Advances in cardiovascular-related biomarkers to predict diabetic peripheral neuropathy.

Diabetic peripheral neuropathy (DPN) is a common chronic complication of diabetes mellitus. One of the most common types is distal symmetric poly-neuropathy, which begins as bilateral symmetry pain and hyperesthesia and gradually progresses into hypoesthesia with nerve fibre disorder and is frequently accompanied by depression and anxiety. Notably, more than half of patients with DPN can be asymptomatic, which tends to delay early detection. Furthermore, the study of adverse outcomes showed that DPN is a prominent risk factor for foot ulceration, gangrene and nontraumatic amputation, which decreases quality of life. Thus, it is essential to develop convenient diagnostic biomarkers with high sensitivity for screening and early intervention. It has been reported that there may be common pathways for microvascular and macrovascular complications of diabetes. The pathogenesis of both disorders involves vascular endothelial dys-function. Emerging evidence indicates that traditional and novel cardiovascular-related biomarkers have the potential to characterize patients by subclinical disease status and improve risk prediction. Additionally, beyond traditional cardiovascular-related biomarkers, novel cardiovascular-related biomarkers have been linked to diabetes and its complications. In this review, we evaluate the association between major traditional and nontraditional car-diovascular-related biomarkers of DPN, such as cardiac troponin T, B-type natriuretic peptide, C-reactive protein, myeloperoxidase, and homocysteine, and assess the evidence for early risk factor-based management strategies to reduce the incidence and slow the progression of DPN.

Hydromorphone vs sufentanil in patient-controlled analgesia for postoperative pain management: A meta-analysis.

BACKGROUND: Patient-controlled analgesia (PCA) is an effective method of postoperative pain, there have been many studies performed that have compared the efficacy of hydromorphone with continuous sufentanil. The purpose of this systematic review is to compare the efficacy and safety of hydromorphone and sufentanil. METHODS: Seven databases were searched for controlled trials to compare the efficacy and safety of hydromorphone and sufentanil. After selecting the studies, extracting the data, and assessing study quality, the meta-analysis was performed on several of the studies with RevMan 5.3. RESULTS: Thirteen studies comprised of 812 patients were found. The pain intensity of the hydromorphone group was significantly lower than that of the sufentanil group at 12 hours. With no statistical difference at 24 to 48 hours (MD12 = -1.52, 95% CI [-2.13, -1.97], P <.05). The sedation intensity of the hydromorphone group at 12, 24, and 48 hours were lower than those of the sufentanil group, with no statistical difference (MD12 = -0.03, 95% CI [-0.18, 0.12], P > .05; MD24 = -0.20, 95% CI [-0.42, 0.03], P > .05; MD48 = -0.03, 95% CI [-0.18, 0.11)], P > .05). The PCA requests in the hydromorphone group were less than that in the sufentanil group, and there was no significant difference (RR = -0.20, 95% CI [-1.93,1.53], P > .05). The incidence of adverse events in the hydromorphone group was less than that in the sufentanil group, and there was a statistical difference: (RR = 0.61, 95% CI [0.47,0.79], P < .05). CONCLUSION: Compared with sufentanil, PCA with hydromorphone was more effective in relieving pain and PCA requests 12, 24, and 48 hours after operation, and significantly reduced the incidence of adverse events, but it did not have an advantage in sedation intensity.

Hypertriglyceridemia-induced acute pancreatitis: progress on disease mechanisms and treatment modalities.

Acute pancreatitis (AP) is a common and destructive inflammatory condition of the pancreas. Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) has become the second major cause of AP. Although the association between HTG and AP is well established, HTG as a risk factor of AP in the general population is not well identified. In this review, we summarize recent progress in our understanding of the pathogenesis of HTG-AP and clinical management of this disease. The mechanism responsible for HTG-AP is related to high-level free fatty acid (FFA), microcirculatory disorder, oxidative stress, Ca2+ overload, and genetic polymorphism. Heparin and insulin therapy in diabetic patients with HTG can dramatically reduce triglyceride levels. Use of plasmapheresis is still experimental and better-designed studies are needed to evaluate the promise in the management of HTG-AP. Dietary intervention, lifestyle changes, and control of secondary causes are critical to the management and treatment of HTG-AP.