Serum levels of leptin and adiponectin in patients with nonalcoholic fatty liver disease: potential biomarkers

Nonalcoholic fatty liver disease [NAFLD] occurs in 60% -95% of people with obesity. Understanding the pathogenesis of NAFLD is of great importance in ultimately finding a treatment, cure or prevention of this disease. The present study aimed to investigate the role of adipocytokines [leptin and adiponectin] in NAFLD and correlate them with different anthropometric and clinical variables as well as to investigate the relationship between high-sensitivity C-reactive protein [hs-CRP] and NAFLD. Thirty patients [9 males and 21 females] with NAFLD [their diagnosis was based on ultrasonographic finding of bright liver]. Their age was [Mean +/- SD] 38.00 +/- 10.42 years. A control group included fifteen healthy volunteers, who was gender, age and BMI matched. Serum levels of leptin, adiponectin, [hs- CRP], and lipid profile were assayed. NAFLD patients showed significantly higher BMI, AST/ALT ratio, serum levels of total cholesterol, triglycerides, LDL-C, serum NEFFA levels, serum hs-CRP levels and significantly lower serum HDL-C and adiponectin levels in comparison to controls. Among NAFLD patients; these changes were significantly high in females than male patients. Serum leptin levels showed no significant difference between patients and controls. NAFLD patients with BMI >/= 30 and those with AST/ALT ratio >/= 1 showed significantly higher serum levels of NEFFA, leptin, hs-CRP and significantly lower serum levels of adiponectin in comparison to those with BMI<30 and AST/ALT ratio <1. To date adiponectin and hs-CRP has yielded the most promising results. Serum leptin has contradictory results so can not be used as a marker of NAFLD

Inflammatory mediators in plasma and peritoneal fluid in cirrhotic patients with spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis [SBP] in cirrhotic patients is associated with an increased production and decreased metabolism of inflammatory mediators [cytokines] such as tumour necrosis factor a [TNF-alpha], interleukin 6 [IL-6] and interleukin 1-beta [IL-l beta]. The present study was designed to investigate the relationship between the development of SBP and the degree of inflammatory response in patients with liver cirrhosis and to assess the diagnostic value of the inflammatory mediators in cirrhotic patients with SBP. This study was carried out on 46 cirrhotic patients with SBP, 22 cirrhotic patients with ascites but without evidence of SBP, and 12 healthy subjects as a control group. All patients were subjected for history taking, clinical examination and abdominal ultrasound. Blood samples were collected for complete blood count [CBC], liver function tests and measurement of TNF-alpha, IL- l beta, and IL-6 levels [in patients and control]. Ascitic fluid samples were collected for measurement of TNF-alpha, IL- l beta, and IL-6 and for aerobic and anaerobic cultures [only in patients with SBP]. Cirrhotic patients with SBP showed significantly higher plasma and ascitic fluid levels of TNF-alpha, IL- l beta and IL-6 than cirrhotic patients without SBP [despite that severity of liver disease was similar in the two groups] and normal control subjects [p<0.001]. Ascitic fluid TNF-alpha, IL- l beta and IL-6 were also higher in the cirrhotic patients with SBP than in plasma, [p<0.001 for each]. Also the plasma levels of TNF-alpha, IL- l beta and IL-6 in cirrhotic patients with SBP were significantly higher than in healthy control subjects [p<0.001]. There was a strong direct correlation between plasma and ascitic fluid levels of TNF-alpha, [r=0.9624, p<0.001] IL-l beta [r=0.4024, p<0.01], and IL-6 [r=0.2890, p<0.05] at the time of diagnosis of SBP. A significant correlation was also observed between TNF-alpha, IL- l beta, and IL-6 in ascitic fluid [r=1.0000, p<0.001] and in plasma [r=0.8500, p<0.001]. PMN cell count in ascites correlated significantly with the ascitic fluid level of IL- l beta [r=0.3156, p<0.05], but did not correlate with both TNF-alpha [r-0.0953, p>0.05] and IL-6 [r=0.0702, p>0.05]. Patients with culture-positive SBP showed significantly higher plasma and ascitic fluid levels of TNF-alpha, IL- l beta, and IL-6 than patients with culture-negative SBP. The PMN cell count in the ascitic fluid was also significantly higher in the culture-positive vs culture-negative SBP patients [6.813 +/- 0.24 vs 1.36110.07, p<0.001]. Cirrhotic patients with SBP display a marked increase of TNF-alpha, IL- l beta, and IL-6 levels in ascitic fluid and plasma. Specificity and sensitivity of these cytokines detection of SBP in cirrhotic patients strongly favor its measurement during acute phase of the disease