Document Detail

Mean platelet volume: a controversial marker of disease activity in Crohn's disease.
Jump to Full Text
MedLine Citation:
PMID:  23058104     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: We investigated and compared the capacity of mean platelet volume (MPV) and other inflammatory markers in detecting Crohn's disease (CD) activity and differentiating CD patients from healthy controls.
METHODS: MPV, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cells were measured in 61 CD patients and 50 healthy subjects. Disease activity was assessed by the Crohn's Disease Activity Index.
RESULTS: A significant decrease in MPV was noted in patients with CD compared with healthy controls (P <0.0001), but statistical difference was not found between active and inactive CD groups. In CD, no significant correlation was found between MPV and other inflammatory markers. The overall accuracy of MPV (cutoff: 10.35 fl), CRP (cutoff: 4.85 mg/dl) and ESR (cutoff: 8.5 mm/hour) in differentiating CD patients from healthy controls was 76.6%, 65.8% and 72.1% respectively. The overall accuracy of CRP (cutoff: 4.95 mg/dl) and ESR (cutoff: 16.5 mm/hour) in determination of active CD was 80.3% and 73.8%.
CONCLUSIONS: MPV declined in CD patients compared with healthy subjects. MPV had the best accuracy in determination of CD patients and healthy controls. MPV did not show a discriminative value in disease activity.
Authors:
Song Liu; Jianan Ren; Gang Han; Gefei Wang; Guosheng Gu; Qiuyuan Xia; Jieshou Li
Related Documents :
23053754 - A comparative investigation of flexion relaxation phenomenon in healthy and chronic nec...
24314054 - Low-dose oral desmopressin for treatment of nocturia and nocturnal enuresis in patients...
24596514 - Prealbumin is a more sensitive marker than albumin to assess the nutritional status in ...
23088814 - Sensory reweighting in controls and stroke patients.
10957834 - Glycogen storage disease type ia: frequency and clinical course in turkish children.
23053754 - A comparative investigation of flexion relaxation phenomenon in healthy and chronic nec...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-10-12
Journal Detail:
Title:  European journal of medical research     Volume:  17     ISSN:  2047-783X     ISO Abbreviation:  Eur. J. Med. Res.     Publication Date:  2012  
Date Detail:
Created Date:  2012-12-11     Completed Date:  2013-04-01     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  9517857     Medline TA:  Eur J Med Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  27     Citation Subset:  IM    
Affiliation:
Department of Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adult
Biological Markers / analysis*,  metabolism
Blood Platelets / metabolism,  pathology*
Blood Sedimentation
Body Mass Index
C-Reactive Protein / analysis
Case-Control Studies
Cell Differentiation
Crohn Disease / diagnosis*,  metabolism
Female
Humans
Inflammation / metabolism
Leukocytes
Male
Platelet Count
Prospective Studies
ROC Curve
Sensitivity and Specificity
Severity of Illness Index
Chemical
Reg. No./Substance:
0/Biological Markers; 9007-41-4/C-Reactive Protein
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Eur J Med Res
Journal ID (iso-abbrev): Eur. J. Med. Res
ISSN: 0949-2321
ISSN: 2047-783X
Publisher: BioMed Central
Article Information
Download PDF
Copyright ©2012 Liu et al.; licensee BioMed Central Ltd.
open-access:
Received Day: 29 Month: 6 Year: 2012
Accepted Day: 1 Month: 10 Year: 2012
collection publication date: Year: 2012
Electronic publication date: Day: 12 Month: 10 Year: 2012
Volume: 17 Issue: 1
First Page: 27 Last Page: 27
PubMed Id: 23058104
ID: 3519557
Publisher Id: 2047-783X-17-27
DOI: 10.1186/2047-783X-17-27

Mean platelet volume: a controversial marker of disease activity in Crohn’s disease
Song Liu12 Email: medical.lis@gmail.com
Jianan Ren1 Email: jiananr@gmail.com
Gang Han3 Email: hanlaowu53@yahoo.com.cn
Gefei Wang1 Email: Gfwang@163.com
Guosheng Gu1 Email: guguoshengde@163.com
Qiuyuan Xia4 Email: xiaqiuo@163.com
Jieshou Li1 Email: jieshou_li@163.com
1Department of Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, China
2Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA, 02114, USA
3Second Affiliated Hospital of Jilin University, Department of General Surgery, General Surgery Center of Jilin University, 218 Ziqiang Road, Changchun, 130041, China
4Department of Pathology, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, China

Background

The pathogenesis of Crohn’s disease (CD) remains unclear [1,2]. Previous studies suggested that early detection of disease activity could significantly reduce the mortality of CD [3,4]. Non-invasive tests, such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and fecal calprotectin, are therefore being increasingly recognized as important markers for initial diagnosis and disease activity detection.

Recently, several studies have suggested that platelets may be involved in the pathogenesis of CD [5-8]. In addition, mean platelet volume (MPV) has been reported to be influenced in CD [9,10], and has been assumed a potential inflammatory marker and disease activity indicator in several studies [10-12].

However, as these studies involved limited amounts of enrolled patients or did not compare the differential capacity of MPV with previous inflammatory markers, the present study was designed to examine whether MPV would be useful for differentiating CD patients from healthy controls and evaluating CD activity. Furthermore, we analyzed and compared the ability of MPV with other inflammatory markers.


Methods
Patients

We prospectively collected 61 CD patients and 50 healthy subjects between March 2010 and September 2011 (Figure 1). The diagnostic criteria of CD were mainly composed from standard clinical, radiological, endoscopic and histopathologic findings.

The exclusion criteria were acute or chronic infection, hypertension, endocrinological disorder, hematological disease, heart failure, hepatic and renal disorder, cancer and peripheral vascular disease [13]. None of the enrolled subjects had received anticoagulant medications, NSAIDs or contraceptives.

Laboratory parameters

Full blood count (including MPV and white blood cells (WBC)), CRP and ESR were performed on admission (before prescribing any medications).

For MPV measurement in all enrolled patients, the blood samples were anticoagulated by ethylenediamine tetraacetic acid with wortmanin and tyrphostin [14], and then treated with rapid processing (within <4 hours) [14] and the same storage temperature [13,15]. For other parameters, the measurement and process were carried out according to standard laboratory practice.

To calculate the body mass index, height and weight were recorded on admission for each individual. For CD patients, the disease activity was defined according to the Crohn’s Disease Activity Index (CDAI) score. Patients were further divided into an active CD group (CDAI >150) and an inactive CD group (CDAI <150) (Figure 1).

Statistical analysis

Statistical analysis was performed using GraphPad Prism Software (version 5.01; GraphPad, San Diego, CA, USA). All analyses were two-tailed and differences were considered statistically significant when P <0.05. For continuous variables, the mean and standard error of the mean were calculated; Students’ t test was used to compare variance between groups. For categorical variables, percentages were provided and the chi-squared test was used. Pearson analysis was used to calculate the correlation between MPV and other inflammatory markers. Receiver operating characteristic (ROC) curve analysis was performed to identify optimal cutoff values for MPV and other inflammatory markers. The overall accuracy was also calculated by additional true-positive and true-negative test results divided by all tests: (a + d) / (a + b + c + d).

Ethical consideration

This study was approved by the Ethics Committee of Jinling Hospital, and a written informed consent was obtained from each enrolled participant.


Results
Differentiation of Crohn’s disease patients and healthy controls

The demographic features of CD patients and healthy controls are shown in Table 1. The distributions of age, gender, smoking habit and body mass index were not statistically significant between groups.

Table 2 demonstrates comparisons of all inflammatory markers, including MPV, CRP, ESR and WBC. A significant decline in MPV was noted in patients with CD compared with healthy controls (9.55 ± 0.168 fl vs. 11.1 ± 0.160 fl, P <0.0001). Meanwhile, CRP (13.4 ± 2.43 mg/dl vs. 2.89 ± 0.547 mg/dl, P <0.0001) and ESR (19.1 ± 2.15 mm/hour vs. 6.60 ± 0.431 mm/hour, P <0.0001) were statistically higher in the CD group than those in the control group. However, WBC appeared to be similar in both groups (6.83 ± 0.377×109/l vs. 6.90 ± 0.342×109/l, P = 0.8881).

We further investigated the ability of MPV and other markers in differentiating CD patients from healthy controls. As shown in Table 3, the optimal cutoff value for MPV was 10.35 fl, with sensitivity and specificity of 78.7% and 74.0% respectively (area under the curve (AUC): 0.8303). The overall accuracy of MPV in detecting CD patients was 76.6%.

Moreover, ROC analysis also suggested 4.85 mg/dl and 8.5 mm/hour as optimal cutoff points for CRP (sensitivity: 52.5%, specificity: 82%, AUC: 0.6849) and ESR (sensitivity: 68.9%, specificity: 76.0%, AUC: 0.7834) respectively (Figure 1).

Differentiation of active and inactive Crohn’s disease

According to CDAI scores, patients with CD were assigned into active and inactive groups. Notably, MPV was similar between active and inactive CD patients (9.52 ± 0.223 fl vs. 9.58 ± 0.251 fl, P = 0.8423) (Table 4). However, CRP (21.8 ± 4.21 mg/dl vs. 5.75 ± 1.81 mg/dl, P = 0.0012) and ESR (26.4 ± 3.26 mm/hour vs. 12.5 ± 2.33 mm/hour, P = 0.0011) of active CD patients were significantly higher than those of inactive CD patients.

Spearman correlation analysis suggested that MPV did not correlate with CRP (r = −0.022, P = 0.8671), ESR (r = −0.059, P = 0.6518) or WBC (r = −0.1549, P = 0.2332) in patients with CD (Table 5).

We further performed ROC analysis to investigate the capacity of all inflammatory markers in differentiating active from inactive CD (Table 6 and Figure 2). The optimal cutoff levels for CRP and ESR were 4.95 mg/dl (sensitivity: 82.8%, specificity: 78.1%, AUC: 0.7877) and 16.5 mm/hour (sensitivity: 65.5%, specificity: 81.3%, AUC: 0.7909), with 80.3% and 73.8% of overall accuracy respectively (Figure 3). However, MPV did not show a statistically discriminative value in differentiate active from inactive CD (AUC: 0.5043, overall accuracy: 55.7%).


Discussion

In the present study we have demonstrated that the MPV level was significantly lower in CD patients than that in healthy participants. We also illustrated that MPV was an accurate marker in distinguishing CD patients from healthy controls. However, the MPV level was statistically similar between active and inactive CD patients, leading to a failure of detecting patients with or without active disease.

Meanwhile, we demonstrated that CRP and ESR were both higher in CD patients compared with healthy controls, and higher in active compared with inactive CD patients. Even though the overall accuracy of CRP and ESRwas lower than that of MPV in detecting CD patients, they were still effective in determination of active CD patients.

Moreover, we found that MPV was not correlated with CRP, ESR or WBC in patients with CD. WBC was not an effective indicator in distinguishing CD patients from healthy subjects and active from inactive CD patients.

CD is characterized by chronic, transmural intestinal inflammation in which periods of remission with variable length are interrupted by relapse episodes. Previous studies have demonstrated that appropriate and effective therapy could significantly control symptoms, maintain remission, prevent relapse, improve quality of life and reduce mortality [3,16]. The early determination of diagnosis and detection of disease activity are therefore essential for tailoring therapy [17].

As invasive techniques, including endoscopic, radiological and histopathologic methods, are routinely used for diagnostic decision and disease activity supervision, an ideal non-invasive test is increasingly expected for initial diagnosis and identification of disease activity [18].

CRP is a valuable inflammatory marker in inflammatory bowel disease (IBD), especially CD [17,19]. Prior studies suggested a sensitivity range for uncovering IBD between 50 and 60% [20,21]. In our study, CRP displayed a high accuracy for differentiating CD patients from healthy controls and for distinguishing patients with and without active disease (65.8% and 80.3% respectively).

ESR and WBC are both nonspecific markers of inflammation. Although they could adjust to and reflect the severity of inflammation, low sensitivity and specificity of gastrointestinal inflammatory status were reported in previous studies [19,22]. However, in the present study, ESR performed as a notable marker in the detection of CD patients (overall accuracy: 72.1%) and in distinguishing active from inactive CD (overall accuracy: 73.8%).

Recently, a series of stool tests, such as fecal lactoferrin, calprotectin and elastase, were investigated as novel inflammatory markers. Even though they may be superior to CRP or ESR with higher sensitivity and specificity in detecting gastrointestinal inflammation [17,23,24], they are not specific markers for IBD; and they are inconvenient and unpleasant for stool sampling.

The link between MPV and inflammation has been well investigated in the literature [13,25]. Previous series of case–control and cohort studies have discovered several important confounders of MPV. Smoking and exposure to nicotine were key factors that would significantly influence platelet morphology and size, and could be confounded by sex, age and duration of smoking [13]. In the current study, the age, sex and smoking histories were statistically similar between healthy controls and patients with CD (Table 1). However, the duration of smoking was not registered and calculated in this study, leading to a difficulty in excluding the influence of duration of smoking on MPV. Nevertheless, as the percentage of participants with a current or previous smoking history was <25% in both healthy control (22.0%) and CD (24.6%) groups, the influence of duration of smoking on MPV was dramatically restricted. Hypertension [13,26] and diabetes [27,28] were confirmed closely correlated with large platelet size, respectively. To prevent their influence on MPV, we excluded patients with hypertension, heart failure, hepatic and renal disorder, vascular disease, endocrinological disorder and hematological disease. Obesity was also found to be associated with elevated MPV [13,29]. However, the normal and similarity of body mass index in both healthy controls and CD patients eliminated the potential influence of obesity on MPV.

Platelets, which are frequently complicated with thromboembolic risks, may play a crucial role in the pathogenesis of IBD [30-33]. The statistically significant declined MPV in CD patients observed in the present study is in accordance with findings of prior studies [9,10], suggesting that MPV may be helpful in clinical practice [34,35].

To our knowledge, prior studies have never analyzed and reported a positive result of MPV in differentiating CD patients from healthy volunteers using ROC analysis. Our study, for the first time, discovered a preliminary but inspiring finding that MPV could be used as a good biomarker in distinguishing CD from healthy controls (Table 3). We are aware that our finding is not sufficient for employing MPV solely in this differential diagnosis, but our finding could provide a suggestion for clinical physicians to pay attention to the value of MPV and take it into account when making decisions of differential diagnosis.

The similar MPV between active and inactive CD patients observed in our study is not in agreement with those in previous studies. The absence of any correlation between MPV and other inflammatory markers in our study supported the hypothesis that MPV was not in a close relationship with CD activity. In the studies by Jaremo and Sandberg-Gertzen [10] and Kapsoritakis and colleagues [12], an activity-dependent diversity of MPV was reported. The reason for this discrepancy is unclear; we assume that the amount of enrolled patients in these studies was limited, and large-sample studies are expected to investigate the real diversity between active and inactive CD patients.

Our study raised several interesting and meaningful controversies that are worthy of discussions and further investigations.

Firstly, we raised controversy about the correlation between MPV and other inflammatory biomarkers in CD.

Although the issue of MPV shifts in inflammatory disorders has been extensively covered in recent publications, studies in the current literature investigating the association of MPV and CD are still limited. Among them, studies discussing the correlation between MPV and other regular inflammatory biomarkers (including CRP, ESR and WBC) in CD are even fewer.

The only and most worthy-of-mention study was published in 2001. Kapsoritakis and colleagues collected data for 66 patients with CD and 38 healthy volunteers, and found a negative correlation of MPV with CRP, ESR and WBC [12]. However, they did not analyze and compare the cutoff point, sensitivity, specificity and overall accuracy of MPV and other biomarkers.

Our results are not in accordance with their findings. As no statistical correlation between MPV and other inflammatory biomarkers was confirmed in our study, an obvious and meaningful controversy appeared. While the sample size was similar between our study (n = 61) and that of Kapsoritakis and colleagues (n = 66), further studies are expected to uncover the real relationship between MPV and other biomarkers. This confirmation of relationship is pivotal in determining the role of MPV in the inflammatory course in CD.

Secondly, we raised a controversy about the decisive value of MPV in the determination of activity in CD.

The similarity of MPV between active and inactive CD in our study is in contrast with several previous remarkable studies. Jaremo and Sandberg-Gertzen collected data for 18 ulcerative colitis patients, nine CD patients and 18 healthy volunteers, and reported an association of lower MPVs with active IBD [10]. However, this excessive small sample size of CD (nine patients) significantly hampered the value of their conclusions. Yuksel and colleagues recruited data for 61 ulcerative colitis patients and 27 healthy controls, and suggested that decreased MPV may be an indicator for increased disease activity in patients with ulcerative colitis [35]. However, they did not collect data for CD patients or provide any information regarding MPV in indicating CD activity.

Douda and colleagues collected data for 56 CD patients and found that decreased MPV is an independent laboratory marker of clinical disease activity [36]. However, MPV’s predictive value is inferior compared with the total platelet count, CRP and CDAI. The latter finding is partly in accordance with our findings. We also discovered that MPV was inferior to CRP and ESR in determination of activity in CD (see Table 6), but it is still a challenge for clinical physicians to find more evidence to prove a definite association between MPV and disease activity.

There has been sufficient evidence derived from numerous prospective and retrospective studies suggesting MPV is a key predictor of thrombotic events in various disorders [13], including cardiovascular disease [37], cerebrovascular disease [38,39], venous thromboembolism [40] and other disorders [41,42].

In IBD, low-sized platelet with an increase of platelet count has been a typical manifestation for both CD and ulcerative colitis [13]. Meanwhile, both a prothrombotic condition and a hypercoagulable state are established features of IBD [43]. Microaggregates and microinfarction of mesenteric vessels unveiled a potential role of platelet as an inflammatory cell in the pathogenesis of CD [8,13]. Wakefield and colleagues demonstrated in their study a consecutive process of microinfarction in mesenteric vasculature [44]. This process was initiated by vascular injury, followed by focal arteritis, fibrin deposition and arterial occlusion at muscularis mucosa. Subsequently, tissue infarction and mucosal ulceration were assumed to be a possible chain of events in the pathogenesis of CD [45]. Notably, the above course of events depended on several key factors – including glycoprotein IIb/IIIa, which is a platelet surface glycoprotein, and platelet surface template for factors V and VIII, which were previously known as platelet factor 3 [46]. Platelets were therefore proposed to be involved, at least partly, in the formation of microinfarction and the pathogenesis of CD [45].

An increased activation of platelet was confirmed by the expression of surface activation markers including P-selectin, GP53 and β-thromboglobulin [43,47]. Moreover, various factors (such as IL-3, IL-6 and thrombopoietin) were responsible for the platelet activation and participated in the stimulation of thrombopoiesis [48]. The reduced size of platelets in CD suggested a possible mechanism in which large activated platelets were consumed or sequestrated in the intestinal vasculature [49].

We are aware of limitations to our study. First, this is a single-center study, leading to a potential selection bias. Second, as only 61 CD cases and 50 healthy subjects were enrolled in our study, the sample size might be too small to detect the real diversity of MPV between active and inactive CD patients.


Conclusions

Our study demonstrated a decline of MPV in CD patients compared with healthy controls. We also compared MPV with other inflammatory markers, including CRP, ESR and WBC, and provided the discriminative talent of MPV and recommended MPV as the best marker for differentiating CD patients from healthy subjects. Finally, we suggested that it should be cautious to use MPV as a marker in determination of CD activity. Large multicenter studies are expected to resolve the controversy.


Abbreviations

AUC: area under the curve; CD: Crohn’s disease; CDAI: Crohn’s Disease Activity Index; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; IBD: inflammatory bowel disease; IL: interleukin; MPV: mean platelet volume; NSAID: nonsteroidal anti-inflammatory drug; ROC: receiver operating characteristic; WBC: white blood cells.


Competing interests

The authors declare that they have no competing interests.


Authors’ contributions

SL and JR participated in the design of the study. SL and GH performed the statistical analysis. GW and GG collected the data and helped to draft the manuscript. JL conceived of the study, and participated in its design and coordination. SL and QX drafted the manuscript. All authors read and approved the final manuscript.


Acknowledgements

This work was supported by grants from the Climb Program in Natural Science Foundation of Jiangsu Province for Distinguished Scholars (No. BK2010017).


References
Xavier RJ,Podolsky DK,Unravelling the pathogenesis of inflammatory bowel diseaseNatureYear: 200744842743410.1038/nature0600517653185
Weersma RK,van Dullemen HM,van der Steege G,Nolte IM,Kleibeuker JH,Dijkstra G,Review article: inflammatory bowel disease and geneticsAliment Pharmacol TherYear: 200726Suppl 2576518081650
Wong A,Bass D,Laboratory evaluation of inflammatory bowel diseaseCurr Opin PediatrYear: 20082056657010.1097/MOP.0b013e32830d3aaf18781120
Sandborn WJ,Loftus EV Jr,Colombel JF,Fleming KA,Seibold F,Homburger HA,Sendid B,Chapman RW,Tremaine WJ,Kaul DK,Wallace J,Harmsen WS,Zinsmeister AR,Targan SR,Evaluation of serologic disease markers in a population-based cohort of patients with ulcerative colitis and Crohn’s diseaseInflamm Bowel DisYear: 2001719220110.1097/00054725-200108000-0000311515844
Ripoche J,Blood platelets and inflammation: their relationship with liver and digestive diseasesClin Res Hepatol GastroenterolYear: 20113535335710.1016/j.clinre.2011.02.01221482218
Bernhard H,Deutschmann A,Leschnik B,Schweintzger S,Novak M,Hauer A,Muntean W,Thrombin generation in pediatric patients with Crohn’s diseaseInflamm Bowel DisYear: 2011172333233910.1002/ibd.2163121287673
Danese S,Motte C,Cde L,Fiocchi C,Platelets in inflammatory bowel disease: clinical, pathogenic, and therapeutic implicationsAm J GastroenterolYear: 20049993894510.1111/j.1572-0241.2004.04129.x15128364
Collins CE,Rampton DS,Platelet dysfunction: a new dimension in inflammatory bowel diseaseGutYear: 1995365810.1136/gut.36.1.57890235
Shah A,Morgan G,Rose JD,Fifield R,Rhodes J,Platelet number and size in relation to serum orosomucoid concentration in Crohn’s diseaseMed Lab SciYear: 19894679802779388
Jaremo P,Sandberg-Gertzen H,Platelet density and size in inflammatory bowel diseaseThromb HaemostYear: 1996755605618743178
Zubcevic N,Mesihovic R,Zubcevic S,Usefulness of laboratory data in estimation of Crohn’s disease activityMed ArhYear: 201064333620422823
Kapsoritakis AN,Koukourakis MI,Sfiridaki A,Potamianos SP,Kosmadaki MG,Koutroubakis IE,Kouroumalis EA,Mean platelet volume: a useful marker of inflammatory bowel disease activityAm J GastroenterolYear: 20019677678110.1111/j.1572-0241.2001.03621.x11280550
Gasparyan AY,Ayvazyan L,Mikhailidis DP,Kitas GD,Mean platelet volume: a link between thrombosis and inflammation?Curr Pharm DesYear: 201117475810.2174/13816121179504980421247392
Diaz-Ricart M,Brunso L,Pino M,Navalon F,Jou JM,Heras M,White JG,Escolar G,Preanalytical treatment of EDTA-anticoagulated blood to ensure stabilization of the mean platelet volume and component measured with the ADVIA countersThromb ResYear: 2010126e30e3510.1016/j.thromres.2010.04.00220427079
Dastjerdi MS,Emami T,Najafian A,Amini M,Mean platelet volume measurement, EDTA or citrate?HematologyYear: 20061131731910.1080/1024533060095416317607580
Kucharzik T,Maaser C,Lugering A,Kagnoff M,Mayer L,Targan S,Domschke W,Recent understanding of IBD pathogenesis: implications for future therapiesInflamm Bowel DisYear: 2006121068108310.1097/01.mib.0000235827.21778.d517075348
Langhorst J,Elsenbruch S,Koelzer J,Rueffer A,Michalsen A,Dobos GJ,Noninvasive markers in the assessment of intestinal inflammation in inflammatory bowel diseases: performance of fecal lactoferrin, calprotectin, and PMN-elastase, CRP, and clinical indicesAm J GastroenterolYear: 200810316216910.1111/j.1572-0241.2007.01556.x17916108
Bruining DH,Loftus EV,Current and future diagnostic approaches: from serologies to imagingCurr Gastroenterol RepYear: 2007948949610.1007/s11894-007-0065-518377802
Vermeire S,Van Assche G,Rutgeerts P,Laboratory markers in IBD: useful, magic, or unnecessary toys?GutYear: 20065542643110.1136/gut.2005.06947616474109
Shine B,Berghouse L,Jones JE,Landon J,C-reactive protein as an aid in the differentiation of functional and inflammatory bowel disordersClin Chim ActaYear: 198514810510910.1016/0009-8981(85)90219-03995779
Poullis AP,Zar S,Sundaram KK,Moodie SJ,Risley P,Theodossi A,Mendall MA,A new, highly sensitive assay for C-reactive protein can aid the differentiation of inflammatory bowel disorders from constipation- and diarrhoea-predominant functional bowel disordersEur J Gastroenterol HepatolYear: 20021440941210.1097/00042737-200204000-0001311943955
Khan K,Schwarzenberg SJ,Sharp H,Greenwood D,Weisdorf-Schindele S,Role of serology and routine laboratory tests in childhood inflammatory bowel diseaseInflamm Bowel DisYear: 2002832532910.1097/00054725-200209000-0000312479647
Sutherland AD,Gearry RB,Frizelle FA,Review of fecal biomarkers in inflammatory bowel diseaseDis Colon RectumYear: 2008511283129110.1007/s10350-008-9310-818543035
Peterson CG,Sangfelt P,Wagner M,Hansson T,Lettesjo H,Carlson M,Fecal levels of leukocyte markers reflect disease activity in patients with ulcerative colitisScand J Clin Lab InvestYear: 20076781082010.1080/0036551070145283818034391
Gasparyan AY,Sandoo A,Stavropoulos-Kalinoglou A,Kitas GD,Mean platelet volume in patients with rheumatoid arthritis: the effect of anti-TNF-alpha therapyRheumatol IntYear: 2010301125112910.1007/s00296-009-1345-120066426
Coban E,Yazicioglu G,Berkant Avci A,Akcit F,The mean platelet volume in patients with essential and white coat hypertensionPlateletsYear: 20051643543810.1080/0953710050016357216236605
Tavil Y,Sen N,Yazici H,Turfan M,Hizal F,Cengel A,Abaci A,Coronary heart disease is associated with mean platelet volume in type 2 diabetic patientsPlateletsYear: 20102136837210.3109/0953710100362842120521863
Schafer A,Bauersachs J,Endothelial dysfunction, impaired endogenous platelet inhibition and platelet activation in diabetes and atherosclerosisCurr Vasc PharmacolYear: 20086526010.2174/15701610878333129518220940
Coban E,Ozdogan M,Yazicioglu G,Akcit F,The mean platelet volume in patients with obesityInt J Clin PractYear: 20055998198210.1111/j.1742-1241.2005.00500.x16033624
Polinska B,Matowicka-Karna J,Kemona H,Assessment of the influence of the inflammatory process on the activation of blood platelets and morphological parameters in patients with ulcerative colitis (colitis ulcerosa)Folia Histochem CytobiolYear: 20114911912421526498
Li Z,Yang F,Dunn S,Gross AK,Smyth SS,Platelets as immune mediators: their role in host defense responses and sepsisThromb ResYear: 201112718418810.1016/j.thromres.2010.10.01021075430
Harris NR,Carter PR,Watts MN,Zhang S,Kosloski-Davidson M,Grisham MB,Relationship among circulating leukocytes, platelets, and microvascular responses during induction of chronic colitisPathophysiologyYear: 20111830531110.1016/j.pathophys.2011.05.00321680162
Mannaioni PF,Di Bello MG,Masini E,Platelets and inflammation: role of platelet-derived growth factor, adhesion molecules and histamineInflamm ResYear: 19974641810.1007/PL000001589117517
Güçlü M,Sakallı H,Yakar T,Mean platelet volume may be reflects the disease activity of ulcerative colitisEur J Gen MedYear: 20107259263
Yuksel O,Helvaci K,Basar O,Koklu S,Caner S,Helvaci N,Abayli E,Altiparmak E,An overlooked indicator of disease activity in ulcerative colitis: mean platelet volumePlateletsYear: 20092027728110.1080/0953710090285678119459134
Douda T,Bures J,Rejchrt S,Kopacova M,Pecka M,Maly J,Mean platelet volume (MPV) in Crohn’s disease patientsCas Lek CeskYear: 200614587087317168422
Chu SG,Becker RC,Berger PB,Bhatt DL,Eikelboom JW,Konkle B,Mohler ER,Reilly MP,Berger JS,Mean platelet volume as a predictor of cardiovascular risk: a systematic review and meta-analysisJ Thromb HaemostYear: 2010814815610.1111/j.1538-7836.2009.03584.x19691485
O’Malley T,Langhorne P,Elton RA,Stewart C,Platelet size in stroke patientsStrokeYear: 19952699599910.1161/01.STR.26.6.9957762052
Greisenegger S,Endler G,Hsieh K,Tentschert S,Mannhalter C,Lalouschek W,Is elevated mean platelet volume associated with a worse outcome in patients with acute ischemic cerebrovascular events?StrokeYear: 2004351688169110.1161/01.STR.0000130512.81212.a215143290
Braekkan SK,Mathiesen EB,Njolstad I,Wilsgaard T,Stormer J,Hansen JB,Mean platelet volume is a risk factor for venous thromboembolism: the Tromso Study, Tromso, NorwayJ Thromb HaemostYear: 2010815716210.1111/j.1538-7836.2009.03498.x19496920
Colkesen Y,Acil T,Abayli B,Yigit F,Katircibasi T,Kocum T,Demircan S,Sezgin A,Ozin B,Muderrisoglu H,Mean platelet volume is elevated during paroxysmal atrial fibrillation: a marker of increased platelet activation?Blood Coag FibrinolYear: 20081941141410.1097/MBC.0b013e3283049697
Yavuz B,Ertugrul DT,Yalcin AA,Kucukazman M,Ata N,Dal K,Increased mean platelet volume in rheumatic mitral stenosis: a possible factor for thromboembolic eventsJ CardiolYear: 20095320420710.1016/j.jjcc.2008.10.01219304123
Danese S,Papa A,Saibeni S,Repici A,Malesci A,Vecchi M,Inflammation and coagulation in inflammatory bowel disease: the clot thickensAm J GastroenterolYear: 200710217418610.1111/j.1572-0241.2006.00943.x17100967
Wakefield AJ,Sawyerr AM,Dhillon AP,Pittilo RM,Rowles PM,Lewis AA,Pounder RE,Pathogenesis of Crohn’s disease: multifocal gastrointestinal infarctionLancetYear: 19892105710622572794
Collins CE,Rampton DS,Review article: platelets in inflammatory bowel disease–pathogenetic role and therapeutic implicationsAliment Pharmacol TherYear: 19971123724710.1046/j.1365-2036.1997.153328000.x9146760
Hudson M,Wakefield AJ,Hutton RA,Sankey EA,Dhillon AP,More L,Sim R,Pounder RE,Factor XIIIA subunit and Crohn’s diseaseGutYear: 199334757910.1136/gut.34.1.758094363
Collins CE,Cahill MR,Newland AC,Rampton DS,Platelets circulate in an activated state in inflammatory bowel diseaseGastroenterologyYear: 19941068408458143990
Mahida YR,Kurlac L,Gallagher A,Hawkey CJ,High circulating concentrations of interleukin-6 in active Crohn’s disease but not ulcerative colitisGutYear: 1991321531153410.1136/gut.32.12.15311773961
Webberley MJ,Hart MT,Melikian V,Thromboembolism in inflammatory bowel disease: role of plateletsGutYear: 19933424725110.1136/gut.34.2.2478432482

Figures

[Figure ID: F1]
Figure 1 

Study design. A total of 111 subjects were enrolled in the current study. Fifty healthy controls were differentiated with 61 Crohn’s disease (CD) patients using mean platelet volume (MPV), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cells (WBC). Furthermore, the 61 CD patients were divided into active (n = 29) and inactive (n = 32) groups and distinguished using the same inflammatory biomarkers. All blood sample collections were obtained on admission (before any medication or procedure).



[Figure ID: F2]
Figure 2 

Mean platelet volume and other inflammatory markers in differentiate Crohns disease patients and controls. Receiver operating characteristic (ROC) curves. The optimal cutoff value for mean platelet volume (MPV) was 10.35 fl (sensitivity: 78.7%, specificity: 74.0%, area under the curve: 0.8303), with 76.6% overall accuracy.



[Figure ID: F3]
Figure 3 

Mean platelet volume and other inflammatory markers in differentiate active and inactive Crohns disease. Receiver operating characteristic (ROC) curves. The optimal cutoff levels for C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were 4.95 mg/dl (sensitivity: 82.8%, specificity: 78.1%, area under the curve (AUC): 0.7877) and 16.5 mm/hour (sensitivity: 65.5%, specificity: 81.3%, AUC: 0.7909), with 80.3% and 73.8% overall accuracy respectively. MPV did not show a statistically discriminative value in differentiating active from inactive Crohn’s disease (CD) (AUC: 0.5043, overall accuracy: 55.7%)



Tables
[TableWrap ID: T1] Table 1 

Demographics of patients and controls


  Crohn’s disease (n = 61) Control group (n = 50) P value
Age (years)
32.4 ± 1.59
34.0 ±1.44
0.133
Male (%)
40 (65.6%)
35 (70.0%)
0.686
Smoking
15 (24.6%)
11 (22.0%)
0.709
Body mass index (kg/m2)
18.4 ± 0.526
19.3 ± 0.507
0.427
Active disease
29 (47.5%)


Age (%)
 
 
 
 A1 (≤16 years)
9 (14.7%)


 A2 (17–40 years)
37 (60.7%)


 A3 (>40 years)
15 (24.6%)


Disease location (%)
 
 
 
 L1 (ileal)
33 (54.1%)


 L2 (colonic)
10 (16.4%)


 L3 (ileocolonic)
18 (29.5%)


 + L4 (upper gastrointestinal tract)
3 (4.92%)


Disease behavior (%)
 
 
 
 B1 (inflammatory)
9 (14.7%)


 B2 (stricturing)
32 (52.5%)


 B3 (penetrating)
20 (32.8%)


 + P (perianal) 3 (4.92%)

[TableWrap ID: T2] Table 2 

Comparison of MPV and other inflammatory markers between Crohn’s disease and control groups


  Crohn’s disease (n = 61) Control group (n = 50) P value
MPV (fl)
9.55 ± 0.168
11.1 ± 0.160
<0.0001
CRP (mg/dl)
13.4 ± 2.43
2.89 ± 0.547
<0.0001
ESR (mm/hour)
19.1 ± 2.15
6.60 ± 0.431
<0.0001
WBC (×109/l) 6.83 ± 0.377 6.90 ± 0.342 0.8881

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; MPV, mean platelet volume; WBC, white blood cells.


[TableWrap ID: T3] Table 3 

Accuracy and ROC analyses of MPV and other inflammatory markers in differentiate patients and controls


  AUC Sensitivity(%) Specificity(%) Overall accuracy(%)
MPV (cutoff: 10.35)
0.8303
78.7
74.0
76.6
CRP (cutoff: 4.85)
0.6849
52.5
82.0
65.8
ESR (cutoff: 8.5)
0.7834
68.9
76.0
72.1
WBC (cutoff: 4.35) 0.5234 18.0 92 51.4

AUC, area under the curve; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; MPV, mean platelet volume; ROC, receiver operating characteristic; WBC, white blood cells.


[TableWrap ID: T4] Table 4 

Comparison of MPV and other inflammatory markers in patients with and without active disease


  Active CD (n = 29) Inactive CD (n = 32) P value
MPV (fl)
9.52 ± 0.223
9.58 ± 0.251
0.8423
CRP (mg/dl)
21.8 ± 4.21
5.75 ± 1.81
0.0012
ESR (mm/hour)
26.4 ± 3.26
12.5 ± 2.33
0.0011
WBC (×109/l) 6.42 ± 0.413 7.19 ± 0.613 0.3047

CD, Crohn’s disease; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; MPV, mean platelet volume; WBC, white blood cells.


[TableWrap ID: T5] Table 5 

Correlation between MPV and other inflammatory markers in Crohn’s disease


MPV r value P value
CRP
−0.022
0.8671
ESR
−0.059
0.6518
WBC −0.1549 0.2332

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; MPV, mean platelet volume; WBC, white blood cells.


[TableWrap ID: T6] Table 6 

Overall accuracy and ROC analyses of MPV and other inflammatory markers in differentiating Crohn’s disease


  AUC Sensitivity (%) Specificity (%) Overall accuracy (%)
MPV (cutoff: 8.80)
0.5043
31.0
78.1
55.7
CRP (cutoff: 4.95)
0.7877
82.8
78.1
80.3
ESR (cutoff: 16.5)
0.7909
65.5
81.3
73.8
WBC (cutoff: 7.20) 0.5474 72.4 40.6 55.7

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; MPV, mean platelet volume; ROC, receiver operating characteristic; WBC, white blood cells.



Article Categories:
  • Research

Keywords: Crohn’s disease, Mean platelet volume, C-reactive protein, Erythrocyte sedimentation rate, Inflammatory bowel disease.

Previous Document:  A closed-loop system for control of the fraction of inspired oxygen and the positive end-expiratory ...
Next Document:  Critical thinking and creativity in nursing: Learners' perspectives.