their any variables concerning plasmin generation (more than DDimers) available? This is 
especially important because the course of DIC was rather acute (Serial repeat lab showed dropping 
Hb and platelets, whereas initial Fg concentration was normal). The rise of D-Dimer alone may be 
due to an exacerbation of UC, as has been shown by several authors. 'A thorough hematologic work-up of the patient did not reveal..'is stated in the discussion, but not in 
the results. What has been measured precisely and what were the values/findings? 
------------------------------------------------------------------------------- Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author can be trusted to correct) 
Data on pre-admission drugs are sparse (ASA, Cipro, Lansoprazole, 6-MP and steroids): what was 
the dosage and duration of the drug usage and what was the indication? Subsequently, a few words 
concerning the therapeutic intervention at the hospital may be given. Why was this regimen/strategy 
chosen, and why did the patient respond to IV steroids whereas such an apparently ineffective, 
abundant immunosuppressive drug strategy was prescribed before? 
Minor errors in language eg ('shistocytes', 'associated' without 'with' in the discussion section)and syntaxis (a fibrin clot consistent with a submucosal hematoma) can be found. Some vital references are missing; eg Bernstein CN, Blanchard JF, Houston DS, Wajda A. The 
incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory 
bowel disease: a population-based cohort study. Thromb Haemost 2001;85:430-4 (------------------------------------------------------------------------------- Discretionary Revisions (which the author can choose to ignore) 
The authors may extend their discussion with regard to the pathogenesis of DIC in the course of UC. 
Eg, do microparticles (generated from activated platelets) play a etiological role? Is this patient prone 
due to the drug or due to his age? 
Moreover, they may suggest that DIC is a rather difficult diagnosis to prove, and may be missed in 
patients, especially when not expected, which is in my opinion an important message of this case report. 
 Accept after minor essential revisions What next?: 
 An article whose findings are important to those with closely related research Level of interest: 
interests 
 Needs some language corrections before being published Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
None 
assistant