|Year : 2018 | Volume
| Issue : 1 | Page : 8-15
Study of platelet indices in cirrhotic patients with spontaneous bacterial peritonitis
Rania M Elkafoury1, Abdelrahman A Kobtan1, Taher E Attia1, Amal H Abdelhamed2
1 Department of Tropical Medicine and Infectious Diseases, Faculty of Medicine, Tanta University, Tanta, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt
|Date of Submission||22-Jun-2017|
|Date of Acceptance||05-Nov-2017|
|Date of Web Publication||26-Jul-2018|
Rania M Elkafoury
Department of Tropical Medicine and Infectious Diseases, Tanta University Hospital, El Geish Street, Tanta, Gharbia Governorate, 31527
Background Ascites are a pathological collection of fluid within the peritoneal cavity and the most common complication of liver cirrhosis. Spontaneous bacterial peritonitis (SBP) is an infection that develops in cirrhotic ascitic patients. Platelets release prothrombotic and proinflammatory agents and participate in the induction and advancement of vascular and inflammatory disorders.
Aim The aim of this study was to evaluate platelet indices as noninvasive predictors for the diagnosis of SBP in cirrhotic patients.
Patients and methods Patients were divided into the following groups: group I included 52 cirrhotic ascitic patients with SBP; group II included 34 cirrhotic ascitic patients without SBP; group III (the control group) included 20 healthy individuals. A complete blood count analysis was carried out using the Erma PCE-210 hematology analyzer. Platelet count, mean platelet volume (MPV), and platelet distribution width (PDW) of all the participating patients were determined.
Results In this study, there were differences in MPV and PDW between the three groups. MPV showed a significant increase in SBP in comparison with ascitic patients and control participants (11.39±1.08, 10.39±1.32, and 9.47±1.29 fl, respectively), with a P value of less than 0.001. Similarly, the PDW was greater in SBP patients compared with those in groups II and III, but with no significant difference (14.14±2.01, 13.96±3.58, and 12.90±3.13, respectively).
Conclusion MPV measurement is an inexpensive, fast, and easy to use test that can predict the development of SBP in cirrhotic ascitic patients.
Keywords: ascites, cirrhosis, mean platelet volume, platelet distribution width, spontaneous bacterial peritonitis
|How to cite this article:|
Elkafoury RM, Kobtan AA, Attia TE, Abdelhamed AH. Study of platelet indices in cirrhotic patients with spontaneous bacterial peritonitis. Tanta Med J 2018;46:8-15
|How to cite this URL:|
Elkafoury RM, Kobtan AA, Attia TE, Abdelhamed AH. Study of platelet indices in cirrhotic patients with spontaneous bacterial peritonitis. Tanta Med J [serial online] 2018 [cited 2019 Jul 22];46:8-15. Available from: http://www.tdj.eg.net/text.asp?2018/46/1/8/237626
| Introduction|| |
Cirrhosis is an advanced liver disease characterized by fibrosis and alteration in hepatic architecture with the development of structurally anomalous nodules . Advanced cirrhosis invariably leads to death, unless liver transplantation is performed .
Ascites is a condition in which pathological collection of fluid occurs within the peritoneal cavity mainly because of portal hypertension. It is a major complication of liver cirrhosis, occurring in over 50% of patients within 10 years of diagnosis. The appearance of ascites in cirrhotic patients indicates a poor prognosis as it is associated with an average mortality rate of 20% every year .
Spontaneous bacterial peritonitis (SBP) is a severe infection, commonly occurring in cirrhotic ascitic patients. By definition, SBP is a bacterial infection of ascitic fluid (AF) and peritoneum in patients with no intra-abdominal source of infection ,,.
The prevalence of SBP in cirrhotic patients with ascites admitted to the hospital ranges from 10 to 30% , and about 3.5% of outpatients are commonly asymptomatic . Recurrence is very high in SBP, reaching 70% in a year. Patients recovering from SBP are considered potential candidates for liver transplantation as their long-term prognosis is extremely poor, with mortality rates of 50–70% at 1 year ,.
SBP is produced by dysfunction in local and systemic immunity, decreased AF opsonic activity, and bacterial translocation (BT) ,,,. Consequently, the most common bacteria causing SBP are the gut microflora including Escherichia More Details coli, Klebsiella spp., Enterobacter spp., enterococci, and streptococci as well as infrequent infection by anaerobes in less than 5% of the cases ,,,.
SBP is diagnosed by analyzing AF. A polymorphonuclear count, greater than 250 cells/mm3, signals a positive diagnosis ,,. It is essential to perform an early bedside AF culture before commencement of antibiotic therapy .
Platelets are attributed to preserve hemostasis. Yet, recently, there has been growing recognition that they also play an essential role in inflammatory and immune response. . Platelets release prothrombotic and proinflammatory agents and participate in the induction and advancement of vascular and inflammatory disorders .
Larger-sized platelets contain many granules, and are therefore more efficient in their hemostatic and proinflammatory actions . This is why the mean platelet volume (MPV) and platelet distribution width (PDW) are worth considering as potential tests for platelet function and activation .
The MPV and PWD can be calculated using almost all automated hematology analyzers. The MPV indicates the average platelet size in femtoliters. The PDW, reflecting homogeneity of platelet size, is calculated from the MPV by the equation (SD of platelet volume divided by MPV×100) or the distribution width at 20% frequency .
The aim of the present work was to study platelet indices as noninvasive predictors for the diagnosis of SBP in cirrhotic ascites.
| Patients and methods|| |
This cross sectional observational study was carried out on 86 patients admitted to the Tropical Medicine Department, Tanta University Hospital, during a 6-month period from April to September 2015, as well as 20 apparently healthy volunteers serving as a control group. Written consents were obtained from all individuals and the study was approved by the ethical committee.
Exclusion criteria included patients with ascites because of causes other than cirrhosis, immunocompromised patients, patients with abnormal thrombocytes because of nonhepatic causes, patients with associated inflammatory diseases, metabolic disorders such as diabetes and hyperlipidemia, patients on antibiotics 2 weeks before hospital admission, a history of heart failure, and neoplastic disorders, and patients receiving anticoagulants or NSAIDs before hospital admission.
All patients were subjected to a precise recording of history, a comprehensive physical examination, laboratory testing [complete blood count (CBC), liver and kidney function tests, coagulation profile, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR)], abdominal ultrasonography, AF aspiration, and analysis.
Sampling and methodology
- A peripheral blood sample was collected from each participant using a completely aseptic technique, and divided into three separate vacutainers: an EDTA vacutainer for estimation of CBC, a sodium citrate vacutainer for estimation of prothrombin time and activity, and a plain vacutainer. These were separated as serum for liver function tests and other routine laboratory investigations.
All blood analyses were carried out at the Hematology Laboratory of the Clinical Pathology Department. CBC analyses were carried out using an Erma (Erma Inc., Yushima, Japan) PCE-210 hematology analyzer. Platelet number, MPV, and PDW of all the participants were recorded.
- Paracentesis was performed to obtain an AF sample under completely aseptic conditions from a puncture site in the left or the right lower quadrant (two finger breadths cephalic and two finger breadths medial to the anterior superior iliac spine was the preferred location) with the patient in the supine position . If the fluid was difficult to localize by examination because of obesity, ultrasonography was performed as a useful adjunct in locating fluid and visualizing the spleen and other structures to be avoided .
The samples were collected at the bedside and processed immediately. The samples were tested for cell counts, albumin, total protein, and sugar concentration.
| Results|| |
This study was carried out on 86 patients with cirrhosis (83 patients had chronic hepatitis C and three patients had autoimmune hepatitis), as well as 20 seemingly healthy volunteers serving as a control group.
For determination of clinical data and AF analysis, patients were divided into groups. Group I included 52 cirrhotic ascitic patients with SBP, 34 (65.4%) men and 18 (34.6%) women. Their mean age was 56.96±6.46 years. Group II included 34 cirrhotic ascitic patients without SBP, 23 (67.6%) men and 11 (32.4%) women. Their mean age was 56.68±9.84 years. In addition, the control group (group III) included 20 healthy individuals, 13 (65%) men and seven (35%) women, mean age 53.55±8.96 years. There were no statistically significant differences between the groups studied.
Among the patients with SBP, hemoglobin levels were significantly lower than those in ascitic patients with no SBP (P<0.0001).
Significant increases in white blood cell counts, total and direct serum bilirubin levels, and transaminases were recorded among SBP patients in comparison with ascitic patients (P<0.05) as shown in [Table 1].
|Table 1 Comparison between the three groups in the complete blood count and liver functions|
Click here to view
Serum albumin, hemoglobin, and platelet counts were significantly decreased in both the SBP group (group I) and the ascitic group (group II) than in the control group (P=0.05) as shown in [Table 1].
CRP positivity showed a statistically significant difference between all study groups, being positive in 80.8, 55.9, and 0% of the patients in groups I, II, and III, respectively (P<0.001) as shown in [Table 2].
|Table 2 Comparison between the three groups in erythrocyte sedimentation rate and C-reactive protein|
Click here to view
ESR was 44.45±28.71, 39.76±28.44, and 10.15±6.37 in the first hour and 73.94±33.28, 64.41±33.63, and 18.2±8.49 in the second hour, respectively, which was significantly higher in SBP and ascitic patients than in the control group, but with no statistically significant difference between SBP and ascites as shown in [Table 2].
In AF analysis, there was a significant increase in AF total leukocytic count and protein in SBP patients than in the ascitic group: 15.08±80.92 vs. 22.63±24.59 and 2.15±0.75 vs. 1.73±0.77, respectively. AF glucose was significantly lower in group I than in group II (87.68±13.73 vs. 106.4±14.95) as shown in [Table 3].
Using the Child–Turcotte–Pugh classification, Child class B was detected in 16 (30.8%) patients in group I and in 16 (47.1%) patients in group II, whereas 36 (69.2%) patients in group I and 16 (47.1%) patients in group II were Child class C.
In this study, there was a significant difference in MPV and PDW between the three groups. The MPV was significantly elevated in cases with SBP (group I) compared with ascitic patients (group II) and the control group (group III) (11.39±1.08, 10.39±1.32, and 9.47±1.29, respectively; P<0.001). The PDW in group I was elevated in comparison with groups II and III, but with no significant difference between groups (14.14±2.01, 13.96±3.58, and 12.90±3.13, respectively) as shown in [Table 4] and [Figure 1] and [Figure 2].
|Table 4 Comparison between the three groups in mean platelet volume and platelet distribution width|
Click here to view
|Figure 1 Comparison between the three groups in mean platelet volume (MPV). SBP, spontaneous bacterial peritonitis.|
Click here to view
|Figure 2 Comparison between the three groups in platelet distribution width (PDW). SBP, spontaneous bacterial peritonitis.|
Click here to view
| Discussion|| |
SBP is a complication of ascites, particularly in cirrhotic patients. A measurement of 250 or more neutrophils/mm3 AF is diagnostic, even with negative ascitic bacterial cultures.
MPV and PDW indicate platelet activation. Platelet size corresponds with activity and function; larger-sized platelets are more active. PDW is an indicator of variation in platelet volume, and may indicate active platelet release ,,.
Our study aimed to determine whether any difference in platelet indices (MPV and PDW) occurs between cirrhotic ascitic patients with SBP and those without SBP.
In the hematological tests in this study, most of the patients in groups I and II had significantly lower hemoglobin levels and platelet counts in comparison with the healthy control group (P<0.001). This was in agreement with Suvak et al.  and Abdel-Razik et al. , but not in agreement with Gálvez-Martínez et al. .
The white blood cell count, a well-known indicator of systemic inflammatory response, was found to be significantly higher in groups I and II compared with the controls (P=0.005) in agreement with Suvak and colleagues ,,,.
In our study, differences between the three groups in CRP were statistically significant at a cut-off value of more than 6 mg/l (P<0.001), in agreement with the findings of Suvak and colleagues ,,,. CRP has been considered a reliable prognosticator of SBP and an evaluator of effective therapy in adults ,.
It is postulated that CRP can aid the humoral and cellular immune systems in recognizing and disposing of pathogens and toxic material produced by diseased tissue .
Cho et al.  reported that CRP levels can independently predict reduced response to antibiotics and increased in-hospital mortality among SBP patients.
The ESR was found to be statistically significant between groups I and II in comparison with group III (P<0.0001), and yet the difference between ESR levels in the two patient groups did not reach significance (P=0.532 and 0.39 in the first and second hours). This is in agreement with Suvak et al.  and indicates that ESR is less sensitive or accurate as a reflection of the acute-phase response than the CRP ,.
The liver function tests including serum bilirubin, serum transaminases (alanine aminotransferase and aspartate aminotransferase), and serum albumin were significantly worse in groups I and II than in group III. The serum total bilirubin levels, alanine aminotransferase, and aspartate aminotransferase were significantly higher in group I than in groups II and III (P<0.001, P=0.016, and 0.0007, respectively). This may be attributed to a more advanced liver disease or a deterioration of the hepatic condition because of the occurrence of SBP.
Advanced disease of the liver is frequently accompanied by an increase in serum bilirubin, one of five parameters of the Child–Pugh scoring that is used in staging the severity of liver disease. The risk of SBP increases with the Child score. Seventy percent of SBP cases are recorded in class C cirrhosis ,.
Our study also showed a statistically significant decrease in serum albumin levels in both patient groups and the control group (P<0.0001), but with no significant difference between groups I and II (P=0.096). Prothrombin activity and the international normalized ratio showed statistically significant differences between the three groups (P<0.001). These results were in agreement with Green and Flamm , who attributed this alteration mainly to a defect in the synthesis of coagulation proteins and albumin by hepatocytes in these conditions.
In the kidney function tests, the serum creatinine level was significantly higher in groups I and II than in group III (P<0.001). This is in agreement with Angeloni et al. , who showed that hospital mortality in SBP is high because of hepatorenal syndrome.
Diagnostic paracentesis is the key for the diagnosis of SBP and its differentiation from secondary peritonitis . It was performed for all patients included in this study on hospital admission.
AF total protein was significantly elevated in the SBP compared with the ascitic group (P=0.013). Nepal et al.  found that SBP patients have lower AF albumin. Runyon and colleagues ,, reported that ascitic protein levels below 1 g/dl render cirrhotic patients ten times more susceptible to the occurrence of SBP. It is suspected that AF protein concentration reflects its antibacterial and opsonic activity. Therefore, patients with low ascitic protein levels are more at risk of contracting SBP .
In terms of the AF glucose concentration, there was a significant difference between groups I and II (P<0.0001). The lower glucose concentration in infected AF can be explained by its consumption by bacteria during uncontrolled infection . Most of the patients in the study were classified by the Child–Turcotte–Pugh classification as Child class C: 69.2% in group I and 47.1% in group II; the others were Child class B. There was a significant difference between the studied groups (P<0.001). This is in agreement with Bandy and Tuttle , who found that 70% of the patients developing SBP were in Child class C, with the rest being class B. Schwabl et al.  reported that Child–Pugh stage C indicates a significant risk for the development of SBP.
The Child class has been considered the only independent BT predictor. Previous studies on cirrhotic patients have found BT to be significantly increased in Child C patients (30%), whereas in classes B and A, it is estimated at 8 and 3%, respectively ,,.
In our study, SBP patients (group I) had a significantly higher MPV compared with cirrhotic ascitic patients without the complication of SBP (group II) or the healthy control group (group III) (P<0.001). This is in agreement with the findings of Suvak and colleagues ,,,.
The PDW was found to be higher in group I than in groups II and III, but with no statistical difference (P=0.242). The PDW echoes platelet uniformity in size; this may indicate platelet activation, and may therefore be associated with the inflammatory course of SBP. Our results are in agreement with those of Suvak et al. , but not Abdel-Razik et al.  or Khorshed et al. , who found a significant difference between ascitic patients with SBP and those without SBP in PDW.
Platelets maintain vascular integrity and hemostasis, in addition to playing a role in inflammation. MPV is a surrogate platelet activation marker as larger platelet volume indicates that the platelet is more active enzymatically and metabolically .
In cirrhosis, the bone marrow is stimulated to increase the production of platelets in response to the presence of variable platelet sizes, increased splenic breakdown, and high IL-6 levels. This will lead to increased MPV and in turn increased PDW because of the presence of variable platelet sizes in the circulation .
In sepsis, Becchi et al.  reported that in their study, the average MPV level in nonsurvivors increased, whereas that of the survivors decreased after sepsis. These results are consistent with Kitazawa et al. , who reported that the average platelet count decreased during blood stream infection (BSI), whereas the average MPV level increased. The degree of MPV elevation in the nonsurvivors was lower than that observed in the survivors. MPV elevation after BSI has been proven to be a negative prognostic indicator for BSI.
SBP in cirrhosis is associated with a systemic inflammatory response with the production of platelets with high MPV and a wide range of sizes. In this study, we noted that the MPV was significantly increased in SBP patients with a cut-off value of 9.8 fl with a sensitivity of 98.08% and a specificity of 41.18%. Therefore, MPV may be useful to predict the occurrence of SBP at an early stage. The role of PDW as an indicator of platelet activation was examined in our research. The PDW mirrors uniformity in platelet size, indicating platelet activation, and therefore associated with the inflammation process of SBP, but we found no statistically significant differences between ascitic, SBP patients or controls in PDW levels.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
McCormick PA. Hepatic cirrhosis. In: Dooley JS, Lok ASF, Burroughs AK, Heathcote EJ, editor. Sherlock’s diseases of the liver and biliary system. 12th ed. Oxford: Wiley-Blackwell 2011. p. 103–120.
Becker E. Diagnosis and therapy of ascites in liver cirrhosis. World J Gastroenterol 2011; 17:1237–1248.
Evans LT, Kim WR, Poterucha JJ, Kamath PS. Spontaneous bacterial peritonitis in asymptomatic outpatients with cirrhotic ascites. Hepatology 2003; 37:897–901.
Nobre SR, Cabral JE, Gomes JJ, Leitão MC. In-hospital mortality in spontaneous bacterial peritonitis: a new predictive model. Eur J Gastroenterol Hepatol 2008; 20:1176–1181.
Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut 2012; 61:297–310.
Gioannini TL, Zhang D, Teghanemt A, Weiss JP. An essential role for albumin in the interaction of endotoxin with lipopolysaccharide binding protein and sCD14 and resultant cell activation. J Biol Chem 2002; 277:47818–47825.
Bonnel AR, Bunchorntavakul C, Reddy KR. Immune dysfunction and infections in patients with cirrhosis. Clin Gastroenterol Hepatol 2011; 9:727–738.
Navasa M, Casafont F, Clemente G, Guarner C, de la Mata M, Planas R et al.
Consensus on spontaneous bacterial peritonitis in liver cirrhosis: diagnosis, treatment and prophylaxis. The Spanish Association for the Study of the Liver. Gastroenterol Hepatol 2001; 24:37–46.
Gines P, Angeli P, Lenz K, Moller S, Moore K, Moreau R. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol 2010; 53:397–417.
Wiest R, Garcia-Tsao G. Bacterial translocation (BT) in cirrhosis. Hepatology 2005; 41:422–433.
Wiest R, Lawson M, Geuking M. Pathological bacterial translocation in liver cirrhosis. J Hepatol 2014; 60:197–209.
Runyon BA. Management of adult patients with ascites due to cirrhosis: an update. Hepatology 2009; 49:2087–2107.
Runyon BA. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis2012. Hepatology 2013; 57:1651–1653.
Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis − bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther 2015; 41:1116–1131.
Strauss E. The impact of bacterial infections on survival of patients with decompensated cirrhosis. Ann Hepatol 2014; 13:7–19.
Semple JW, Italiano JE Jr, Freedman J. Platelets and the immune continuum. Nat Rev Immunol 2011; 11:264–274.
Kilciler G, Genc H, Tapan S, Ors F, Kara M, Karadurmus N et al.
Mean platelet volume and its relationship with carotid atherosclerosis in subjects with non-alcoholic fatty liver disease. Ups J Med Sci 2010; 115:253–259.
Thompson CB, Jakubowski JA, Quinn PG, Deykin D, Valeri CR. Platelet size and age determine platelet function independently. Blood 1984; 63:1372–1375.
Beyazit Y, Sayilir A, Torun S, Suvak B, Yesil Y, Purnak T et al.
Mean platelet volume as an indicator of disease severity in patients with acute pancreatitis. Clin Res Hepatol Gastroenterol 2012; 36:162–168.
Briggs C. Quality counts: new parameters in blood cell counting. Int J Lab Hematol 2009; 31:277–297.
Sakai H, Sheer TA, Mendler MH, Runyon BA. Choosing the location for non-image guided abdominal paracentesis. Liver Int 2005; 25:984–986.
Ekiz F, Yüksel O, Koçak E, Yılmaz B, Altınbaş A, Çoban S et al.
Mean platelet volume as a fibrosis marker in patients with chronic hepatitis B. J Clin Lab Anal 2011; 25:162–165.
Aydogan A, Akkucuk S, Arica S, Motor S, Karakus A, Ozkan OV et al.
The analysis of mean platelet volume and platelet distribution width levels in appendicitis. Indian J Surg 2015; 77:495–500.
Dinc B, Oskay A, Dinc SE, Bas B, Tekin S. New parameter in diagnosis of acute appendicitis: platelet distribution width. World J Gastroenterol 2015; 21:1821–1826.
Suvak B, Torun S, Yildiz H, Sayilir A, Yesil Y, Tas A et al.
Mean platelet volume is a useful indicator of systemic inflammation in cirrhotic patients with ascitic fluid infection. Ann Hepatol 2013; 12:294–300.
Abdel-Razik A, Eldars W, Rizk E. Platelet indices and inflammatory markers as diagnostic predictors for ascitic fluid infection. Eur J Gastroenterol Hepatol 2014; 26:1342–1347.
Gálvez-Martínez M, Servín-Caamaño AI, Pérez-Torres E, Salas-Gordillo F, Rivera-Gutiérrez X, Higuera-de la Tijera F. Mean platelet volume as a novel predictor of systemic inflammatory response in cirrhotic patients with culture-negative neutrocytic ascites. World J Hepatol 2015; 7:1001–1006.
Khorshed SE, Ibraheem HA, Awad SM. Macrophage inflammatory protein-1 beta (MIP-1β) and platelet indices as predictors of spontaneous bacterial peritonitis. Open J Gastroenterol 2015; 5:94–102.
Wehmeyer MH, Krohm S, Kastein F, Lohse AW, Lüth S. Prediction of spontaneous bacterial peritonitis in cirrhotic ascites by a simple scoring system. Scand J Gastroenterol 2014; 49:595–603.
Guler K, Vatansever S, Kayacan SM, Salmayenli N, Akkaya V, Erk O et al.
High sensitivity C-reactive protein in spontaneous bacterial peritonitis with non neurocytic ascites. Hepatogastroenterology 2009; 56:452–455.
Kasztelan-Szczerbinska B, Słomka M, Celinski K, Serwacki M, Szczerbinski M, Cichoz-Lach H. Prevalence of spontaneous bacterial peritonitis in asymptomatic in patients with decompensated liver cirrhosis − a pilot study. Adv Med Sci 2011; 56:13–17.
Du Clos TW. Function of C-reactive protein. Ann Med 2000; 32:274–278.
Cho Y, Park SY, Lee JH, Lee DH, Lee M, Yoo JJ et al.
High-sensitivity C-reactive protein level is an independent predictor of poor prognosis in cirrhotic patients with spontaneous bacterial peritonitis. J Clin Gastroenterol 2014; 48:444–449.
Liu S, Ren J, Xia Q, Wu X, Han G, Ren H et al.
Preliminary case-control study to evaluate diagnostic values of C-reactive protein and erythrocyte sedimentation rate in differentiating active Crohn’s disease from intestinal lymphoma, intestinal tuberculosis and Behcet’s syndrome. Am J Med Sci 2013; 346:467–472.
Such J, Runyon BA. Review spontaneous bacterial peritonitis. Clin Infect Dis 1998; 27:669–674. quiz 675–676.
Green RM, Flamm S. AGA technical review on the evaluation of liver chemistry tests. Gastroenterology 2002; 123:1367–1384.
Angeloni S, Leboffe C, Parente A, Venditti M, Giordano A, Merli M et al.
Efficacy of current guidelines for the treatment of spontaneous bacterial peritonitis in the clinical practice. World J Gastroenterol 2008; 14:2757–2762.
Nepal N, Pande PR, Pande R, Khatri R. Study of frequency of spontaneous bacterial peritonitis in patients with alcoholic liver cirrhosis with ascites. Postgrad Med J NAMS 2009; 9:45–49.
Runyon BA, Morrisey R, Hoefs JC, Wyle FA. Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. Hepatology 1985; 5:634–637.
Runyon BA. Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology 1986; 91:1343–1346.
Alaniz C, Regal RE. Spontaneous bacterial peritonitis: a review of treatment options. P T 2009; 34:204–210.
Bala L, Sharma A, Yellapa RK, Roy R, Choudhuri G, Khetrapal CL. 1H NMR spectroscopy of ascitic fluid: discrimination between malignant and benign ascites and comparison of the results with conventional methods. NMR Biomed 2008; 21:606–614.
Schwabl P, Bucsics T, Soucek K, Mandorfer M, Bota S, Blacky A et al.
Risk factors for development of spontaneous bacterial peritonitis and subsequent mortality in cirrhotic patients with ascites. Liver Int 2015; 35:2121–2128.
Cirera I, Bauer TM, Navasa M, Vila J, Grande L, Taurá P et al.
Bacterial translocation of enteric organisms in patients with cirrhosis. J Hepatol 2001; 34:32–37.
Wong F, Bernardi M, Balk R, Christman B, Moreau R, Garcia-Tsao G et al.
International Ascites Club. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club. Gut 2005; 54:718–725.
Gasparyan AY, Sandoo A, Stavropoulos-Kalinoglou A, Kitas GD. Mean platelet volume in patients with rheumatoid arthritis: the effect of anti-TNF-alpha therapy. Rheumatol Int 2010; 30:1125–1129.
Kaser A, Brandacher G, Steurer W, Kaser S, Offner FA, Zoller H et al.
Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis. Blood 2001; 98:2720–2755.
Becchi C, Al Malyan M, Fabbri LP, Marsili M, Boddi V, Boncinelli S. Mean platelet volume trend in sepsis: is it a useful parameter? Minerva Anestesiol 2006; 72:749–756.
Kitazawa T, Yoshino Y, Tatsuno K, Ota Y, Yotsuyanagi H. Changes in the mean platelet volume levels after bloodstream infection have prognostic value. Intern Med 2013; 52:1487–1493.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]