No abstract

A total of 117 patients with pancreatitis were studied during the acute attack and after remission, and 32.5% were found to have hyperlipidemia, nearly all of type IV. There did not seem to be a relationship between hyperlipidemia and alcohol intake, although nearly 80% of the patients were alcoholics. No defect in triglyceride turnover could be demonstrated by intravenous fat tolerance tests or postheparin lipolytic activity measurements. No correlation was found between hyperlipidemia and steatosis of the liver or diabetes.It is suggested that the increase in serum triglyceride levels might be due to an increased synthesis or mobilization. It is also suggested that the hypertriglyceridemia does not directly induce an attack of pancreatitis, but might predispose a patient to develop pancreatitis when other provoking factors are also present.

The underlying molecular mechanisms for anastomotic leakage (AL) after colorectal surgery are unknown and there are no therapeutics for AL prevention. Our aim was to correlate endogenous matrix metalloproteinase (MMP) activity, collagen concentration, and collagen/MMP/cytokine mRNA levels with anatomic location in human colorectal tissue. We enrolled 22 patients in this prospective study: 7 underwent elective laparoscopic sigmoid resection and 15 underwent low anterior resection for colorectal cancer. Full-thickness intestinal tissue rings from anastomoses constructed with a circular stapler were used for the determination of the MMP activity, tissue collagen concentration and mRNA levels. COL1A1 (p = 0.017) and COL3A1 (p = 0.0013) mRNA levels were lower in rectal tissue than in colonic samples. Neither MMP activities nor collagen concentrations differed significantly between the two anatomic locations. By elucidating the factors responsible for the decreased collagen production we may identify specific molecular targets in AL prophylaxis.

The increased use of glucagon in the treatment of acute pancreatitis led us to study plasma glucagon in 26 patients with acute pancreatitis and 33 patients with chronic pancreatitis. In all patients simultaneous measurements of plasma glucagon, serum amylase, and serum calcium were performed. In acute pancreatitis there was a tendency toward elevated plasma glucagon and low serum calcium levels, but there was no significant correlation between the concentrations of plasma glucagon, serum calcium, and serum amylase. The plasma glucagon concentrations were found to be low in only 2% of the measurements during the first week of the acute attack. These findings do not support the use of glucagon in the treatment of pancreatitis.