Effect of pentoxifylline on serum hyaluronic acid in patients with non-alcoholic fatty liver disease

Liver fibrosis is the excessive accumulation of extracellular matrix proteins that occurs in most types of chronic liver diseases. Non-alcoholic fatty liver disease [NAFLD] can be associated with progressive hepatic fibrosis. In this study we evaluated the effect of pentoxifylline [PTX] on serum hyaluronic acid [HA] levels as a marker of fibrosis. In this study we included 30 subjects [14 males and 16 females], divided into three groups. The NAFLD group included 20 patients with fatty livers as shown by ultrasound examination. Patients were randomised into a placebo group of 10 patients who received a placebo, and a pentoxifylline PTX group of 10 patients who received pentoxifylline at 400 mg/day for 6 months. The control group included 10 normal individuals. In the NAFLD group the mean value of the base line serum HA was 133 +/- 150.48, while in the control group it was 33.5 +/- 10.01; the difference between the groups was statistically significant [p < 0.001]. The mean value of the base line serum HA in the PTX treated group was 169.5 +/- 156.19, while after 6 months of treatment it was 59 +/- 44.34, with a statistically significant difference [p = 0.007]. In the placebo treated group the mean value of the base line serum HA was 96.5 +/- 143.004, while after 6 months of treatment it was 59.7 +/- 44.29; this difference was not statistically significant [p = 0.594]. Our showed that, when administered for 6 months, PTX caused a significant decline in HA levels, which may be an index reflecting improvement of hepatic fibrosis. Further investigations should be conducted with a large number of patients to confirm our and correlate this with histological findings

Plasma interleukin-8 level changes in acute renal failure patients treated with different therapeutic modalities

Acute renal failure is defined as rapid deterioration [hours to weeks] of kidney function. Introduction of continuous renal replacement therapy, with its advantages as regards hemodynamic stability, is expected to improve the outcome in patients with multi-organ failure MOF. It's also claimed to help in removal of IL-8, a pro-inflammatory chemokine that shares in leukocyte trafficking towards the kidney, where its removal could help in attenuating acute renal injury. The aim of our study was to test the effect of dialytic treatment opposed to non-dialytic treatment on the outcome of ARF. We also tested the difference between dialytic modalities on patients' outcome and on the ability to remove IL-8 from circulation. This study included 30 patients who suffered form acute renal failure [ARF] divided into two groups: Group A [15 patients] who received dialytic treatment and group B [15 patients] who did not receive dialysis. Group A was further subdivided into 3 groups according to the mode of dialysis used: Group A 1 [n=5]: Received continuous renal replacement therapies [CRRT], Group A 2 [n=5]: Received intermittent hemodialysis [IHD] and Group A 3 [n=5]: Received peritoneal dialysis [PD]. Plasma IL-8 level was determined pre and post dialysis. There is no significant difference in IL-8 pre in group A patients versus group B patients [p>0.05]. No significant difference was found between the outcome in group A versus group B [p>0.05]. There was no significant correlation between IL-8 pre and outcome in the whole population [p>0.05]. IL-8 is significantly higher in patients with septicemia [2233.5 +/- 1606.6] than that in patients without septicemia [202.4 +/- 256.7] [p<0.001]. Death was significantly higher in PD group compared with IHD [p<0.05], while there was no significant difference between IHD and CRRT, CRRT and IPD [p>0.05]. Death among patients with isolated ARF was significantly lower [16.6%] than death in patients with ARF as part of MOF [75%] [p<0.001]. Our results have shown that different dialytic modalities could remove the pro-inflammatory chemokine IL-8, from the plasma. Further studies aiming to evaluate the impact of variable dialytic modalities on ARF, need to be conducted using larger number of patients and more homogenous population as regard illness severity

Serum leptin level in nonalcoholic steatohepatitis

Nonalcoholic steatohepatitis [NASH] has increasingly been recognized as a common form of chronic liver disease over the past 20 years. Activated stellate cells have been shown to produce leptin and studies of leptin in NASH are lacking. The aim of this work was to assess the correlation between the serum leptin level and the degree of the histopathological changes of the liver in patients with NASH. Thirty patients with NASH and ten healthy controls were studied to identify the serum leptin level in such patients and compare its level with the histopathologic changes of liver biopsy. All patients were negative for HBsAg, AntiHCV antibodies, circulating autoantibodies and negative history of alcohol use. 90% were females, 83.3% were obese [BMI >30 kg/m2], 43.3% were diabetics, 43.3% had hypercholesterolemia and 63.3% had high triglycerides level. 3.3% had elevated AST, 6.7% had elevated ALT and 53.3% had AST/ALT ratio >1. Histopathologically, all patients had steatosis, ballooning of hepatocytes and lobular inflammation, 86.7% had portal inflammation, 93.3% had perisinusoidal fibrosis, 90% had periportal fibrosis, 16.7% had bridging fibrosis and 3.3% had cirrhosis. The serum leptin level was higher in the patient group [33 +/- 24.63 ng/ml] compared with the control group [12.9 +/- 10.01 ng/ml]. Leptin level was higher in females diabetics and obese hyperlipidemic patients. There was an increase in the level of serum leptin with the increased severity of the pathologic grade of NASH. Also, there was an insignificant relation between the leptin level and the pathologic stage of fibrosis in NASH. The study suggested that there was no significant relation between serum leptin level and the grade of necroinflammation or the stage of fibrosis in patients with NASH

Molecular diagnosis of helicobacter pylori in patients with chronic liver disease.

Fifty individuals were included in this study; 30 patients [group I] were diagnosed as liver cirrhosis and were subjected to injection sclerotherapy with follow up and 20 individuals with matched age and sex serving as normal controls [group II]. Beside the routine laboratory investigations, HP IgG, PCR for HP ure A and ure C were determined in the mucosal biopsy of both groups and PCR for HP ure A in the liver biopsy obtained from 18 patients of group I whose prothrombin time allowed the performance of liver biopsy. HP IgG was detected in 29 out of 30 liver cirrhosis patients and the highest incidence of HP IgG was found in patients over the age of 30 years and in those with gastric and duodenal erosions rather than peptic ulcer, while HP IgG was detected in 17 out of 20 cases of the control group. HP urec C was detected in 13 out of 30 gastric mucosal biopsy samples and HP urec A was detected in 23 out of 30 gastric mucosal biopsy samples. Concomitant HP urec A and C were detected in 9 out of 30 gastric mucosal biopsy samples. HP urec A was detected in all liver biopsy samples