The role of calprotectin and ghrelin in diagnosis of post ERCP pancreatitis.

Acute pancreatitis is a common and dreaded complication of endoscopic retrograde cholangiopancreatography (ERCP) patients. The study identified the incidence of post ERCP pancreatitis and role of serum calprotectin and ghrelin in its diagnosis. One hundred forty two patients underwent ERCP-related procedures were studied. Serum amylase, lipase, calprotectin and ghrelin concentrations were measured 24 hours after the procedure using ELISA, kinetic and colorimetric methods. Thirty two healthy controls were enrolled. In post ERCP group, mean level of amylase was 146.03 +/- 57.40 U/L, lipase 328.37 +/- 133.95 U/L, calprotectin 3.26 +/- 2.99 U/L and gherkin 2.56 +/- 1.76 mg/l. In controls mean level of amylase was 58.13 +/- 15.96U/L, lipase 181.63 +/- 51.94 U/L, calprotectin 0.49 +/- 0.17 U/L and ghrelin 2.59 +/- 0.19 mg/l. A statistical significant increase was reported (p < 0.001) in levels of amylase, lipase and calprotectin between the two groups without significant in ghrelin level.

Hepatocellular integrity during sevoflurane anesthesia with induced hypotension.

The effect of sevoflurane anesthesia with or without induced hypotension on hepatocellular integrity was studied. Forty adult consented patients scheduled for various urological procedures were allocated randomly to either NTG group (nitroglycerin-induced hypotension) or a control group of twenty patients each. Anesthesia was induced and maintained by fentanyl, sevoflurane & vecuronium in both groups. In NTG group, nitro-glycerin infusion was adjusted to maintain mean arterial pressure (MAP) of 50-65 mm Hg. Specific and sensitive hepatic biomarkers; alpha (alpha) and pi (pi) glutathione S-transferases (GST) and hyaluronic acid (HA), also traditional liver enzymes; aspartate (AST) and alanine (ALT) aminotransferases were measured at: TO (pre-induction), T1, T2, T3 (15, 30 & 60 minutes after MAP stabilization respectively) and T4 (24 hours after anesthesia end). Plasma alpha-GST significantly increased at T3 in control group (p < 0.05) and in NTG group (p < 0.01) compared to TO in same group. In NTG group, hyaluronic acid con-centrations was significantly increased at T1, T2 (p < 0.05) and T3 (p < 0.01) from T0. Compared to control group, alpha- GST & HA concentrations showed significant increases in NTG group at T3 with p < 0.05 then returned back to normal range at T4. But, pi-GST, AST and ALT showed no significant changes throughout the study in both groups.

Clinical significance of aflatoxin, mutant P53 gene and sIL-2 receptor in liver cirrhosis and hepatocellular carcinoma.

The incidence of hepatocellular carcinoma (HCC) varies widely worldwide. Chronic infection with hepatitis B virus (HBV) and exposure to aflatoxins in foodstuffs are the main risk factors. AAG to AGT transversion at codon 249 of the P53 gene arg-ser (249ser) has been identified as a hotspot, reflecting DNA damage caused by aflatoxin B1 metabolites in HCC. Because HBV infection is often endemic in high aflatoxin exposure areas, it is still not clear whether HBV acts as a con-founder or as a synergistic partner in the development of the 249ser P53 mutation. Serum levels of soluble interleukin 2 receptor (sIL-2R) correlated with the progression of liver cirrhosis independently of its etiology. This fact may reflect the stimulation of T-lymphocytes, monocytes and macrophages in liver cirrhosis. The inter-relationship among aflatoxin exposure, HBV & HCV infections, P53 & sIL-2R in patients with liver cirrhosis and hepatocellular carcinoma was studied. The results revealed significant increase in serum levels of mutant P53, sIL-2R and aflatoxin B1 in patients with cirrhosis and those with HCC compared to the controls. HCC patients showed levels of all the three parameters significantly higher than both cirrhotics and controls (P<0.001). Correlations were found between serum aflatoxin B1, mutant P53 and sIL-2R in HCC group. The results were discussed.