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Query: UMLS:C0011849 (diabetes)
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In a prospective study the perioperative results of plug-and-patch repair were investigated in patients > or = 65 years, and quality of life was assessed using the SF36 preoperatively and 3 months after the procedure in 34 consecutive patients. From August 1994 to February 1999 147 patients with a mean age of 73 +/- 5 years (65-92 years) were operated on using the plug-and-patch technique, mostly under local anesthesia (LA: n = 124, 84%, ITN: n = 23, 16%). Preoperative risk factors were alcohol consumption, hypertonus, diabetes mellitus, ischemic heart disease, smoking, cerebrovascular disease, hyperlipidaemia and pulmonary disease. Most of the patients were ASA II (ASA I: n = 14, 9%, ASA II: n = 82, 56%, ASA III: n = 51, 35%). No intraoperative complications occurred, postoperative complications consisted of superficial wound hematoma (n = 6, 3.7%) and infection (n = 1, 0.6%), seroma (n = 7, 3.8%), urinary retention (n = 3, 1.8%) and ilioguinal pain syndrome (n = 3, 3.8%). The total amount of postoperative analgesic consumption was 4.9 +/- 1.8 g Novalgin for about 4 +/- 3 days. The duration of postoperative hospitalization was 2 +/- 1 days and limitation of daily activities 6 +/- 3 days. Clinical examinations after 3 months revealed no recurrence or late complications. Investigation of quality of life showed a significant improvement in the SF36 domains of physical activity, pain, vitality, and social functioning after the operation. No significant change was observed for physical, emotional, and global health.
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PMID:[Repair of inguinal hernia in the elderly. Results of the plug-and-patch repair with special reference to quality of life]. 1087 15

Hypocholesterolemia seems to represent a significant predictive factor of morbidity and mortality in critically ill patients. The authors, on the basis of recent literature data, aim to clarify the possible correlation between preoperative hypocholesterolemia and the risk of septic postoperative complications .205 patients undergoing to surgery for gastrointestinal diseases were the object of the study. Patients undergoing "minor" abdominal surgery or video-laparoscopic surgery and classified ASA III-IV were excluded. In all the patients, we considered retrospectively risk factors for postoperative septic complications as follows: preoperative blood concentration of cholesterol, malnutrition, obesity, diabetes, neoplasm, preoperative sepsis, type and duration of operations, antibiotics and regimen of use. Type and incidence of postoperative local or systemic septic complications were recorded. The patients have been stratified according to blood concentration of cholesterol and to the presence or absence of other risk factors. The incidence of postoperative sepsis was 35.1%. The highest incidence of postoperative septic complications (72.7%) was encountered, significantly (X2 = 7.6, p < 0.001), in the patients (11 cases, 5.9%) with cholesterol levels below 105 mg/dl). The results of this study seems to indicate a significant relationship between preoperative hypocholesterolemia and the incidence of septic complications after surgery. Moreover, evaluation of blood cholesterol levels before major surgery might represent a predictive factor of septic risk in the postoperative period.
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PMID:[Blood levels of cholesterol and postoperative septic complications]. 1092 Apr 96

The creation of arteriovenous fistula is an established form of therapy for patients with chronic renal failure. Anesthetic management in such patients is governed by the presence of risk factors such as hypertension, ischemic heart disease, diabetes, chronic pulmonary disease, anemia, coagulopathy, metabolic acidosis and/or hyperkalemia. In an attempt to improve the quality of anesthetic care and outcome we designed the present study to compare the different anesthetic techniques which are used for creation of arteriovenous fistula. Retrospectively we reviewed 164 patients who underwent creation of arteriovenous fistula. We retrieved the data concerning the age, sex, ASA class, and coexisting diseases. The patients were classified into three groups depending on the anesthetic technique received. Group A (n = 48) patients received general anesthesia; group B (n = 39), patients received brachial plexus block and group C (n = 77), patients received local infiltration anesthesia. Chi-square test was used to compare between the percentages among the different groups. The percentages of cardiac patients showed significant differences between groups A and B and also between groups A and C. There was a significant difference between the groups A and B also between the groups A and C but not between groups B and C concerning age. ASA classes were not significantly different among the groups. Among the total number of patients, 34 were diabetics and 75 patients were cardiac. Axillary brachial plexus block was complete in 70% of patients and incomplete in 27% and failed in 3% of patients. We conclude that chronic renal failure patients are at increased risk during anesthesia. We conclude that brachial plexus blockade or local anesthetic infiltration are good alternatives to general anesthesia in these patients undergoing creation of arteriovenous fistula. Age, ASA class and cardiac status were the three determining factors for the choice of the anesthetic technique. Further multivariate prospective study are needed to confirm these results.
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PMID:Arteriovenous fistula in chronic renal failure patients: comparison between three different anesthetic techniques. 1093 89

The state of pharmacotherapy in the Czech Republic in 1998 was analysed in a group of 548 patients with coronary heart disease and diabetes mellitus. 83.0% of the group were treated by antiplatelet drugs, mostly ASA (with the most frequent dose being 100 mg). 7.3% of the patients were treated by anticoagulation treatment. Beta-blocking agents were used in 56.9% of the group (most frequently metoprolol and atenolol). The optimal dose of metoprolol, 100 mg b.i.d., was used in only 12.4% of the patients treated by metoprolol. Older patients and patients with left ventricular systolic dysfunction were treated significantly less frequently than younger patients or patients without left ventricular systolic dysfunction. ACE inhibitors were used in 52.2% of the patients. The optimal daily target dosages of captopril 100-150 mg were used in only 6% of patients treated by captopril. The optimal target daily dosages of enalapril were used in only 35.1% of patients treated by enalapril. 65% of patients with left ventricular systolic dysfunction were treated by ACE inhibitors. Calcium-channel blockers were used in 24.6% of the patients. However, in 20.1% of patients treated by calcium-channel blockers, shortacting or inadequately retarded nifedipine was used. 69.8% of the patients had total cholesterol values higher than 5.2 mmol/l, 18.1% higher than 6.2 mmol/l and 13.5% of patients had total cholesterol values higher than 7.0 mmol/l. 34.3% of the group were treated by hypolipidemic drugs (most frequently fenofibrate). Statins were used by 45.5% of patients treated by hypolipidemic drugs. When compared to our analysis of pharmacologic treatment in patients after myocardial infarction, performed in 1995, ACE inhibitors and hypolipidemic treatment are used more frequently. However, in spite of this improvement, only about 15% of patients with CHD are treated by statins. Furthermore, 35% of patients with left ventricular systolic dysfunction due to CHD are not treated by ACE inhibitors. Elderly patients with CHD and diabetes mellitus or patients with left ventricular systolic dysfunction due to CHD are less frequently treated than younger patients or those with normal left ventricular systolic function despite the fact that patients at highest risk benefit most from treatment with beta-blocking agents. Also unsatisfactory is the use of not retarded or inadequately retarded nifedipine although data show its use may increase total mortality in CHD patients. By contrast, use of antiplatelet therapy is satisfactory.
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PMID:[Pharmacotherapy in patients with ischemic heart disease and diabetes mellitus in 1998 in the Czech Republic]. 1095 43

We compared the gastric toxic effect of aspirin (ASA) in both normal and diabetic rats, with that of NCX-4016, a derivative of ASA with nitric oxide (NO) releasing moiety. Animals were injected with streptozotocin and used after 5 weeks of diabetes with blood glucose levels of >350 mg/dl in the presence of omeprazole. Oral administration of ASA (with 150 mM HCl) did not produce damage at 30 mg/kg in the conscious rat but caused hemorrhagic gastric lesions in STZ-diabetic rats. By contrast, NCX-4016 even at 190 mg/kg (a dose equimolar to 100 mg/kg of ASA) did not cause damage in both normal and STZ-diabetic rat stomachs. Plasma salicylic acid levels were not different between normal and diabetic rats after administration of ASA or NCX-4016, though the latter gave significantly lower levels as compared to ASA. Intragastric application of ASA (80 mM in 50 mM HCl) for 30 min caused a reduction of transmucosal PD and increase of luminal H+ loss with a minimal effect on mucosal blood flow (GMBF) in both normal and diabetic rats, yet resulting in much severe damage in the stomach of the latter group. Mucosal application of NCX-4016, however, did not cause PD reduction and luminal H+ loss, but produced a marked hyperemia, resulting in no damage in the stomach of both normal and STZ-diabetic rats. The increased gastric toxicity of ASA in STZ-diabetic rats was significantly mitigated by co-application of a NO donor FK-409 together with ASA, with an increase of GMBF, despite similar degrees of PD reduction and luminal H+ loss being observed. We conclude that NCX-4016 does not have a toxic effect in either normal or diabetic rat stomachs, although the diabetic rat stomach is more vulnerable to ASA-induced damage. NCX-4016, though absorbed more slowly than ASA, counteracts the injurious effect of aspirin on the gastric mucosa, probably by increasing GMBF mediated by NO.
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PMID:Lack of gastric toxicity of nitric oxide-releasing aspirin, NCX-4016, in the stomach of diabetic rats. 1098 57

We and others have previously documented increased resting and exercise-induced skeletal muscle blood flow in young subjects with Type I (insulin-dependent) diabetes mellitus compared with healthy controls. Both NO and prostanoids are important regulators of vascular tone and may therefore contribute to this hyperaemia. The aim of the present study was to determine the contribution of NO and vasodilator prostanoids to this skeletal muscle hyperaemia in diabetes. We assessed the effects of infusion into the intrabrachial artery of the cyclo-oxygenase inhibitor acetylsalicylic acid (ASA; aspirin) and of the L-arginine analogue N(G)-monomethyl-L-arginine (L-NMMA) on skeLetal muscle blood flow in subjects with Type I diabetes mellitus (DM subjects) and control subjects. Blood flow was measured by venous occlusion plethysmography. Isotonic forearm exercise involved 2 min of wrist flexion and extension. Resting flow (forearm blood flow; FBF) was augmented in DM subjects, as was peak exercise-related blood flow (PFBF) and the volume repaid to the forearm 5 min after exercise (AUC 5, where AUC is area under the flow-time curve) (P<0.05), even when accounting for differences in basal flow. Infusion of L-NMMA reduced resting flow by 48% in controls (P<0.005) and by 12% in DM subjects (not significant). L-NMMA reduced PFBF and AUC 5 by 29% (P<0.05) and 39% (P<0.0005) respectively in controls, but had no significant effect on these parameters in DM subjects. Infusion of ASA reduced FBF, PFBF and AUC 5 in both DM (P<0.05) and control (P<0.05) subjects, but the magnitude of this reduction was greater in DM than in control subjects (ANOVA, P<0.05), even when differences in resting FBF were accounted for. Indeed, ASA eliminated the differences in FBF, PFBF and AUC 5 between DM and control subjects. Thus increased release of vasodilator prostanoids, rather than of NO, appears to account for skeletal muscle hyperaemia in Type I diabetes.
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PMID:Vasodilator prostanoids, but not nitric oxide, may account for skeletal muscle hyperaemia in Type I diabetes mellitus. 1105 18

Recent studies suggest that aggregation of platelets from patients with coronary artery and cerebrovascular disease may be resistant to low-dose aspirin (ASA) treatment, which may promote plaque-associated thrombus formation. However, the underlying mechanisms of platelet ASA resistance are poorly understood. ASA is thought to inhibit platelet aggregation primarily by inactivating the cyclooxygenase (COX), thus decreasing the synthesis of the pro-aggregatory arachidonic acid metabolite thromboxane A(2) (TxA(2)). However, recent studies also identified a non-enzymatic, oxidation-dependent pathway for the synthesis of the arachidonic acid derivative isoprostanes, which exhibit potent vasoconstrictor and pro-aggregatory effects similar to that of TxA(2). Because the pathophysiological conditions that promote arteriosclerotic vascular diseases (e.g. hypercholesterolemia, diabetes, hyperhomocysteinemia) are thought to be associated with an increased formation of reactive oxygen species and increased plasma isoprostane levels, it can be hypothesized that increased COX-independent isoprostane formation in platelets contribute to ASA resistance.
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PMID:Oxidative stress-induced isoprostane formation may contribute to aspirin resistance in platelets. 1214 79

The glycosphingolipid sulfatide is present in secretory granules and at the surface of pancreatic beta-cells, and antisulfatide antibodies (ASA; IgG1) are found in serum from the majority of patients with newly diagnosed type 1 diabetes. Here we demonstrate that sulfatide produced a glucose- and concentration-dependent inhibition of insulin release from isolated rat pancreatic islets. This inhibition of insulin secretion was due to activation of ATP-sensitive K(+)-(K(ATP)) channels in single rat beta-cells. No effect of sulfatide was observed on whole-cell Ca(2+)-channel activity or glucose-induced elevation of cytoplasmic Ca(2+) concentration. It is interesting that sulfatide stimulated Ca(2+)-dependent exocytosis determined by capacitance measurements and depolarized-induced insulin secretion from islets exposed to diazoxide and high external KCl. The monoclonal sulfatide antibody Sulph I as well as ASA-positive serum reduced glucose-induced insulin secretion by inhibition of Ca(2+)-dependent exocytosis. Our data suggest that sulfatide is important for the control of glucose-induced insulin secretion and that both an increase and a decrease in the sulfatide content have an impact on the secretory capacity of the individual beta-cells.
Diabetes 2002 Aug
PMID:Sulfatide controls insulin secretion by modulation of ATP-sensitive K(+)-channel activity and Ca(2+)-dependent exocytosis in rat pancreatic beta-cells. 1214 65

Metabolomic mapping is an emerging discipline geared at providing information on a large number of metabolites as a complement to genomics and proteomics. Here we have probed ascorbic acid homeostasis and degradation in diabetes using 6-deoxy-6-fluoro ascorbic acid (F-ASA) and 750 MHz (19)F-nuclear magnetic resonance (NMR) spectroscopy with proton decoupling In vitro, Cu(2+)-mediated degradation of F-ASA revealed the formation of 4 major stable degradation products at 24 hours. However, when normal or diabetics rats were injected with F-ASA intraperitoneally (IP) for 4 days, up to 20 fluorine-labeled compounds were observed in the urine. Their composition resembled, in part, metal catalyzed degradation of F-ASA and was not explained by spontaneous degradation in the urine. Diabetes led to a dramatic increase in urinary F-ASA loss and a relative decrease in most other urinary F-compounds. Diabetes tilted F-ASA homeostasis toward oxidation in liver (P <.01), kidney (P <.01), spleen (P <.01), and plasma (P <.01), but tended to decrease oxidation in brain, adrenal glands, and heart. Surprisingly, however, besides the major oxidation product fluoro-dehydroascorbic acid (F-DHA), no F-ASA advanced catabolites were detected in tissues at 5 micromol/L sensitivity. These findings not only confirm the key role of the kidney in diabetes-mediated loss of ascorbic acid, but demonstrate that only selected tissues are prone to increased oxidation in diabetes. While the structure of most degradation products needs to be established, the method illustrates the power of high resolution (19)F-NMR spectroscopy for the mapping of complex metabolomic pathways in disease states.
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PMID:Vitamin C metabolomic mapping in experimental diabetes with 6-deoxy-6-fluoro-ascorbic acid and high resolution 19F-nuclear magnetic resonance spectroscopy. 1280 Jan 4

There is an increased risk of stroke and other cardiovascular events in patients with atrial fibrillation (AF). Three meta-analyses of randomized clinical trials (RCTs) comparing oral anticoagulants (OAC) with aspirin (ASA) arrived at different conclusions regarding the relative efficacy of these agents to prevent ischemic stroke in AF patients. This article summarizes a recently published individual patient meta-analysis of all published RCTs comparing OAC and ASA in AF. In total, 4052 patients randomized to OAC or ASA were similar regarding important prognostic factors. Patients receiving OAC had a significantly lower risk of any stroke (hazard ratio [HR] 0.54 [95% CI 0.43-0.71]), ischemic stroke (HR 0.48 [0.37-0.63]), or cardiovascular events (HR 0.71 [0.59-0.85]). Patients receiving OAC were more likely to experience major bleeding (HR 1.71 [1.21-2.41]). The benefit of OAC was most prominent in patients at a high risk of stroke and other cardiovascular events, such as patients with hypertension, diabetes, or previous cerebrovascular events. Overall, OAC improves outcomes for cardiovascular events in AF patients but modestly increases the absolute risk of major bleeding. Since high-risk AF patients appear to benefit most from OAC, determining stroke risk in AF patients is very important.
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PMID:Oral anticoagulants vs. aspirin for stroke prevention in patients with non-valvular atrial fibrillation: the verdict is in. 1507 Dec 58


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