Lymphocyte to Monocyte Ratio and C-Reactive Protein Combination as the Best Simple Predictor of Treatment Response in Cirrhotic Patients With Culture Negative Neutrocytic Ascites

Abstract

A scites is the most common complication and reason of the hospitalization in the cirrhotic patients. Almost 60% of patients with cirrhosis will develop ascites within 10 years after diagnosis of the disease. [1] Cirrhotic patients with ascites are generally prone to developing bacterial infection of ascitic fluid. The prevalence of spontaneous bac- Objectives:The aim of this study was to evaluate the most ideal inflammatory markers for treatment response and to determine a cutoff value that could predict response to treatment for culture negative neutrocytic ascite (CNNA) patients. Methods: This is a retrospective cross-sectional case-controlled study. Patients with CNNA were evaluated by taking ascites fluid sampling at the beginning and on the 5 th day of treatment. Neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), and neutrophil-to-monocyte ratio were calculated. Results: Of the 123 cases with cirrhotic ascites disease, 59 were CCNA and 64 were the control group without ascite-fluid infection. There were statistically significant differences for blood monocyte count, NLR (p<0.01), LMR, and C-reactive protein (CRP) (p<0.001) between two groups. Patients in the CNNA group were compared before and after treatment among themselves for the treatment response. There was statistically significant difference in mean platelet volume, monocyte, LMR, and CRP (p<0.05) between two groups. After receiver operator characteristics curve analysis, the best cutoff value for monocyte was <0.64 × 10³/µL (sensitivity 49.2%, specificity 74.6%, positive predictive value [PPV] 65.9%, and negative predictive value [NPV] 59.5%) (p<0.01), for LMR was ≥1.7 (sensitivity 76.3%, specificity 78%, PPV 77.6%, and NPV 76.7%), and for CRP was ≤18 mg/L (sensitivity 91.5% specificity 57.6%, PPV 68.4%, and NPV 87.2%) (p<0.001). When LMR and CRP were used together, sensitivity (86.5%), specificity (83.1%), PPV (83.6%), and NPV (86%) were found to be statistically significantly higher (p<0.001). Conclusion: Our results showed that in cirrhotic patients with CNNA, combined LMR + CRP can be used as a novel, low cost and non-invasive test to predict treatment response.

Impact of Serum and Ascitic Fluid Procalcitonin on Diagnosis and Outcome of Patients with Spontaneous Bacterial Peritonitis

“…Our study results are in agreement with Barutcu et al (13) who enrolled 50 patients with cirrhotic ascites who were divided into three groups: Group A: 20 patients with SBP diagnosed laboratoraly. Group B: 20 patients with criteria suggestive of SBP, but shows neutrophil count in ascitic fluid <250.…”

Culture-Negative Neutrocytic Ascites in a Patient With Cardiac Ascites From End-Stage Heart Failure

“…A study demonstrated the use of LMR and C-reactive protein to monitor treatment response. In the study, after the study group received antibiotic treatment, C-reactive protein levels were significantly lower, and LMR was elevated [ 3 ]. We did not use these markers upon initial diagnosis and treatment of our patient’s care of CNNA.…”

“…There are two significant groups of infection regarding ascitic fluid: spontaneous bacterial peritonitis (SBP) and culture-negative neutrocytic ascites (CNNA). Diagnostic criteria for CNNA are an ascitic fluid polymorphonuclear leukocyte count >250/mm, an ascitic fluid culture negative for bacterial growth, no prior antibiotic therapy within 30 days, and no infectious source within the abdomen [ 3 - 5 ]. CNNA generally has a lower risk for mortality, which was demonstrated across multiple studies [ 5 ].…”

Hyperammonemia and Hepatic Encephalopathy in Pediatric and Adult Liver İntensive Care Unit

“…[ 12 , 13 ] HE who develops CLF, on the other hand, presents with a wide variety of neurological symptoms, including mood swings, impaired sleep-wake cycles, changes in muscle tone, and severe cognitive deficits. [ 14 , 15 ] Just as in the presence of sepsis and inflammation, blood levels of inflammation mediators such as tumor necrosis factor-alpha, Interleukin (IL)-1β, and IL-6 have been found to increase in patients with HE. Moreover, the development of astrocyte swelling-brain edema by these mediators suggests the possibility of exacerbation in HE.…”

“…Moreover, the development of astrocyte swelling-brain edema by these mediators suggests the possibility of exacerbation in HE. [ 14 , 15 ] Despite all the studies in the literature, it is suggested that these inflammatory factors other than ammonia, including infection, cytokines, and other blood and brain immune factors, play a potential role in the pathogenesis of HE, but the data on these factors are basic. [ 15 , 16 ]…”