Physical activity and sitting time in bariatric surgery patients 1-16 years post-surgery.

Physical activity (PA) is an important adjunct to bariatric surgery in the treatment of severe obesity; however, patient PA levels prior to and in the short-term following surgery are usually low. Scarce data exist describing PA and sedentary behaviours in the long term following surgery. The objectives were to describe PA and sitting time in bariatric patients 1-16 years post-surgery and assess their associations with patient, surgery and weight-loss characteristics. A total of 398 bariatric patients (73% female; mean age 47 ± 11 years, mean 6 ± 4 years since surgery) completed a telephone questionnaire. Patients reported moderate-to-vigorous PA (MVPA: # sessions week(-1) ≥30 min), sitting time (h d(-1)) and change in PA and sitting time vs. pre-surgery (more/same/less). Associations with patient, surgery and weight-loss characteristics were assessed. Only 53% of patients reported ≥1 session week(-1) MVPA, mean sitting time was 7 ± 4 h d(-1), 74% of patients reported more PA and 53% reported less sitting, now vs. pre-surgery. Age, sex, smoking status, pre-surgery body mass index, time-since-surgery and percent excess weight lost were significantly associated with PA and/or sitting outcomes. Patients currently experiencing ≥50% excess weight loss had over three times the odds of reporting ≥1 session week(-1) MVPA (odds ratio [95% confidence interval] 3.28 [1.57, 6.89]) and almost four times greater odds of reporting 'more' PA vs. pre-surgery (3.78 [2.15, 6.62]) compared with their less successful counterparts. Results point to low PA and high sedentariness among bariatric patients in the long-term following surgery, associated with several characteristics. Associations with long-term weight management highlight the need for tailored interventions to promote active living in this patient population.

The role of excess subcutaneous fat in pain and sensory sensitivity in obesity.

BACKGROUND: Previous studies suggest pain sensitivity may be decreased in obesity, but it is unknown whether this is a global or a site-specific phenomenon related to the amount of excess fat. DESIGN: a cross-sectional study comparing obese and non-obese participants on body sites with much and little excess subcutaneous fat in obesity. Hot and cold sensory detection thresholds, pain thresholds, pain tolerance and subjective ratings for a cold (0 °C) and hot (48 °C) stimulus were assessed using a 16 × 16 mm thermode (Medoc, Israel) on the forehead and abdomen. Pressure pain thresholds were measured on the hand. Cold water immersion tolerance duration and subjective ratings were assessed on the hand. Two indices of central pain processing, i.e., temporal summation and heterotopic noxious stimulation, were assessed. RESULTS: A total of 20 obese participants [10M/10F, BMI mean (SD) =41.5 kg/m(2) (9.4 kg/m(2) )] and 20 age- and gender-matched non-obese controls [10M/10F, BMI mean (SD) =23.5 kg/m(2) (2.9 kg/m(2) )] were studied. Compared with non-obese, obese participants had higher thresholds and lower subjective ratings, indexing decreased sensitivity, for painful and non-painful thermal stimuli on the abdomen, an area with much excess subcutaneous fat. Decreases in abdominal sensitivity correlated with measures of adiposity (i.e., waist-to-hip ratio and subcutaneous fat thickness). On areas with little excess subcutaneous fat (forehead and hand), obese and non-obese groups did not differ in measures of thermal or pressure sensitivity, nor for indices of central pain processing. CONCLUSION: Obese participants are less sensitive than non-obese individuals, but only on areas with excess subcutaneous fat.

Soluble L-selectin at levels present in septic patients diminishes leukocyte-endothelial cell interactions in mice in vivo: a mechanism for decreased leukocyte delivery to remote sites in sepsis.

OBJECTIVE: Recent in vivo studies of both septic humans and animals demonstrate that leukocyte delivery is attenuated to sites remote from the primary infection. The mechanisms for this are not entirely clear. L-selectin is integral to rolling, the first step in leukocyte recruitment to an inflammatory site. L-selectin is shed from leukocytes in sepsis, resulting in increased levels of soluble L-selectin in plasma (2.33 microg/mL). This study investigates the effects of soluble L-selectin at levels found in sepsis on leukocyte trafficking in vivo. DESIGN: Prospective, controlled trial. SETTING: Surgical research laboratory in a university hospital. SUBJECTS: Swiss white male mice of 25-35 g. INTERVENTIONS: Mice were randomized to one of three study groups: soluble L-selectin 2.33, soluble L-selectin 8.0, or albumin. Intravital microscopy was performed on postcapillary venules of 20-40 microm in diameter in the cremaster muscle of mice. Leukocyte-endothelial cell interactions (rolling, adherence, and rolling velocity) were measured pre- and post- (1, 15, 30, and 45 mins) intravenous infusion of human recombinant soluble L-selectin (2.33 and 8.0 microg/mL) or human albumin (8.0 microg/mL). MEASUREMENTS AND MAIN RESULTS: The intravenous administration of soluble L-selectin to a systemic concentration of 2.33 microg/mL diminished rolling significantly. Soluble L-selectin at 8.0 microg/mL decreased rolling and increased rolling velocity to a greater degree. Injection of albumin did not alter leukocyte-endothelial cell interactions at any time point. No difference between groups in blood pressure, shear rate, or leukocyte counts was detected. CONCLUSIONS: Soluble L-selectin diminishes leukocyte rolling at levels present in sepsis (2.33 microg/mL). This effect is dose dependent, and could not be explained by differences in blood pressure, shear rate, or leukocyte counts. These findings identify increased soluble L-selectin levels as one of the mechanisms for decreased leukocyte delivery and exudation to remote sites in septic patients.

Results of a clinical trial of clinafloxacin versus imipenem/cilastatin for intraabdominal infections.

OBJECTIVE: Clinafloxacin is a novel quinolone with wide activity against the plethora of microorganisms encountered in intraabdominal infections. This trial was performed to examine its clinical efficacy. SUMMARY BACKGROUND DATA: Clinafloxacin is representative of a new class of quinolones with considerable antimicrobial activity resulting from their mechanisms of action and pharmacodynamics. There is, however, concern about specific potential toxicities, including photosensitivity. METHODS: This prospective, randomized, double-blind trial was conducted to compare clinafloxacin with imipenem/cilastatin as adjuncts in the management of complicated intraabdominal infections. RESULTS: Five hundred twenty-nine patients were included in the intent-to-treat population, with 312 meeting all criteria for the valid population. Patients with a wide range of infections were enrolled; perforated or abscessed appendicitis was the most common (approximately 50%). One hundred twenty-three of the 150 valid patients treated with clinafloxacin (82%) had successful outcomes, as did 130 of the 162 (80%) treated with imipenem. For the intent-to-treat groups, 219 of 259 patients treated with clinafloxacin (85%) had successful outcomes, as did 219 of 270 patients treated with imipenem/cilastatin (81%). Treatment failure occurred in 39 patients who underwent drainage. There were substantially more gram-negative organisms recovered from the patients with treatment failure who were initially treated with imipenem/cilastatin. CONCLUSIONS: The results of this study clearly demonstrate the safety and efficacy of clinafloxacin in the treatment of a range of intraabdominal infections, and in patients with a broad range of physiologic disturbances.

Hemorrhagic shock resuscitation with a low molecular weight starch reduces neutrophil-endothelial interactions and vessel leakage in vivo.

BACKGROUND: The polymorphonuclear neutrophil (PMN) has been implicated in the pathogenesis of endothelial cell (EC) damage and organ injury following hemorrhagic shock. Pentastarch (PTS), a low substituted medium molecular weight (MW) colloid, improves hemodynamics in hypovolemic shock and cardiac surgery. No data exist comparing the immunomodulation of PTS and Ringer's lactate (RL) on the activation of PMN in hemorrhagic shock in vivo. METHODS: Using an in vivo murine hemorrhagic shock model (blood withdrawal to maintain 50 mmHg x 45 min), circulating PMN were observed every 15 minutes using intravital microscopy on cremaster muscle. EC-PMN interactions (videorecorded and subsequently analyzed blindly), vessel leakage (live epifluorescence after injection of 50 mg/kg fluorescent albumin) and PMN expression of L-selectin (immunofluorescent monoclonal antibodies and flow cytometry) were evaluated in three resuscitation groups: PTS (7.14 mL/kg 10% pentastarch/0.9% NaCl + shed blood, n = 13), RL (RL [2 x shed blood volume] + shed blood, n = 13) and SHAM (0 hemorrhage, 0 resuscitation, n = 9). Significance was evaluated by ANOVA with Bonferroni correction. RESULTS: PMN rolling was significantly diminished in PTS and SHAM as compared to RL animals at all time points. Similar differences were found in PMN adherence to EC at most time points onwards from 15 minutes following resuscitation. In vivo vessel permeability was lowest in SHAM and PTS animals (mean 0.274 +/- 0.07 and 0.356 +/- 0.15, respectively, p > 0.05) and highest in RL animals (0.667 +/- 0.09, p < 0.001 vs PTS or SHAM). PMN L-selectin expression tended to be higher in the RL group than either SHAM and PTS groups. There were no flow-mechanics differences between groups (vessel diameter, mean red cell velocity, shear stress, shear rate). CONCLUSIONS: 10% pentastarch reduces RL-associated EC-PMN interactions and vessel leakage following hemorrhagic shock. These results support the use of low MW starches to resuscitate hemorrhagic shock, potentially reducing PMN-mediated tissue injury.

Plasma complement C5 protects endothelial cells from polymorphonuclear neutrophil-derived, H2O2-mediated cytotoxicity.

BACKGROUND: In vitro studies suggest that polymorphonuclear neutrophils (PMN) can damage endothelial cells (EC) by releasing hydrogen peroxide. In vivo this can lead to anasarca secondary to capillary leakage of fluid, protein, and electrolytes. The result is multiple organ dysfunction syndrome, which is associated with high mortality. In vivo, circulating PMN-EC interactions take place in the presence of plasma, and we have shown previously that plasma affords protection to EC from PMN-mediated damage. METHODS: Human umbilical vein endothelial cells were primed with cytokines, cultured to a confluent monolayer, and coincubated with normal human PMNs. Cytotoxicity was assayed by gamma scintigraphy, plasma C5 was determined by sepharose column elution, and H(2)O(2) was assayed by R-Phycoerythrin fluorescence. RESULTS: Addition of C5, but not C3, to RPMI resulted in EC cytoprotection equivalent to adding whole serum. Removal of C5 from serum using F(ab')(2) rabbit IgG anti-human C5 coupled to CNBr-activated 4 sepharose beads resulted in significant loss of EC cytoprotection against H(2)O(2)-mediated damage, whereas adding back C5 restored the cytoprotection. C5 also reduced H(2)O(2)-mediated destruction of R-Phycoerythrin. CONCLUSIONS: The data suggest that the protection of EC against hydrogen peroxide-mediated damage is partly mediated through complement component C5.

Multiple organ dysfunction syndrome: exploring the paradigm of complex nonlinear systems.

OBJECTIVES: The objectives of this article are to introduce and explore a novel paradigm based on complex nonlinear systems, and to evaluate its application to critical care research regarding the systemic host response and multiple organ dysfunction syndrome (MODS). DATA SOURCES: Published original work, review articles, scientific abstracts and books, as well as our personal files. STUDY SELECTION: Studies were selected for their relevance to the applications of nonlinear complex systems, to critical care medicine, and to the concepts presented. DATA EXTRACTION: We extracted all applicable data. DATA SYNTHESIS: Following a brief review of MODS, an introduction to complex nonlinear systems is presented, including clear concepts, definitions, and properties. By examining the multiple, nonlinear, interrelated, and variable interactions between the metabolic, neural, endocrine, immune, and inflammatory systems; data regarding interconnected antibody networks; and the redundant, nonlinear, interdependent nature of the inflammatory response, we present the hypothesis that the systemic host response to trauma, shock, or sepsis must be evaluated as a complex nonlinear system. This model provides a new explanation for the failure of trials using various antimediator therapies in the treatment of patients with sepsis and MODS. Understanding the host response as a complex nonlinear system offers innovative means of studying critical care patients, specifically by suggesting a greater focus on systemic properties. We hypothesize that analysis of variability and connectivity of individual variables offer a novel means of evaluating and differentiating the systemic properties of a complex nonlinear system. Current applications of evaluating variability and connectivity are discussed, and insights regarding future research are offered. CONCLUSION: The paradigm offered by the study of complex nonlinear systems suggests new insights to pursue research to evaluate, monitor, and treat patients with MODS.

Decreased systemic polymorphonuclear neutrophil (PMN) rolling without increased PMN adhesion in peritonitis at remote sites.

BACKGROUND: Previous in vitro studies have demonstrated that the host response to intra-abdominal infection produces increased generalized polymorphonuclear neutrophil (PMN) adherence to vascular endothelial cells (ECs), which may lead to subsequent endothelial damage, leaky capillaries, and organ dysfunction. There are scant data to demonstrate this enhanced systemic PMN adherence in vivo or the influence of PMN rolling on PMN endothelial adherence. HYPOTHESIS: Systemic PMN adherence in the animal with sepsis is increased. DESIGN: In vivo murine model of a 2-front infection using intravital microscopy of the cremasteric muscle to quantify PMN-EC adherence in a septic response. SETTING: Basic science laboratory and animal surgical facility. PATIENTS OR OTHER PARTICIPANTS: One hundred CD1 male mice. INTERVENTIONS: Animals underwent cecal ligation and puncture peritonitis, cremasteric muscle Escherichia coli infection, both infections, or neither (controls). Eighteen hours later, the mice underwent exteriorization of the cremasteric muscle under an intravital microscope for measurement of PMN-EC interactions. Blood was then drawn for calculation of circulating PMN counts. MAIN OUTCOME MEASURES: Adherence of PMNs, PMN rolling flux, PMN rolling velocity, and circulating PMN counts. RESULTS: Circulatory mechanics did not differ between the groups. Unlike static in vitro systems, we could not detect an increase in PMN adherence after peritonitis with this dynamic in vivo model. A local (cremasteric) infection was associated with marked PMN adherence. Peritonitis was associated with reduced PMN adherence at a local infection site as well as reduced rolling adhesion and PMN rolling velocity. CONCLUSIONS: The data suggest that intra-abdominal infection does not increase remote PMN adherence, and may actually result in reduction of systemic adherence via modulation of PMN rolling.

Polymorphonuclear neutrophil (PMN) recruitment in a 2-front murine injury model: triage of PMNs to competing stimuli of recruitment.

BACKGROUND: Intensive care unit patients as a group have the highest rate of nosocomial infections, such as pneumonia, urinary tract infections, and wound infections. The triage of polymorphonuclear neutrophils (PMNs) during an acute inflammatory response was investigated to determine if the severity of injury or infection contributes to PMN delivery. METHODS: A murine cecal ligation and puncture-induced peritonitis model with polyvinyl sponge discs were used to collect the PMNs in the abdomen (primary site) and in the subcutaneous tissue of the dorsum (remote site). Eighty CD1 male mice--20 in each of 4 groups--were assigned to the following: cecal ligation and puncture (CLP), sham laparotomy with cecal manipulation (CM), polyvinyl sponge placement in the abdomen and back only (SP), and sponge placement in the back alone (CON [control]). After 24 hours, the sponges were harvested, and the PMNs were collected and counted on a hemocytometer. RESULTS: These data, reported as mean PMN cells x 10(5) +/- SEM, demonstrated that back sponges contained significantly fewer PMNs in the CLP group (3.29 +/- 1.1) than in the CM group (7.77 +/- 1.61, P = .04), the SP group (8.69 +/- 1.67, P = .01), and the CON group (11.04 +/- 1.91, P < .001). CONCLUSIONS: These results demonstrate that PMN delivery to sites of secondary injury are inversely correlated to the severity of the primary injury or peritonitis.

Mechanisms for the diminished neutrophil exudation to secondary inflammatory sites in infected patients with a systemic inflammatory response (sepsis).

OBJECTIVE: To determine the mechanism for the reduced polymorphonuclear neutrophil exudation to secondary inflammatory sites in critically ill patients with infection and systemic inflammatory response (sepsis). DESIGN: Prospective cohort study. SETTING: Research laboratory and integrated intensive care unit of a tertiary care university-affiliated teaching hospital. PATIENTS: Healthy subjects or critically ill patients with confirmed infection and a systemic inflammatory response (septic patients). MEASUREMENTS AND MAIN RESULTS: We found that polymorphonuclear neutrophil delivery to a secondary inflammatory site (skin window blisters) is reduced by >70% in humans with sepsis, defined as serious infection and a systemic inflammatory response compared with healthy controls. The expression of the endothelial adhesion molecules intercellular adhesion molecule-1, E-selectin and P-selectin in microvessels from skin biopsies was comparable in the two study groups. Also, CD11a and CD11b levels were equal in circulating polymorphonuclear neutrophils (PMNs) from both study groups. Both adhesion molecules were markedly and equally up-regulated during exudation. Circulating PMNs from septic patients showed marked shedding of L-selectin compared to those of healthy controls, with a corresponding increase in their plasma L-selectin levels. An increased concentration gradient between plasma and exudate fluid was found for tumor necrosis factor-alpha and interleukin-8 in septic patients, but not for C5a. The phagocytic and bactericidal capacity of septic patient circulating PMNs was higher then in healthy control patients, but these differences were lost after exudation. There were no major differences in oxidative burst or intracellular calcium flux of circulating PMNs from the two study groups. Polymorphonuclear neutrophil exudation primed both responses to different extents. CONCLUSIONS: Septic patients deliver fewer PMNs to secondary inflammatory sites. In addition, neutrophil exudation results in loss of the small priming effect for phagocytosis and bactericidal function induced by sepsis. Failure to produce a gradient to C5a and intravascular shedding of L-selectin may be responsible for this sepsis-induced reduction in neutrophil exudation to secondary inflammatory sites.

Iron absorption and therapy after gastric bypass.

BACKGROUND: Iron deficiency anemia is a common complication of gastric bypass. The authors assessed the value of taking vitamin C with oral iron in correcting deficiencies in iron stores and anemia postoperatively. MATERIALS AND METHODS: Iron absorption tests were performed on 55 patients 3.2+/-2.0 years after isolated gastric bypass to identify those at higher risk for the late development of anemia. Twenty-nine of this group agreed to a therapeutic trial of iron alone or with vitamin C over a 2-month period. All 55 patients were followed up for 27.1+/-1.0 months following the study. RESULTS: The iron absorption test identified patients with low iron stores, as indicated by low serum ferritin, and those with sufficient absorption surface to benefit from oral iron. The addition of vitamin C appears to enhance the therapeutic effect of iron by correcting ferritin deficits (P < 0.01) and anemia (P < 0.05). Differences in intestine length bypassed by the operation (10 vs. 100 cm) did not affect late ferritin and hemoglobin values. CONCLUSION: This study suggests but does not prove that the addition of vitamin C to iron therapy after gastric bypass is more effective in restoring ferritin and hemoglobin than iron alone. These results are in contrast with the outcome 22.8 months later, when approximately 50% of study patients were again anemic. Closer follow-up of patients is urgently needed.

Reduction in neutrophil cell surface expression of tumor necrosis factor receptors but not Fas after transmigration: implications for the regulation of neutrophil apoptosis.

OBJECTIVES: To test the hypothesis that loss of polymorphonuclear neutrophil tumor necrosis factor alpha (TNF-alpha) receptors during transmigration renders the exudate neutrophil refractory to TNF-alpha-mediated stimulation of apoptosis; and to investigate the surface expression of Fas on both circulating and exudate neutrophils. DESIGN: A prospective cohort study. SETTING: Surgical laboratory of a tertiary care hospital. PARTICIPANTS: Twenty-one healthy human volunteers. INTERVENTIONS: All subjects had circulating neutrophils and exudate neutrophils collected by venipuncture and skin window methods, respectively. MAIN OUTCOME MEASURES: Circulating and exudate neutrophils were incubated in culture medium (1.0x10(6) neutrophils per milliliter) alone or with TNF-alpha (100 ng/mL). Apoptosis was evaluated by flow cytometry (annexin V-fluorescein isothiocyanate and propidium iodide). Tumor necrosis factor alpha-phycoerythrin and anti-human Fas-fluorescein isothiocyanate were used to evaluate neutrophil TNF-alpha receptors and surface expression of Fas. RESULTS: Exudate neutrophils had a significant delay in apoptosis rates when compared with circulating neutrophils. The percentage of neutrophils expressing TNF-alpha receptors was significantly diminished after exudation (80%+/-15% vs 33%+/-9%; P<.001), as was the median channel number of TNF-alpha phycoerythrin fluorescence (8.1+/-1.6 vs 5.2+/-0.5; P=.001). However, the expression of Fas was unchanged after transmigration (percentage positive for Fas: 98.7%+/-0.7% vs 92.8%+/-3.4%, P=.89; Fas antibody-fluorescein isothiocyanate median channel fluorescence: 12.2+/-1.1 vs 13.1+/-1.2; P=.80). Exposure of exudate neutrophils to TNF-alpha failed to increase their rate of apoptosis. CONCLUSIONS: Exudate polymorphonuclear neutrophils are confirmed to have delayed apoptosis. Loss of TNF-alpha receptors during transmigration is necessary for neutrophil survival in the extravascular inflammatory milieu.

Increased plasma von Willebrand factor in the systemic inflammatory response syndrome is derived from generalized endothelial cell activation.

OBJECTIVES: Von Willebrand factor antigen (vWf) is an essential hemostatic protein. Increased plasma levels have been documented in patients suffering from the systemic inflammatory response syndrome (SIRS) and resulted presumably from endothelial cell damage specific to the site of injury. We hypothesize that increased plasma levels result from systemic endothelial cell activation and degranulation. DESIGN: We compared immunohistochemical vWf staining in dermal biopsy specimens from patients with SIRS to healthy control subjects in the presence and absence of recombinant human tumor necrosis factor (rhTNF)-alpha. Also, we quantified plasma levels of vWf in these groups using a newly available antibody. SETTING: A tertiary care surgical intensive care unit in a university teaching hospital. SUBJECTS: Patients with SIRS and healthy controls. INTERVENTIONS: Biopsies and blood samples were obtained from study groups. MEASUREMENTS AND MAIN RESULTS: Decreased baseline vWf staining was noted in SIRS patients. The rhTNF-alpha caused a statistically significant decrease in vWf staining in control subjects but not in SIRS patients. Plasma vWf levels were increased an average of 11-fold in SIRS patients compared with control subjects. CONCLUSION: We postulate that the increased plasma levels of vWf and the decreased staining in the peripheral dermal plexus represent the generalized activation and degranulation of endothelium in vascular beds remote from the original inflammatory focus.

Protective effect of plasma in polymorphonuclear neutrophil-mediated cytotoxicity of endothelial cells in the systemic inflammatory response syndrome.

Polymorphonuclear neutrophil (PMN)-mediated endothelial cell (EC) cytotoxicity is well described in many in vitro systems. These observations have been extended in vivo and suggest that circulating PMNs adherent to endothelial cells can damage these endothelial cells and produce the capillary leak that is central to the evolution of a systemic inflammatory response to multiple organ failure. However, most PMC-EC interactions in the circulation must occur in the presence of plasma, therefore we studied PMN-induced endothelial cell cytotoxicity in the absence and presence of autologous plasma from healthy human volunteers and patients with the systemic inflammatory response syndrome (SIRS) requiring admission to an intensive care unit. PMNs from patients with SIRS had increased endothelial cell adherence compared with controls, but equivalent endothelial cell cytotoxicity. Endothelial cell activation with TNF-alpha and IL-1beta markedly increased PMN adherence to endothelial cells. Plasma had a minimal effect on the adherence of PMNs to endothelial cells at baseline or after endothelial cell activation. In contrast, plasma provided endothelial cells with almost complete protection from PMN-induced cytotoxicity at baseline, as well as after endothelial cell activation in both human volunteers and patients with SIRS. The data suggest that PMNs may cause cytotoxic damage in end organs such as the lung only after they diapedese through the endothelial barrier into the extracellular matrix removed from the protective effect of circulating plasma.

Endothelial cells: role in infection and inflammation.

Infection and resulting sepsis continue to be important causes of morbidity and mortality in surgical patients. Although much has been learned about the pathogens and the leukocyte responses to these pathogens, we are only beginning to understand the role of the host in these pathologies. The endothelium is a dynamic participant in cellular and organ function rather than a static barrier as it was once believed. Emerging evidence implicates the endothelium as a central effector in the inflammatory response. Through the expression of surface proteins and secretion of soluble mediators, the endothelium controls vascular tone and permeability, regulates coagulation and thrombosis, and directs the passage of leukocytes into areas of inflammation. Derangements in these normal functions may contribute significantly to a maladaptive inflammatory response leading to systemic inflammation and multiple organ failure.

Association between preoperative acute phase response and postoperative complications.

OBJECTIVE: To find out if there is an association between the acute phase response preoperatively and the development of postoperative infective complications. DESIGN: Prospective open study. SETTING: Teaching hospital Germany. SUBJECTS: 229 patients who were to undergo major abdominal operations. INTERVENTIONS: Measurements of serum concentrations of interleukin 6 (IL-6), alpha-1-antitrypsin, C-reactive protein (CRP), albumin, and prealbumin. MAIN OUTCOME MEASURES: Abnormal values of substances measured. RESULTS: Serum concentrations of IL-6, alpha-1-antitrypsin and CRP were raised, and those of albumin and prealbumin were reduced in 5% to 14% of patients. 25 (11%) developed major complications, of whom 9 (4%) died. 9 Patients (4%) had a severe systemic inflammatory response caused by infective complications that did not result from technical failure of the operative technique. Of these 9 patients, 7 (78%) already had signs of an increased acute phase response before operation that was significantly different from the incidence among patients who recovered without complications (21/204. p < 0.001) CONCLUSION: These data suggest that if there are signs of an acute phase response preoperatively the patient's response to operation and infection during the postoperative period may be adversely affected.

Decreased neutrophil L-selectin expression in patients with systemic inflammatory response syndrome.

OBJECTIVE: To determine whether the expression of L-selectin is reduced in patients with systemic inflammatory response syndrome (SIRS) compared with control subjects, to test the effect of exudation of neutrophil L-selectin expression, and to measure soluble serum concentrations of shed L-selectin in the two groups. DESIGN: Prospective study. SETTING: Intensive care unit in a tertiary care hospital (Royal Victoria Hospital, Montreal). PATIENTS: Twenty-five patients with SIRS and 20 healthy, age-matched controls. INTERVENTIONS: Collection of exudate neutrophils from skin window and circulating neutrophils from venous blood. OUTCOME MEASURES: Neutrophil L-selectin levels, measured with the use of fluorocytometry, and soluble L-selectin levels, measured with the use of enzymelinked immunosorbent assay. RESULTS: There is a significant reduction in L-selectin expression on circulating neutrophils in patients with SIRS, compared with control subjects. Exudation of neutrophils to an extravascular site resulted in a dramatic down-regulation of L-selectin in both groups. Serum levels of soluble L-selectin were higher in patients with SIRS than in control subjects. CONCLUSIONS: The loss of L-selectin may be partly responsible for reduced neutrophil exudation to extravascular sites in patients with SIRS.