Ascites is the pathological accumulation of fluid in the peritoneal cavity, commonly resulting from portal hypertension due to cirrhosis, which accounts for 80% of cases. The onset of ascites marks the transition from compensated to decompensated cirrhosis, with increased mortality, often due to complications like SBP (Spontaneous Bacterial Peritonitis) and hepatorenal syndrome. Mortality in decompensated liver disease is approximately 15% within the first year and 44% over five years. Other causes of ascites include cancer (10%), heart failure (3%), tuberculosis (2%), dialysis (1%), pancreatic disease (1%), and others (2%).[1] Pathogenesis of Ascites in Cirrhosis Portal hypertension in cirrhosis is driven by hepatic structural changes, including nodular formation and collagen deposition, which increase vascular resistance.[2] Stellate cells play a key role by secreting contractile proteins and vasoconstrictor substances such as endothelin, ADH, and angiotensin II.[3] Splanchnic vasodilation further exacerbates ascites formation by increasing blood flow to the mesenteric and splenic vascular beds, activating the renin-angiotensin-aldosterone system and causing sodium and water retention.[4] Hypoalbuminemia, due to impaired hepatic protein synthesis, and increased peritoneal lymphatic flow also contribute to ascitic fluid accumulation.[5] Theories of Ascites Formation Several theories explain ascites formation: the Underfill Theory, suggesting that portal hypertension leads to sodium and water retention;[6] the Overflow Theory, which posits renal sodium retention due to impaired hepatic clearance;[7] and the Arterial Vasodilation Theory, which links portal hypertension and splanchnic vasodilation to sodium retention by the kidneys.[8] SBP (Spontaneous Bacterial Peritonitis) SBP is an infection of ascitic fluid without a surgically treatable source, occurring in 10-30% of cirrhotic patients. Gram-negative bacteria lie E. coli and Klebsiella are common perpetrators, though gram-positive organisms are increasingly implicated.[9] Risk factors include low ascitic fluid protein, high bilirubin, variceal hemorrhage, previous SBP episodes, malnutrition, and proton pump inhibitor use. AIMS AND OBJECTIVES The study aims to evaluate the diagnostic significance of ascitic fluid LDH (Lactate Dehydrogenase) levels in the assessment of SBP in patients with liver cirrhosis and ascites. The specific objectives include calculating the prevalence of SBP in cirrhotic patients using ascitic fluid cytology and culture criteria, measuring both ascitic fluid and serum LDH levels, and determining the correlation between ascitic fluid LDH levels and serum LDH levels in patients with and without SBP.

Study Design This cross-sectional observational study was conducted at the Department of Medicine, Sri Guru Ram Das Institute of Medical Sciences and Research, Vallah, Sri Amritsar. The study population consists of patients of either sex, admitted either in the emergency or the ward of the Department of Medicine, who were diagnosed with cirrhosis of the liver with ascites. These patients, who were admitted between July 2023 and February 2025, were included in the study after obtaining written informed consent. The study was conducted over a period from July 2023 to February 2025. Inclusion and Exclusion Criteria The study included patients aged 18-65 years, diagnosed with cirrhosis of the liver with ascites, confirmed through clinical and radiological evaluation. Exclusion criteria included patients with a known history of malignancy and those suffering from vasculitic diseases such as Polyarteritis nodosa, eosinophilic granulomatosis with polyangiitis (Churg-Strauss vasculitis), granulomatosis with polyangiitis (Wegener's), Behçet's syndrome, or sarcoidosis. Additionally, patients who had already been administered oral or intravenous antibiotics prior to admission, those with evidence of haemolytic anemia with jaundice, and pregnant women or those in the postpartum period (within 6 months of delivery) were excluded from the study. Data Collection Procedure Data collection was carried out using a structured proforma that included detailed history, clinical examination, and relevant investigations. All patients diagnosed with liver cirrhosis and ascites underwent radiological evaluation (USG/CT abdomen) to assess liver morphology and ascitic fluid volume. Diagnostic paracentesis was performed within 24 hours of admission, prior to initiation of antibiotics, and ascitic fluid was collected in three sterile containers-one each for culture and sensitivity, biochemical analysis (including total proteins, albumin, and LDH levels), and cytological examination. Routine laboratory investigations included complete blood count, renal function tests, serum electrolytes, liver function tests (including serum proteins and bilirubin), serum LDH, serum ammonia, PTI (Prothrombin Time Index), and viral markers (HBsAg, HCV, HIV). Radiological imaging with abdominal ultrasound was performed using a 3–5 MHz curvilinear probe, and upper GI endoscopy was done where indicated. Based on clinical and laboratory findings, patients were assessed and scored using the Child-Pugh classification and MELD-Na score to evaluate liver disease severity. Statistical Analysis Data collected during the study were compiled in Microsoft Excel and analyzed using SPSS version 26. Categorical variables were expressed as numbers and percentages and analyzed using the chi-square test. Parametric data were presented as mean ± SD and compared using the Student’s t-test. For data not normally distributed, non-parametric tests were applied, with results summarized as median and interquartile range, and the Mann-Whitney U test used for group comparisons. Pearson correlation was used to assess the relationship between ascitic fluid LDH, serum LDH, and their ratio. A p-value <0.05 was considered statistically significant, and p≤0.001 as highly significant.

Age (in years) Number Percentage ≤30 5 3.3 31-40 28 18.4 41-50 53 34.9 51-60 41 27.0 ≥61 25 16.4 Table 1: Age Distribution Table 1 shows the age distribution of the study population, with the maximum number of subjects belonging to the 41–50 years age group, followed by the 51–60 years group. Gender Number Percentage Female 21 13.8 Male 131 86.2 Table 2: Gender Distribution Table 2 observes gender distribution, highlighting that the study population was predominantly male (86.2%). Presenting Complaints SBP Number (%) Non-SBP Number (%) Yellow Discolouration 27 (60%) 67 (62.6%) Abdominal Distension 45 (100%) 107 (100%) Altered Talks 22 (48.8%) 37 (34.5%) Hematemesis 7 (15.5%) 19 (17.75%) Melena 10 (22.2%) 32 (29.9%) Table 3: Presenting Complaints Table 3 presents the distribution of major presenting complaints between SBP and non-SBP patients, showing abdominal distension was present in all cases, while altered talks were more common in SBP. Grade SBP Number (%) Non-SBP Number (%) 0 23 (51.11%) 69 (64.49%) MHE 1 (2.22%) 4 (3.73%) 1 2 (4.45%) 8 (7.48%) 2 9 (20%) 10 (9.35%) 3 9 (20%) 9 (8.41%) 4 1 (2.22%) 7 (6.54%) Table 4: Hepatic Encephalopathy Grades Table 4 illustrates the grades of hepatic encephalopathy (West Haven criteria) in SBP and non-SBP patients, where grade 0 was most frequent in both groups. Etiology SBP Number (%) Non-SBP Number (%) Alcoholic 31 (68.89%) 71 (66.36%) HCV 3 (6.67%) 7 (6.54%) HCV + Alcoholic 5 (11.11%) 10 (9.35%) HBV 1 (2.22%) 0 (0%) HBV + Alcoholic 0 (0%) 1 (0.93%) HIV 0 (0%) 0 (0%) HIV + Alcoholic 3 (6.67%) 1 (0.93%) Others 2 (4.44%) 17 (15.89%) Table 5: Etiologies Table 5 summarizes the etiologies of liver disease, with alcohol use being the most common cause among both SBP and non-SBP patients. Parameter SBP Median (IQR) Non-SBP Median (IQR) P-Value Hb (gm/dl) 9.5 (8.1–11.05) 8.7 (7.2–10.5) 0.127 TLC (cells/mm³) 11800 (6850–19600) 8600 (5500–13400) 0.051 Platelets (lakhs/mm³) 1.4 (0.88–1.78) 1.5 (1.3–1.6) 0.111 PT-INR 1.68 (1.35–2.23) 1.35 (1.1–1.85) 0.002 Table 6: Lab Parameters Comparison Table 6 compares different laboratory parameters, showing higher TLC and PT-INR levels in SBP patients compared to non-SBP patients. MELD-Na Score Number Percentage <17 26 17.11 17-20 22 14.47 21-22 11 7.24 23-26 26 17.11 27-31 29 19.07 ≥32 38 25.0 Table 7: MELD-Sodium Score Table 7 shows the MELD-Sodium score distribution, with 25% of the study population having a score ≥32, indicating severe liver dysfunction.

Gender In the present study, there was a clear male predominance (86.2%) among cirrhotic patients with ascites, which is consistent with earlier reports. Kamal et al. (2012) observed a higher number of males in both SBP and non-SBP groups,[10] while Sandhya et al. (2021) also reported that nearly 70% of their cohort were males.[11] Similarly, Kumar et al. (2022) and Lal Krishna et al. (2024) found that two-thirds to over 90% of cirrhotic patients were men.[12,13] Other studies, including those by Khan et al.[14] Deepika et al.[15] Verma et al.[16] Chaudhary et al.[17] and Punekar et al.[18] have consistently shown male predominance. This gender disparity may be attributed to higher prevalence of alcohol consumption among men, delayed healthcare-seeking behavior in males, and possible hormonal protective effects in females. Age Most patients in our study belonged to the age group of 41–50 years (34.9%), followed by 51–60 years (27%). The median age was comparable between SBP and non-SBP groups (48 vs. 50 years). These findings are similar to Kamal et al.[10] who reported mean ages of 51 and 50 years in SBP and non-SBP groups respectively. Kumar et al.[13,19] Lal Krishna et al.[12] Khan et al.[14] Punekar et al.[18] Chaudhary et al.[17] and Mohan et al.[20] all noted that cirrhosis most frequently affects middle-aged adults, particularly between 40 and 60 years. This trend highlights the chronic progressive nature of liver disease, where years of alcohol intake or viral infection culminate in cirrhosis during midlife. Etiology Alcohol was the most common etiological factor in our cohort (≈68%), followed by viral hepatitis, which aligns with observations from Sandhya et al.[11] Khan et al.[14] Patira et al.[21] Chaudhary et al.[17] Mishra et al.[22] Mohan et al.[20] and Punekar et al.[18] Most of these studies consistently identified alcohol as the leading cause of cirrhosis, although regional variation exists depending on viral hepatitis prevalence. The dominance of alcohol-related cirrhosis in our study reflects prevailing lifestyle and sociocultural factors. Ascitic Fluid LDH and SBP Our findings showed significantly higher ascitic fluid LDH levels in patients with SBP compared to those without SBP. Similar associations were demonstrated by Kamal et al.[10] El Motasem et al.[23] Sandhya et al.[11] Mortada et al.[24] Khan et al.[14] Amany Talaat et al.[25] and Reginato et al.[26] The elevation of LDH in SBP likely reflects increased neutrophil activity and cellular breakdown during infection. Thus, LDH can serve as a useful adjunctive marker in differentiating SBP from sterile ascites. Ascitic Fluid LDH/Serum LDH Ratio The ascitic fluid LDH/serum LDH ratio was significantly higher in SBP patients in our study. This agrees with Sandhya et al.[11] Tounyet al.[27] and Khan et al.[14] who also reported elevated ratios in SBP cases. The raised ratio reflects disproportionate increases in peritoneal fluid LDH due to local inflammatory processes, and its diagnostic role has been validated across different populations. Ascitic Fluid Culture In our study, culture-negative neutrocytic ascites was the most common SBP variant, while Gram-negative organisms such as E. coli, Klebsiellapneumoniae, and Acinetobacter were frequently isolated in culture-positive cases. Kamal et al.[10] Mohan et al.[20] Ning et al.[28] and Reginato et al.[26] similarly reported that Gram-negative bacteria, particularly Enterobacteriaceae, predominate in SBP. However, some studies also identified Gram-positive organisms such as Streptococcus and Staphylococcus species, which were not observed in our series. This difference could be due to variations in antibiotic exposure, nosocomial infection rates, and regional microbial profiles. Child–Pugh Score Most patients in our study, both with and without SBP, belonged to Child–Pugh class C, indicating advanced liver dysfunction. Similar findings were reported by El Motasem et al.[23] Sandhya et al.[11] Kumar et al.[13] Lal Krishna et al.[12] and Mohan et al.[20] This pattern emphasizes that SBP typically occurs in advanced liver disease, where reduced immune defense and altered gut permeability increase susceptibility to infection. Our findings align with the majority of previous studies, confirming that cirrhosis with ascites predominantly affects middle-aged males, is most often caused by alcohol, and frequently progresses to Child–Pugh class C. SBP is characterized by elevated ascitic fluid LDH and LDH/serum LDH ratio, with Gram-negative bacteria as the predominant pathogens. These insights reinforce the need for early diagnosis and preventive strategies in high-risk cirrhotic patients. LIMITATIONS The present study had several limitations. It was a single-center study, and future research should involve multi-center approaches to include patients from diverse geographical areas. Additionally, the sample size was insufficient, highlighting the need for studies with larger cohorts to better validate the findings. Furthermore, in cases where no clear cause for cirrhosis was identified, further diagnostic evaluations such as fibroscan or liver biopsy were not performed due to cost constraints.

The median (IQR) value of ascitic fluid LDH was significantly higher in patients with SBP compared to the non-SBP group. Our study suggests that ascitic fluid LDH, along with the ascitic fluid LDH to serum LDH ratio, may serve as a potential diagnostic marker in patients with cirrhosis of the liver. However, further research is needed to explore the diagnostic significance of ascitic fluid LDH in cirrhotic patients with ascites.

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