Comparison of staple-line leakage and hemorrhage in patients undergoing laparoscopic sleeve gastrectomy with or without Seamguard.

Laparoscopic sleeve gastrectomy (LSG) has been recognized as a primary procedure for the surgical management of morbid obesity. Staple-line leaks and hemorrhage are two associated complications. Staple-line buttressing materials have been suggested to decrease these complications. When used during LSG, few published papers exist that compare the incidence of leak or hemorrhage to that of nonreinforced staple-lines. The purpose of this study was to compare the incidence of leak and hemorrhage in patients who did and did not receive reinforcement with Seamguard (W.L. Gore & Associates, Flagstaff, AZ). This is a retrospective analysis of patients undergoing LSG. All patients met National Institutes of Health criteria and each had an extensive preoperative evaluation. Data was collected from inpatient and outpatient medical records. Fifty-nine patients received reinforcement and 80 patients did not. There was no significant difference in mean body mass index, age, or gender make-up between the two groups. The overall incidence of leak was 3.60 per cent. The incidence was 3.39 per cent in patients who received reinforcement and 3.75 per cent in those who did not. This was not statistically significant. There was no incidence of staple-line hemorrhage in either group. There is no conclusive evidence that Seamguard reduces staple-line leakage or hemorrhage. Studies involving a larger number of patients are necessary before recommending staple-line reinforcement.

Differential regulation of angiotensin II-induced expression of connective tissue growth factor by protein kinase C isoforms in the myocardium.

Protein kinase C (PKC) and angiotensin II (AngII) can regulate cardiac function in pathological conditions such as in diabetes or ischemic heart disease. We have reported that expression of connective tissue growth factor (CTGF) is increased in the myocardium of diabetic mice. Now we showed that the increase in CTGF expression in cardiac tissues of streptozotocin-induced diabetic rats was reversed by captopril and islet cell transplantation. Infusion of AngII in rats increased CTGF mRNA expression by 15-fold, which was completely inhibited by co-infusion with AT1 receptor antagonist, candesartan. Similarly, incubation of cultured cardiomyocytes with AngII increased CTGF mRNA expression by 2-fold, which was blocked by candesartan and a general PKC inhibitor, GF109203X. The role of PKC isoform-dependent action was further studied using adenoviral vector-mediated gene transfer of dominant negative (dn) PKC or wild type PKC isoforms. Expression of dnPKCalpha, -epsilon, and -zeta isoforms suppressed AngII-induced CTGF expression in cardiomyocytes. In contrast, expression of dominant negative PKCdelta significantly increased AngII-induced CTGF expression, whereas expression of wild type PKCdelta inhibited this induction. This inhibitory effect was further confirmed in the myocardium of transgenic mice with cardiomyocyte-specific overexpression of PKCdelta (deltaTg mice). Thus, AngII can regulate CTGF expression in cardiomyocytes through a PKC activation-mediated pathway in an isoform-selective manner both in physiological and diabetic states and may contribute to the development of cardiac fibrosis in diabetic cardiomyopathy.

Oxidative stress and antioxidant treatment in diabetes.

The many studies on oxidative stress, antioxidant treatment, and diabetic complications have shown that oxidative stress is increased and may accelerate the development of complications through the metabolism of excessive glucose and free fatty acids in diabetic and insulin-resistant states. However, the contribution of oxidative stress to diabetic complications may be tissue-specific, especially for microvascular disease that occurs only in diabetic patients but not in individuals with insulin resistance without diabetes, even though both groups suffer from oxidative stress. Although antioxidant treatments can show benefits in animal models of diabetes, negative evidence from large clinical trials suggests that new and more powerful antioxidants need to be studied to demonstrate whether antioxidants can be effective in treating complications. Furthermore, it appears that oxidative stress is only one factor contributing to diabetic complications; thus, antioxidant treatment would most likely be more effective if it were coupled with other treatments for diabetic complications.