Leptin to adiponectin ratio - A surrogate biomarker for early detection of metabolic disturbances in obesity.

AIM: To study if the leptin to adiponectin (L:A) ratio, can be a potential biomarker for postprandial triglyceride clearance, insulin resistance (IR) or leptin resistance (LR) in apparently healthy obese, and obese individuals with established metabolic disease. METHODS AND RESULTS: Fifty adult subjects with obesity (BMI ≥30); of which 36 metabolic healthy obese (MHO), and 14 metabolic dysregulated obese (MDO), with clinical and/or biochemical signs of metabolic disease were included. Seventeen healthy, normal weight subjects represented the control group. Postprandial triglyceride (TG) levels were measured in an 8 h oral fat tolerance test (OFTT). IR by HOMA-IR, L:A ratio and indirect LR were measured. In the MHO group, 71.4%, 69.4% and 86.1%, had delayed TG clearance, IR and LR, respectively; whereas in the MDO group this was detected in 85.7%, 71.4% and 91.7%, respectively. A combination of all three metabolic risk factors was found in 39.8% of the MHO and in 42.9% of the MDO patients. Receiver operating characteristics (ROC) analysis revealed that a cut-off value for the L:A ratio of >1.65 for the control group (PPV 1.0, NPV 0.91) and >3.65 for the obese subjects (PPV 0.86, NPV 0.48) predicted the delayed TG clearance with a good specificity and sensitivity. Detecting a combined risk with at least 2/3 metabolic risk factors, the ROC yielded the most suitable L:A ratio cut-off at >1.88. CONCLUSION: L:A ratio was able to detect early metabolic disturbances in obese individuals, and may be a potential useful clinical surrogate biomarker of metabolic disorders.

Future complications of chronic hepatitis C in a low-risk area: projections from the hepatitis c study in Northern Norway.

BACKGROUND: Hepatitis C (HCV) infection causes an asymptomatic chronic hepatitis in most affected individuals, which often remains undetected until cirrhosis and cirrhosis-related complications occur. Screening of high-risk subjects in Northern Norway has revealed a relatively low prevalence in the general population (0.24%). Despite this, late complications of HCV infection are increasing. Our object was to estimate the future prevalence and complications of chronic HCV infection in the period 2013-2050 in a low-risk area. METHODS: We have entered available data into a prognostic Markov model to project future complications to HCV infection. RESULTS: The model extrapolates the prevalence in the present cohort of HCV-infected individuals, and assumes a stable low incidence in the projection period. We predict an almost three-fold increase in the incidence of cirrhosis (68 per 100,000), of decompensated cirrhosis (21 per 100,000) and of hepatocellular carcinoma (4 per 100,000) by 2050, as well as a six-fold increase in the cumulated number of deaths from HCV-related liver disease (170 per 100,000 inhabitants). All estimates are made assuming an unchanged treatment coverage of approximately 15%. The estimated numbers can be reduced by approximately 50% for cirrhosis, and by approximately one third for the other endpoints if treatment coverage is raised to 50%. CONCLUSION: These projections from a low-prevalence area indicate a substantial rise in HCV-related morbidity and mortality in the coming years. The global HCV epidemic is of great concern and increased treatment coverage is necessary to reduce the burden of the disease.

Delayed clearance of triglyceride-rich lipoproteins in young, healthy obese subjects.

Obesity is associated with the metabolic syndrome. The aims were, first, to study the postprandial triglyceride clearance in young, healthy obese subjects and, second, to investigate if fasting triglycerides can predict delayed postprandial triglyceride clearance. Eighteen apparently healthy, obese subjects with no clinical signs of metabolic disturbances participated. Controls were age- and sex-matched, healthy, normal weight subjects. Subclinical markers of metabolic disturbances were assessed by measuring postprandial triglycerides in serum and in chylomicrons by oral fat tolerance test. Postprandial triglyceride clearance for 8 h was assessed indirectly as removal of the lipid from serum during the oral fat tolerance test. Insulin resistance was measured by the homeostasis model assessment of insulin resistance (HOMA-IR). Twelve (66%) of the apparently healthy obese individuals had insulin resistance measured by HOMA-IR. There was a delayed clearance of serum triglycerides and chylomicron triglycerides at 6 h when compared with the control group, while, at 8 h, the differences were only detected for the chylomicron triglyceride clearance. Triglyceride response was significantly greater in the obese subjects. Fasting triglycerides in upper normal level predicted a delayed postprandial triglyceride clearance and insulin resistance. In young, apparently healthy obese subjects early metabolic disturbances including insulin resistance and delayed postprandial triglyceride clearance can be detected. Fasting serum triglyceride in upper normal level predicted delayed postprandial triglyceride clearance and insulin resistance.

Cardioprotective effects of the MR contrast agent MnDPDP and its metabolite MnPLED upon reperfusion of the ischemic porcine myocardium.

PURPOSE: To evaluate whether manganese dipyridoxyl diphosphate (MnDPDP) or its metabolite manganese dipyridoxyl ethyldiamine (MnPLED) reduces post-ischemic myocardial injury. MATERIAL AND METHODS: Left anterior descending artery (LAD) in anesthetized pigs was occluded (30 min) followed by reperfusion (120 min) during hemodynamic monitoring and infarct assessment. Three micromol/kg MnDPDP, 1 micromol/kg MnPLED (or a mixture of both) or saline was injected i.v. 10 min before reperfusion followed by infusion of either 3 micromol/kg/h MnDPDP, 1 micromol/kg/h MnPLED (or a mixture of both) or saline. The plasma concentrations of MnDPDP, MnPLED and other metabolites (e.g., ZnDPDP and ZnPLED) were analyzed. RESULTS: Femoral blood flow was reduced by 60% during early reperfusion in controls, whereas only 23 and 31% reductions were seen in animals treated with MnDPDP and MnPLED. During that time, +LV/dP and -LV/dP (maximum rate of left ventricular isovolumic contraction and relaxation, respectively), systolic pressure and diastolic pressure fell significantly less in animals treated with MnDPDP or MnPLED. Three out of 5 control animals experienced ventricular fibrillation (VF) during reperfusion, whereas VF was not seen in any of the pigs treated with MnPLED or/and MnDPDP. The infarct sizes in saline- and MnPLED-treated animals were 39+/-6 and 16+/-5%, respectively, of the occluded areas. MnDPDP did not reduce the infarct size. A mixture of MnDPDP and MnPLED significantly reduced infarct size (10+/-4%). When reperfusion started and throughout reperfusion, almost all injected MnDPDP was present as Zn-metabolites. CONCLUSION: MnPLED seems to reduce reperfusion-induced cardiac dysfunction and infarct size in pigs. MnDPDP does not reduce infarct size in the pig, probably because of the rapid exchange of Mn2+ for Zn2+ taking place in the pig.

What are the basic dimensions of movements? A psychometric evaluation of the Comprehensive Body Examination III.

The movements were examined in accordance with the Comprehensive Body Examination. The study objects were 99 persons: 17 pain syndrome patients (PSP group), 27 psychotic patients (PP group), 4 non-psychotic patients (NPP group), and a comparison group consisting of 51 students and staff members (SS group). On the basis of factor analysis three subscales were made: 1) Resistance to Passive Movements (RPM), with nine items, 2) Assistance to Passive Movements (APM), with six items, and 3) Motor Disturbances (MD), with three items. The internal consistency of the subscales was high (Chronbach's alpha, 0.81-0.96), and the intercorrelation low to moderate. The RPM subscale distinguished significantly between the SS group and both patient groups; the APM and MD subscales distinguished between the SS group and the PP group. The MD subscale also distinguished between patients taking drugs and those who did not, but there was no difference between patients without medication and the SS group.

NMR relaxation studies with MnDPDP.

PURPOSE: Our studies were designed to compare the efficacy of mangafodipir trisodium (MnDPDP, Teslascan) as a tissue-specific MR agent with that of manganese chloride (MnCl2), to compare the efficacy of different doses and rates of administration of MnDPDP, and to collect the data needed for predicting optimum pulse sequences. MATERIAL AND METHODS: The dose response for the relaxation rates R1 and R2 at 0.47 T, and the manganese (Mn) concentrations in rat liver and in the liver, pancreas, heart and adrenals of pigs was determined for both MnDPDP and MnCl2 administered i.v. Computer simulations were carried out to model the effects of different tissue Mn concentrations and TR on signal intensities and contrast-to-noise ratios. RESULTS: In rat liver and pig organs both compounds produced a positive dose-response in R1 and tissue Mn concentration, and only small or no response in R2. The Mn concentration in rat liver was positively correlated with R1, regardless of the form in which Mn was given, or the rate of administration. Optimal imaging parameters are therefore expected to be different pre- and post-MnDPDP administration. CONCLUSION: The added cardiovascular safety of MnDPDP compared with MnCl2 does not result in loss of efficacy in increasing RI at the intended clinical dose of 5 mumol/kg MnDPDP. The changes in R2 were too small to affect T2-weighted images. The data give the basis for choosing the appropriate pulse sequences for MnDPDP-enhanced MR imaging.

Endothelin-1 and neutrophil activation during heparin-coated cardiopulmonary bypass.

BACKGROUND: Heparin-coated circuits attenuate the systemic inflammatory response to cardiopulmonary bypass. The present study compares two different heparin coatings in terms of the release of endothelin-1 and neutrophil glycoproteins. METHODS: Forty low-risk patients undergoing coronary artery bypass grafting were investigated, having cardiopulmonary bypass with a Duraflo II heparin-coated circuit (n = 10), an identical but uncoated circuit (n = 10), a Carmeda BioActive Surface heparin-coated circuit (n = 10), or an identical but uncoated circuit (n = 10). A standard systemic heparin dosage was used in all patients. Endothelin-1 and the neutrophil glycoproteins lactoferrin and myeloperoxidase were quantified throughout the operation and 3 hours postoperatively. RESULTS: Enhanced plasma levels of endothelin-1, lactoferrin, and myeloperoxidase were observed during and after uncoated cardiopulmonary bypass, but this was not associated with clinical side effects. Compared with the respective uncoated controls, Duraflo II attenuated only the lactoferrin levels, whereas Carmeda BioActive Surface was associated with lower levels of both endothelin-1, lactoferrin, and myeloperoxidase. Of the two heparin coatings, Carmeda BioActive Surface proved more effective than Duraflo II in attenuating the levels of these substances. CONCLUSIONS: The plasma levels of endothelin-1, lactoferrin, and myeloperoxidase increase during cardiopulmonary bypass in coronary artery bypass grafting, but this has no clinical side effects in low-risk patients. The increase is attenuated using heparin-coated extracorporeal circuits, and then more effectively by Carmeda BioActive Surface than by Duraflo II.

Both plasma- and leukocyte-associated C5a are essential for assessment of C5a generation in vivo.

BACKGROUND: Measurement of C5a in plasma is hampered by the rapid clearance of C5a as a result of cell binding. Therefore, an assessment of whether cell-bound C5a might better reflect C5a generation in vivo is essential. METHODS: We quantified plasma and leukocyte-bound C5a in samples from patients undergoing cardiopulmonary bypass, which is known to be associated with complement activation. C3 activation products and the terminal complement complex were measured as well. RESULTS: Plasma levels of C3 activation products and the terminal complement complex increased rapidly and significantly after the onset of cardiopulmonary bypass until they reached a plateau after 30 minutes. The concentration of plasma C5a increased steadily to twice baseline at the end of bypass. The concentration of leukocyte-associated C5a increased threefold after 10 minutes of cardiopulmonary bypass, when a plateau was reached. A positive correlation was found between levels of plasma C3 activation products or terminal complement complex and plasma C5a plus cell-associated C5a but not between C3 activation products or terminal complement complex and either one of the C5a variables. CONCLUSIONS: We conclude that both plasma C5a and leukocyte-associated C5a are needed for monitoring in vivo C5a generation.

Effects of heparin coating on the expression of CD11b, CD11c and CD62L by leucocytes in extracorporeal circulation in vitro.

Leucocyte adhesion molecules are involved in the leucocyte-endothelial interaction and in the activation of coagulation and binding of complement and endotoxin. Thus, they are important in inflammation, systemic acute phase reaction, ischaemia reperfusion injury and resistance against infections. The expression of the adhesion molecules CD11b, CD11c and CD62L on leucocytes and changes in plasma products of neutrophil activation (myeloperoxidase, lactoferrin) and complement activation (C3bc, SC5b-9 (TCC)) were examined in an extracorporeal circulation (ECC) model and the effects of Carmeda bioactive surface (CBAS) heparin coating (n = 7) of the circuits were compared to uncoated control circuits (n = 5). In this model, new 'unactivated' cells mobilized from the bone marrow could not interfere with descriptive measures of cell activation as seen in in vivo studies. In the control group, CD11b and CD11c were upregulated on monocytes and granulocytes during ECC, whereas CD62L was downregulated. Heparin coating reduced the increase in CD11b and CD11c on granulocytes (p < 0.02 at 2 h), but the delayed increase in CD11c on monocytes and the delayed downregulation of CD62L on granulocytes and monocytes did not reach statistical significance. Further, heparin coating also reduced the initial decrease in the absolute cell counts of monocytes and granulocytes (p = 0.01 at 2 h), reflecting reduced adhesion to the oxygenator/tubing. The increases in plasma myeloperoxidase, lactoferrin, C3bc and TCC were lower in the heparin-coated group compared to the control group. The increases in plasma myeloperoxidase and lactoferrin correlated significantly to the increase in CD11b (r = 0.71, p = 0.02 and r = 0.64, p = 0.05, respectively) and CD11c (r = 0.72, p = 0.008 and r = 0.72, p = 0.008, respectively) on granulocytes, suggesting interacting regulatory pathways in the process of neutrophil adhesion, activation and degranulation. Thus, in this in vitro ECC model, heparin coating of oxygenator/tubing sets reduced leucocyte activation and leucocyte adhesion-related phenomena.

Duraflo II coating of cardiopulmonary bypass circuits reduces complement activation, but does not affect the release of granulocyte enzymes : a European multicentre study.

OBJECTIVE: This study was carried out to: (a) compare complement and granulocyte activation during cardiac operations in patients operated with cardiopulmonary bypass coated with heparin by the Duraflo II method, with activation in patients operated with uncoated circuits; and (b) relate complement, and granulocyte activation to selected adverse effects. METHODS: In a multicentre study among Rikshospitalet, Ullevaal Hospital in Norway and Uppsala University Hospital in Sweden, plasma concentrations of the complement activation products C4b/iC4b/C4c (C4bc), C3b/iC3b/C3c (C3bc), the terminal SC5b-9 complement complex (TCC), and the granulocyte proteins myeloperoxidase and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass. Seventy-six patients underwent surgery operated with circuits coated by the Duraflo II heparin coating and 75 uncoated circuits. The same amount of systemic heparin was administered to all patients. RESULTS: In both groups a significant increase in C4bc was first seen by the end of operation, from 86.7 +/- 12.5 to 273.0 +/- 277.4 nM in controls and from 86.9 +/- 18.5 to 320.2 +/- 190.5 nM in the control group, confirming previous documentation that the classical pathway is not activated during CPB, but as a consequence of protamin administration. The formation of C4bc did not differ significantly between the two groups. In the uncoated group the C3bc concentration increased from 124.0 +/- 15.3 to a maximum of 1176.1 +/- 64.7 nM (P < 0.01) and in the coated group it increased from 129.8 +/- 16.1 to a maximum of 1019.4 +/- 54.9 nM (P < 0.01) during CPB. Summary values but not peak values differed significantly between the groups. In the uncoated group the TCC concentration increased from 0.52 +/- 0.03 to a maximum value of 8.09 +/- 0.57 AU/ml (P < 0.01) while in the coated group the TCC concentration increased from a baseline of 0.53 +/- 0.03 to a peak value of 5.2 +/- 0.24 AU/ml (P <0.01). The difference between the peak values was statistically significant (P = 0.00002). In both groups a significant increase in myeloperoxidase and lactoferrin release was observed by the end of operation. There was no difference in myeloperoxidase or lactoferrin release between the two groups. TCC levels were compared to the occurrence of perioperative infarction, development of lung or renal failure, postoperative bleeding, time on ventilator and days in hospital. Three patients developed perioperative infarction; the peak levels of TCC were significantly higher in these patients than in the 148 patients that did not develop infarction. The reduction in TCC formation in the heparin-coated group was not associated with differences in any of the other clinical parameters. Few adverse effects occurred in the study. The peak values of C3bc were higher in the patients needing inotropic support that in those who did not, the relevance of this finding remains uncertain. CONCLUSION: It is concluded that the Duraflo II heparin coating reduces complement activation, particularly TCC formation, during CPB, but not the release of specific neutrophil granule enzymes. No certain correlation was established between complement and granulocyte activation and clinical outcome.

Attenuation of changes in leukocyte surface markers and complement activation with heparin-coated cardiopulmonary bypass.

BACKGROUND: The inflammatory response induced by cardiopulmonary bypass can result in severe organ dysfunction in some patients. This postperfusion response is caused mainly by contact between blood and the foreign surface of the cardiopulmonary bypass equipment and includes adhesion of leukocytes to vascular endothelium, which precedes a series of events that mediate inflammatory damage to tissues. METHODS: Low-risk patients accepted for coronary artery bypass grafting were randomized to operation with the cardiopulmonary bypass surface either completely heparin coated (Duraflo II) or uncoated. There were 12 patients in each group. Blood plasma sampled during cardiopulmonary bypass was analyzed for complement activation (C3bc and terminal SC5b-9 complement complex) and neutrophil activation (lactoferrin and myeloperoxidase). In addition, neutrophils, monocytes, and platelets were counted, and the expression of surface markers on the neutrophils and monocytes (complement receptor [CR] 1, CR3, CR4, and L-selectin) and on the platelets (P-selectin and CD41) was quantified with flow cytometry. RESULTS: Clinical and surgical results were similar in both groups. In the group with the heparin-coated surface, the formation of the terminal SC5b-9 complement complex was significantly reduced, and the counts of circulating leukocytes and platelets were significantly less reduced initially but were higher at the end of cardiopulmonary bypass compared with baseline. Also, the expression of CR1, CR3, and CR4 was significantly less upregulated and the L-selectin, significantly less downregulated on monocytes and neutrophils. CONCLUSIONS: We conclude that heparin coating reduces complement activation and attenuates the leukocyte integrin and selectin response that occurs when uncoated circuits are used.

Centrifugal pump and heparin coating improves cardiopulmonary bypass biocompatibility.

BACKGROUND: Centrifugal pumps are being used increasingly for short-term extracorporeal circulation purposes such as during heart operations. Whether the centrifugal pump improves the cardiopulmonary bypass biocompatibility has not been fully documented. METHODS: A roller pump (n = 20) was compared in vivo with a centrifugal pump (n = 20) in groups of patients in which cardiopulmonary bypass circuits that were either totally heparin coated (Carmeda BioActive Surface; n = 20) or uncoated (n = 20) were used. We expected the heparin coating to attenuate blood activation, thus possibly making the comparison of the two pumps easier with respect to their different blood activation potentials. Samples of blood plasma, obtained during cardiopulmonary bypass from low-risk coronary artery bypass grafting patients, were analyzed for hemolysis (plasma haemoglobin), complement activation (C3bc and the terminal complement complex), a complement lytic inhibitor (vitronectin), coagulation activation (fibrinopeptide A), granulocyte activation (lactoferrin), and platelet activation (beta-thromboglobulin). RESULTS: The concentrations of terminal complement complex, lactoferrin, and beta-thromboglobulin were significantly lower in association with heparin-coated surfaces. The concentration of plasma hemoglobin was significantly lower in association with the centrifugal pump. In uncoated circuits, the beta-thromboglobulin level was significantly higher in association with the roller pump than with the centrifugal pump, but this significant reduction in the beta-thromboglobulin level did not hold true for the heparin-coated circuit group. CONCLUSIONS: A heparin-coated cardiopulmonary bypass surface reduces the blood activation potential during cardiopulmonary bypass, and the centrifugal pump causes less hemolysis than the roller pump.

Differences in blood activation related to roller/centrifugal pumps and heparin-coated/uncoated surfaces in a cardiopulmonary bypass model circuit.

An in vitro model cardiopulmonary bypass (CPB) circuit consisting ot tubing, oxygenator and venous reservoirs with either a roller or a centrifugal pump, and with either heparin-coated (Carmeda Bioactive Surface, CBAS) or uncoated surfaces, was studied with respect to 'blood activation', using small-scale-based blood volume (450 + 500 ml). Sixteen circuits were tested in each pump group, eight with and eight without heparin-coated surfaces, by circulating heparinized fresh human blood for 72 hours at 30 degrees C. Blood plasma, sampled at defined intervals, was analysed for haemolysis (lactate dehydrogenase and potassium), complement activation (C3bc and C5b-9 (TCC)), complement lytic inhibitors (vitronectin and clusterin), coagulation activation (fibrinopeptide A), granulocyte (lactoferrin and myeloperoxidase) and platelet (beta-thromboglobulin) activation and contaminating endotoxin. The heparin coating significantly reduced the concentrations of C3bc, TCC, fibrinopeptide A, lactoferrin, myeloperoxidase and beta-thromboglobulin. The two pump types did not differ with respect to these parameters, but the roller pump caused significantly higher increases in plasma LDH and potassium and significantly greater reductions in clusterin and vitronectin than the centrifugal pump. Endotoxin concentration was low at the start and after 24 hours in all groups. These results confirm that heparin-coated CPB surfaces reduce blood activation, and suggest that centrifugal pumps cause less haemolysis and less reduction in lytic complement inhibitors than roller pumps.

Disparity in blood activation by two different heparin-coated cardiopulmonary bypass systems.

BACKGROUND: Several studies have indicated reduced "blood activation" in heparin-coated cardiopulmonary bypass systems. The present study compares the effect of two different heparin coatings on different blood activation indices. METHODS: Low-risk patients (n = 40) were randomized to coronary artery bypass grafting using cardiopulmonary bypass with surfaces coated entirely by either the Duraflo II heparin coat or the Carmeda Biological Active Surface, or with identical uncoated equipment. In all cases, a standard systemic heparin dosage was used. Complement activation (C3 activation products C3bc and C3a and formation of fluid phase terminal SC5b-9 complement complex), neutrophil activation (lactoferrin and myeloperoxidase), and lytic inhibitors (vitronectin and clusterin) were quantified during cardiopulmonary bypass and 6 hours postoperatively. RESULTS: Heparin coating by either method reduced the formation of terminal SC5b-9 complement complex and the release of lactoferrin and myeloperoxidase compared with uncoated systems. Lactoferrin and myeloperoxidase levels increased significantly during cardiopulmonary bypass in the Duraflo II group, whereas no significant increase was observed in the Carmeda Biological Active Surface group. The least formation of terminal SC5b-9 complement complex and neutrophil activation was observed with the Maxima Carmeda Biological Active Surface-coated equipment. The vitronectin and clusterin concentrations were significantly less reduced in the Duraflo II compared with the control group. This study underlines the importance of terminal SC5b-9 complement complex as a suitable marker in the evaluation of complement activation during cardiopulmonary bypass. CONCLUSIONS: Both heparin coatings reduce blood activation, probably more so with Carmeda Biological Active Surface than with Duraflo II.

Reduced complement and granulocyte activation with heparin-coated cardiopulmonary bypass.

Plasma concentrations of the complement activation products C3b, iC3b, and C3c; the terminal C5b-9 complement complex; and the granulocyte proteins calprotectin, myeloperoxidase, and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass procedures. In 10 patients operated on, the bypass circuits were coated by the Carmeda Bio-Active Surface and systemic heparinization was reduced to 1.5 mg/kg; in another 10, the systems were uncoated and the dosage of systemic heparinization was 4 mg/kg. In both groups, significant complement activation was observed after the onset of cardiopulmonary bypass, but the maximum levels of C3b, iC3b, and C3c and the terminal C5b-9 complement complex were significantly lower in the heparin-coated group. In both groups, a significant increase in calprotectin, myeloperoxidase, and lactoferrin release was observed by the end of operation. The maximum myeloperoxidase levels were significantly lower in the heparin-coated group than those in the uncoated group (p = 0.03). There was a correlation of borderline significance between the formation of terminal C5b-9 complement complex and lactoferrin release, as well as between the formation of terminal C5b-9 complement complex and myeloperoxidase release (p = 0.05). The postoperative blood loss did not differ significantly between the two groups. We conclude that coating by end point-attached and functionally active heparin allows a significant reduction in the amount of systemic heparinization, and significantly reduces complement and granulocyte activation.

[Ulcer surgery and anti-ulcer agents. Changes in surgical activities and sale of anti-ulcer agents in Nord-Trøndelag 1975-89]. / Ulcuskirurgi og ulcusmidler. Endringer i operasjonsaktivitet og salg av ulcusmidler i Nord-Trøndelag 1975-89.

During recent decades the number of operations for peptic ulcer has decreased significantly. The incidence of operations for peptic ulcer or related complications during the period 1975-89 in persons older than 15 years was investigated in the Nord-Trøndelag region of Norway, with a population of approximately 100,000. The number of elective surgical procedures decreased by 72% from 1975 to 1989. The greatest reduction was found for duodenal ulcers. The incidence of acute operations decreased by 35%. The main reason was fewer surgical interventions in patients with haemorrhage, since the number of operations for perforation remained almost constant during the period of 15 years. The reduction in surgical treatment can be explained mainly by the introduction of new H2-antagonists in the seventies, leading to more successful pharmacological treatment of peptic ulcer.

Roller and centrifugal pumps compared in vitro with regard to haemolysis, granulocyte and complement activation.

A Biomedicus centrifugal pump and a Polystan roller pump were compared in vitro with regard to differences in haemolysis, granulocyte and complement activation. Six circuits of tubing and oxygenators were connected to each pump. Heparinized fresh human blood was circulated for 72 hours in the systems. Blood samples were drawn at defined intervals. Haemolysis was assessed by determination of lactate dehydrogenase (LD) and potassium, and granulocyte activation by quantification of the granulocyte proteins calprotectin, lactoferrin and myeloperoxidase. Complement activation was assessed by measuring C3 activation products (C3b, iC3b and C3c), and the terminal C5b-9 complement complex (TCC). The results indicate more haemolysis and complement activation in the roller pump group, revealed by significantly higher concentrations of LD, potassium, C3 activation products and TCC. Calprotectin, lactoferrin and myeloperoxidase were all significantly increased in both groups, but the rise appeared earlier in the roller pump group. The concentrations of LD and potassium both correlated significantly with C3 activation products, indicating that complement activation may at least partly be responsible for the haemolysis.

Slotted versus non-slotted locked intramedullary nailing for femoral shaft fractures.

Experimentally, two slotted nails, the Grosse-Kempf nail and the AO/ASIF universal femoral nail, were compared to the non-slotted Grosse-Kempf nail and control bone using a cadaver femoral osteotomy. The stiffnesses and strengths of the osteotomies fixed with slotted nails in 10-30 degrees torsion were 6-8% and the values of non-slotted nails 40% of control bone. The maximal moments were 14-18% and 48%, respectively. In the "clinical range" of torsion, the implant-bone construct never failed or was deformed. Clinically, 46 femoral shaft fractures were randomized to treatment with Gross-Kempf nails, 24 with slotted nails and 22 with non-slotted nails. Four complications in the slotted nail group and three in the non-slotted nail group were considered to be independent of the choice of nail and did not affect the end result. Three splinterings of the distal fragment, one resulting in a change of the osteosynthesis implant to a condylar plate, were considered to result from the high stiffness of the non-slotted nail. Osteosynthesis of femoral shaft fractures using slotted nails has not resulted in healing disturbances, which could be accounted for by the high torsional elasticity of the nail; there seems to be no indication for high-stiffness nails in femoral fractures.

The value of the prophylactic use of doxycycline and tinidazole in elective colorectal surgery.

The present study was undertaken in order to compare the effect of different antimicrobial regimens on the incidence of postoperative wound infections after elective colorectal surgery. The series consists of 84 patients, randomized in the following three groups: Group I was treated with bacitracin/neomycin tablets during the 3 days immediately prior to operation. Group II received doxycycline 200 mg orally 12-18 hours preoperatively and 200 mg intravenously during the subsequent 4 days. Group III is identical with group II, but in addition, 2 grams of tinidazole were given orally as a single dose 12-18 hours preoperatively. The ordinary preoperative treatment with low residue diet and bowel cleansing was the same for all groups. The wound infection rate was 37% (10 patients) in group I, 18.2% (6 patients) in group II, and 8.3% (2 patients) in group III. No serious side effects were observed in any of the groups.