Intervention-related increases in preoperative physical activity are maintained 6-months after Bariatric surgery: results from the bari-active trial.

Higher preoperative physical activity (PA) strongly predicts higher post-operative PA in bariatric surgery (BS) patients, providing rationale for preoperative PA interventions (PAIs). However, whether PAI-related increases can be maintained post-operatively has not been examined. This study compared PA changes across pre- (baseline, post-intervention) and post-operative (6-month follow up) periods in participants randomized to 6 weeks of preoperative PAI or standard care control (SC). Of 75 participants initially randomized, 36 (PAI n=22; SC n=14) underwent BS. Changes in daily bout-related (⩾10-min bouts) moderate-to-vigorous PA (MVPA) and steps were assessed via the SenseWear Armband monitor. PAI received weekly counseling to increase walking exercise. Retention (86%) at post-operative follow up was similar between groups. Intent-to-treat analyses showed that PAI vs SC had greater increases across time (baseline, post-intervention, follow up) in bout-related MVPA minutes/day (4.3±5.1, 26.3±21.3, 28.7±26.3 vs 10.4±22.9, 11.4±16.0, 18.5±28.2; P=0.013) and steps/day (5163±2901, 7950±3286, 7870±3936 vs 5163±2901, 5601±3368, 5087±2603; P<0.001). PAI differed from SC on bout-related MVPA at post-intervention (P=0.016; d=0.91), but not follow up (P=0.15; d=0.41), and steps at post-intervention (P=0.031; d=0.78) and follow up (P=0.024; d=0.84). PAI participants maintained preoperative PA increases post-operatively. Findings support preoperative PAIs and research to test whether PA changes can be sustained and influence surgical outcomes beyond the initial post-operative period.

Intestinal adaptation and amino acid transport following massive enterectomy.

Morphological and physiological adaptation in residual small intestine occurs after massive enterectomy and is influenced significantly by different growth factors and hormones. The mechanism of adaptation occurs through hypertrophy and hyperplasia as well as nutrient transporter changes. These transporters are classified into different classes dependent on its biological properties. The adaptation process evolves over time and different nutrient absorption profiles occur at different postoperative stages. There is an initial decrease in amino acid transport after resection followed by a return to approximately normal levels. Glucose also follows a similar pattern of changes but returns to normal later than amino acids. The time course of these changes are different for different animals with rat adaptation being much faster than rabbit. Growth hormone (GH) induces increased amino acid transport during this adaptation period, however, appears not to affect small intestine hypertrophy or hyperplasia. The increase in transport occurs via an increase in transport numbers rather than affinity. Epidermal growth factor (EGF) also increases amino acid transport in postoperative animals. Its advantage is it is orally stable when given with a protease inhibitor. EGF also reverses the down-regulating effects of the somatostatin analogue Octreotide (SMS) post resection. EGF in combination with GH has additive effects. However, the effects of the growth factors are site specific. GH and EGF combination therapy significantly increased alanine and arginine transport in distal small bowel after 70 % enterectomy but not in the proximal small bowel. The same combination increases leucine and glutamine transport in the proximal small intestine only. Understanding the specific changes that occur with these therapies may improve quality of life for patients and also reduce that need for total parenteral nutrition.

Hepatic steatosis in total parenteral nutrition: failure of fatty infiltration to correlate with abnormal serum hepatic enzyme levels.

Total parenteral nutrition (TPN) is associated with hepatic biochemical and morphologic changes. Suggested causes include excessive glucose calories, fatty acid deficiency, and enterically derived hepatotoxins escaping atrophied bowel. Male Sprague-Dawley rats were cannulated or sham operated with internal jugular ligation. The cannulated groups received TPN with a 25% dextrose base, or TPN 12.5% dextrose and given nothing by mouth, or saline solution and allowed to eat ad lib. Sham animals ate ad lib. After 6 days the animals were killed and portal blood was assayed for endotoxin and cultured. Cultures were also taken of the liver. Serum hepatic enzyme concentration and hepatic fat were determined. All cultures and endotoxin assays were negative. Microscopy revealed nonlipid vacuolization in both TPN groups, a finding reproduced by direct portal infusion of endotoxin. There was significant hepatic steatosis in the 25% dextrose base TPN versus all other groups (28.6% liver weight versus 6.3% liver weight; p less than 0.05). This was correlated with caloric intake (28.7 calories/100 gm/day versus 21.2 calories/100 gm/day; p less than 0.05). Liver enzymes were not significantly different among groups. We conclude that hepatic steatosis in TPN is a result of overfeeding a glucose only substrate and that fatty infiltration is independent of changes in blood hepatic enzyme concentrations. Although other morphologic changes of hepatotoxin-induced injury were seen in the TPN group, portal endotoxemia to the level of 1 ng/ml could not be documented.

Total parenteral nutrition-induced changes in gut mucosal function: atrophy alone is not the issue.

BACKGROUND: Total parenteral nutrition (TPN) has been implicated in gut atrophy and breakdown of barrier function leading to bacterial translocation (BT) in animals. BT during TPN, however, is not found consistently, and it has therefore been suggested that macromolecular permeability may occur independently of BT during TPN. METHODS: Male Sprague-Dawley rats were administered isocaloric standard TPN enterally, parenterally, or split equally between the two routes or allowed food ad lib. A second group of rats was administered isocaloric TPN with and without 4% lipids, and changes in gut barrier function were assessed by measuring lactulose permeability. RESULTS: Rats receiving TPN both enterally and parenterally maintained histologic intestinal structure to the same degree as rats fed enterally and those allowed food. Although parenteral feeding led to significant gut atrophy and cecal bacterial overgrowth, BT was not increased. Gut permeability to lactulose, however, was increased significantly in the TPN groups. Lipid content did not affect outcome. CONCLUSIONS: These results suggest that gut atrophy, BT, and permeability to macromolecules are not necessarily related. Gut-origin septic states during TPN or trauma may be caused by an increased escape of macromolecules from the gut, and BT may be an end result rather than a primary cause of such septic episodes.

Starvation induces differential small bowel luminal amino acid transport.

BACKGROUND: The importance of small intestinal mucosa functions has been emphasized in recent years because gut metabolism becomes better defined. One of the major activities of the enterocyte is amino acid transport, which is important not only for the organism but also for the integrity of the mucosa. Bowel rest during the postoperative period is marked by decreased calorie and protein intake with atrophy of the brush border mucosa. We sought to determine whether active amino acid transport is altered during 72 hours of fasting. METHODS: New Zealand white rabbits were fed (control) or fasted for 72 hours. Brush border membrane vesicles were prepared from scraped jejunal mucosa, and their purity was assessed by marker enzyme enrichment (17- to 25-fold). Transport of tritiated glutamine, arginine, alanine, methylamino-isobutyric acid (MeAIB), and leucine into brush border membrane vesicles was measured by rapid mixing filtration. RESULTS: Fasted animals lost on average 138 +/- 51 gm of body weight. Glutamine and arginine transport were decreased in rabbits fasted for 72 hours compared with controls; alanine, MeAIB, and leucine transport were maintained. The decrease in Glutamine transport was due to a decrease in Vmax (545 +/- 22 versus 836 +/- 93 pmol/mg protein/10 sec; p < 0.05), consistent with a decrease in the number of functional transporter proteins. Km values were similar in both groups (644 +/- 25 versus 624 +/- 18 mumol/L), indicating no change in carrier affinity. CONCLUSION: Differential changes occur in brush border amino acid transport during a 3-day period of bowel rest. The apparent gut nutritive transporters for Glutamine and arginine are decreased, although the gluconeogenic transporters for alanine, MeAIB, and leucine are maintained. These adaptive changes may help explain the difficulties seen in postoperative and critically ill patients on prolonged bowel rest.

Sequential alterations in gut mucosal amino acid and glucose transport after 70% small bowel resection.

BACKGROUND: Studies in animals with short bowel syndrome (SBS) suggest that up-regulation of nutrient transporter activity occurs as an adaptive response to the loss of absorptive area. It is unclear, however, whether nutrient transport is altered at the cell membrane in SBS. The purpose of this study is to clarify amino acid and glucose transport in small intestinal luminal mucosa after 70% small bowel resection in rabbits. METHODS: New Zealand white rabbits underwent 70% jejunoileal resection (n = 27) or a sham operation (n = 19). Brush border membrane vesicles were prepared from small intestinal mucosa at 1 week, 1 month, and 3 months by magnesium aggregation-differential centrifugation. Transport of L-glutamine, L-alanine, L-leucine, L-arginine, and D-glucose was assayed by a rapid mixing-filtration technique. RESULTS: We observed no difference in uptake of all amino acids and glucose at 1 week. The uptake of amino acids and glucose was decreased by 20% to 80% in animals with SBS at 1 month. By 3 months all uptake values except that of glucose returned to normal. Kinetic studies of the system B transporter for glutamine indicate that the decrease in uptake at 1 month was caused by a reduction in the Vmax (1575 +/- 146 versus 2366 +/- 235, p < 0.05) consistent with a decrease in the number of functional carriers on the brush border membrane. CONCLUSIONS: In addition to the anatomic loss of absorptive area after massive bowel resection, alterations in enterocyte transport function may be responsible for malabsorption in patients with SBS.

Epidermal growth factor and human growth hormone accelerate adaptation after massive enterectomy in an additive, nutrient-dependent, and site-specific fashion.

BACKGROUND: After massive enterectomy (ME), remnant intestine undergoes compensatory adaptation. Epidermal growth factor (EGF) and human growth hormone (hGH) have each been shown to enhance total length small intestine nutrient transport after ME. This study aims to determine the differential effects of EGF and hGH on proximal and distal small intestinal remnants after ME. METHODS: New Zealand white rabbits underwent 70% mid-jejunoileal resection. After 1 week, animals received hGH (0.2 mg/kg/day), EGF (1.5 micrograms/kg/hr), hGH + EGF, or vehicle (equal volume) for 7 days. Sodium-dependent uptake of glucose, glutamine, alanine, leucine, and arginine into brush border membrane vesicles was quantitated. Serum insulin-like growth factor-I concentrations as well as proximal and distal villus and microvillus heights were measured. IGF binding protein-3 and -4 mRNA expression was determined in full-thickness proximal and distal gut remnants. RESULTS: Concomitant hGH and EGF treatment up-regulates glucose (100%), glutamine (80%), and leucine (60%) transport in the proximal remnant; alanine (150%) and arginine (400%) transport in the distal remnant; and microvillus height (25% to 35%) both proximally and distally. Serum IGF-I levels and gross villus heights were not different among groups. CONCLUSIONS: Co-infusion of hGH and EGF accelerates intestinal adaptation after ME in an additive, nutrient-dependent, and site-specific fashion via enhanced nutrient transport as well as microvillus hypertrophy.

Characterization of L-leucine transport system in brush border membranes from human and rabbit small intestine.

The branched-chain amino acids (BCAAs) leucine, isoleucine, and valine are beneficial to catabolic patients by improving hepatic protein synthesis and nitrogen economy, yet their transport from the intestinal lumen is not well-defined. The leucine transport system in human and rabbit small intestine was characterized using a brush border membrane vesicle (BBMV) model. Sodium and pH dependence and transport activity along the longitudinal axis of the small bowel were determined. Transport kinetics and inhibition profiles were defined. Although previous studies in other tissues show leucine transport to be mostly a Na+-independent process, our studies show that leucine transport is a predominantly Na+-dependent process occurring mainly via a single saturable pH-independent transporter resembling system B0 in the intestine. This system B0 transporter demonstrates stereoisomeric specificity. There is also a minor Na+-independent transport component (<6% in rabbits). Leucine uptake in both rabbits and humans is significantly greater than the uptake of other clinically relevant nutrients such as glutamine. In the rabbit, ileal leucine transport is significantly greater than jejunal uptake. While the affinities of the human and rabbit transporters are similar, the rabbit transporter has greater carrier capacity (maximal transport velocity [Vmax]). These findings suggest that the transport of leucine in the gut mucosa is significantly different from the transport in other tissues.

Clinical use of branched-chain amino acids in liver disease, sepsis, trauma, and burns.

The branched-chain amino acids (BCAAs)--leucine, isoleucine, and valine--share unique biochemical properties that may make them useful in altered physiologic states. They can be metabolized independently of liver function to provide energy, other amino acids, or small nitrogenous compounds. This unique ability makes the BCAAs a desirable supplement in liver disease with encephalopathy and, to a lesser extent, in sepsis with hepatic dysfunction. Furthermore, the BCAAs play a role in the regulation of protein synthesis, suggesting beneficial effects in catabolic states such as postoperative stress, trauma, renal failure, and burns. However, initial studies in these areas have presented equivocal results.

Current concepts of protein turnover and amino acid transport in liver and skeletal muscle during sepsis.

The metabolic response to trauma and sepsis is characterized by a negative nitrogen balance, accelerated muscle proteolysis, increased ureagenesis, and stimulated acute-phase protein synthesis in liver. Inhibited uptake of amino acids and accelerated protein breakdown in muscle increase the flux of amino acids from the periphery to the liver. Concomitantly, hepatic uptake of amino acids is stimulated and protein synthesis and gluconeogenesis in the liver are enhanced. These events are important to the survival of patients with sepsis. Stimulated ureagenesis resulting in nitrogen loss from the body is another important aspect of hepatic nitrogen metabolism following trauma and sepsis. The mediator(s) initiating metabolic changes is not yet exactly defined, although regulatory protein(s) released from stimulated macrophages (particularly interleukin 1 and tumor necrosis factor) may play a major role in altered amino acid and protein metabolism in muscle and liver during sepsis. However, these factors alone are probably not responsible for the metabolic disturbances, since the catabolic hormones cortisol, glucagon, and the catecholamines can simulate the metabolic pattern observed in sepsis. Other possible mediators include prostaglandins and thyroid hormones. It is possible that the interaction between different types of mediators is necessary for the full manifestation of host responses to severe injury and sepsis.

Postoperative enteral vs parenteral nutrition. A randomized controlled trial.

Twenty patients undergoing major upper-gastrointestinal-tract or pancreaticobiliary surgery were randomized to receive postoperative nutritional support by total parenteral nutrition (TPN) or elemental diet administered by needle-catheter jejunostomy (NCJ). Both routes of administration provided adequate nutritional support. No unexpected complications were encountered. The NCJ group compared favorably with the TPN group at the end of the seven-day trial. The NCJ group provided significant cost efficiency while maintaining adequate nutritional support.

Preoperative fasting improves survival after 90% hepatectomy.

OBJECTIVE: To assess whether alterations in preoperative fatty acid oxidation and gluconeogenesis induced by fasting will affect survival and liver regeneration following 90% hepatectomy in the rat. DESIGN: In a randomized, controlled trial, Wistar rats (N = 157) were separated into two groups. Rats in the first group fasted for 24 hours. Rats in the second group were allowed to eat ad libitum until the time of operation. These groups were further randomized to receive either 20% glucose or tap water ad libitum postoperatively. INTERVENTIONS: Ninety percent hepatectomy; 24-hour fast; 5% glucose feeding. MAIN OUTCOME MEASURES: Survival, DNA synthesis in the hepatic remnant along with glucokinase activity (GKA) and glycogen content, serum ketone bodies (KB), free fatty acid (FFA), glucose, and ad libitum glucose consumption (GC) were serially quantified. RESULTS: Fasting rats that were offered glucose (fasted/glucose) after hepatectomy demonstrated better survival at 48 hours than the rats that were fed before the procedure and given glucose following hepatectomy (fed/glucose), 95% vs 52% (P < .05). The fasted/glucose group also had a greater peak rate of DNA synthesis (550 +/- 110 vs 275 +/- 40 disintegrations per minute per 0.001 mg of DNA, P < .05). Survival was poor in both groups when only tap water was offered to the animals after hepatectomy (31% vs 12%). In the fasted/glucose group, GC 1 hour after hepatectomy was greater than that for fed rats (1.3 +/- 0.175 vs 0.73 +/- 0.176 g/h, P < .05), yet GKA was suppressed (3.4 +/- 0.42 vs 8.05 +/- 2.77 nmol/min per milligrams of protein, P < .05). Fasting before hepatectomy and consuming glucose after causes elevations in both FFA (1.26 +/- 0.19 vs 0.82 +/- 0.13 mol/mL., P < .05) and KB (18.96 +/- 2.82 vs 11.4 +/- 3.94 mmol/mL, P < .05). Normal glucose was maintained in the fasted/glucose group, but fell to 63 +/- 14 mg/dL at 8 hours after hepatectomy in the fed/glucose group. CONCLUSIONS: Fasting before hepatectomy shifts energy utilization to fat oxidation and gluconeogenesis, which appears to ameliorate liver failure after hepatectomy in this severe model of hepatic resection.

Incidental appendectomy in the era of managed care and laparoscopy.

BACKGROUND: In a study carried out before laparoscopy or managed care, there was no cost or patient benefit for routine incidental appendectomy. With the onset oflaparoscopy, a change in indications for surgery, and increased prevalence of capitated contracts, a reanalysis of the cost-effectiveness of incidental appendectomy is warranted. STUDY DESIGN: Financial data from 251 patients undergoing appendectomy for acute appendicitis without complication at a single institution were identified. Age-specific epidemiology data from the Centers for Disease Control, Atlanta, were applied to assess risk and cost of future appendectomy. The net cost or savings for incidental appendectomies necessary to prevent one case of acute appendectomy was determined and stratified by gender and age to the population as a whole. Further adjustment was made for the variable level of surgeon reimbursement for incidental appendectomy. RESULTS: At 10% surgeon reimbursement, open incidental appendectomy was cost-effective in those less than 25 years of age (< 35 years of age in a capitated system). Applied to the general population, open incidental appendectomy in those less than 25 years represented savings of up to $1,100 per 10,000 population per year. A surgeon fee of greater than 50%, or the laparoscopic approach using staplers, accrued no savings in any age groups. CONCLUSIONS: Open incidental appendectomy at low physician reimbursement is a cost-effective procedure for patients of less than 35 years of age. A decrease in equipment cost for laparoscopic approach will extend these indications.

Are prophylactic antibiotics required for elective laparoscopic cholecystectomy?

BACKGROUND: Some clinicians administer prophylactic antibiotics routinely before laparoscopic cholecystectomy, and the results of some of the studies in the literature support this practice. We conducted a prospective randomized trial to determine whether administration of prophylactic antibiotics is necessary during routine laparoscopic cholecystectomy in low-risk patients. STUDY DESIGN: Two hundred fifty patients without evidence of acute inflammation, common duct stones, or other indications for antibiotics were randomized to receive three perioperative doses of cefazolin or no prophylaxis and followed up for complications up to 30 days postoperatively. The primary end point was the occurrence of a major infectious complication, defined as that causing a systemic response, delaying discharge, or leading to readmission. Minor infectious problems were also noted, defined as those causing local symptoms only. RESULTS: One hundred twenty-eight patients were randomized to receive prophylactic antibiotics (PA group), 122 to receive none (NONE group; two patients in this group were actually given preoperative antibiotics). Only one major complication occurred (in a patient in the NONE group), an abscess in the presence of a bile leak, despite the administration of antibiotics when the leak was discovered several days before infectious problems arose. There were four minor problems: two lower urinary tract infections and one superficial wound infection in a NONE patient and one urinary tract infection in a PA patient (not significant); all were easily managed. The prophylactic antibiotics did not sterilize the bile, and infectious complications were not associated with weight, inflammation found at the time of operation, reported stone or bile spill-age, or conversion to open operation. CONCLUSIONS: Prophylactic antibiotics are not necessary for elective laparoscopic cholecystectomy in low-risk patients.

Enteral and parenteral feedings. Guidelines and recommendations.

The clinician is confronted with many options in choosing appropriate nutritional support for a patient. Several major issues emerge. 1. Supplemental nutritional support is appropriate in patients who will not be able to take oral calories for more than 7 days. Individuals with preexisting deficits due to lifestyle or disease should have support started more promptly. 2. The use of TPN as a preoperative adjunct in surgical patients appears to be beneficial only to those with severe malnutrition. 3. In the vast majority of patients, the enteral route is preferred. Total parenteral nutrition appears to be beneficial in those with inadequate absorptive capacity, fistula, acute hepatic/renal failure, inflammatory bowel disease, and as an adjunct to cancer therapy. 4. Complications associated with enteral and parenteral nutrition delivery can be minimized by careful attention to detail and adequate monitoring of responses. 5. An exciting area beyond the scope of this monograph is the emergence of the field of "Nutritional Pharmacology" where one manipulates the patient's diet to achieve a desired physiologic result, just as one will change antibiotics or pressors. This will provide an additional tool to the clinician in the treatment of critically ill patients.

Glucocorticoids upregulate intestinal nutrient transport in a time-dependent and substrate-specific fashion.

Glucocorticoids mediate skeletal muscle proteolysis during critical illness to provide substrates for hepatic acute-phase protein synthesis and gluconeogenesis. The effects of hypercortisolemia on splanchnic substrate uptake are not well defined. This study characterizes intestinal nutrient transport in response to acute elevations of plasma glucocorticoid levels. New Zealand White rabbits were randomized to receive either dexamethasone (2 mg/kg intramuscularly) or vehicle and were killed 8, 16, or 24 hours after steroid treatment. Brush-border membrane vesicles were prepared from pooled small intestinal mucosa and the uptake of tritiated substrates was quantified. Serum insulin-like growth factor 1 (IGF-1) levels, mucosal DNA content, and mucosal morphology were determined. Glucocorticoids increased glucose and leucine uptake at 8 hours (80% and 24%, respectively) and 24 hours (147% and 50%, respectively). Glutanmine, alanine, and arginine transport increased by 42%, 96%, and 236%, respectively, at 24 hours. Sodium-independent transport (diffusion) of all substrates was increased by 240% by dexamethasone treatment at 24 hours. Mucosal DNA content increased by 32%, whereas microvillus heights decreased by 27% at 24 hours. No effects were noted on IGF-1 levels or gross villus heights. Glucocorticoids acutely accelerate intestinal nutrient transport in a time-related and substrate-specific fashion. Although the mechanism of glucocorticoid action remains unclear, both genomic and plasma membrane effects are implicated.

Epidermal growth factor and neurotensin induce microvillus hypertrophy following massive enterectomy.

The compensatory hypertrophy that develops after massive enterectomy is rarely adequate to prevent the development of short bowel syndrome. Trophic hormones such as epidermal growth factor (EGF) and neurotensin (NT) may be useful in improving and accelerating this adaptive response. This study delineates the effects of NT and EGF on remnant small bowel at the microvillus cellular level, which is the prime determinant of surface area. New Zealand white rabbits (2 kg) underwent midgut transection (sham) or 70% jejunoileal resection. Alzet pumps containing saline solution (control), EGF (1.5 microg /kg/hr), or NT (900 microg/kg/day) were implanted in resected animals after which they underwent 1 week of infusion. A second group of EGF animals was killed 2 weeks after infusion completion to assess delayed effects (EGF-delayed). Proximal jejunum was fixed for light and electron microscopy; villus and microvillus parameters were read in a blinded fashion. EGF (2.17+/-0.05 microm), EGF-delayed (2.26+/-1.5 microm, and NT (1.96+/-0.02 microm) animals had significantly increased microvillus heights compared to the control group (1.49+/-0.04 microm). Calculated brush-border surface areas were increased in a similar fashion. EGF and NT failed to elicit increases in jejunal gross villus heights. EGF and NT induce enterocyte microvillus hypertrophy and increase absorptive surface area in remnant bowel after massive enterectomy. In addition, the trophic effects of EGF persist after cessation of infusion. These peptides may be useful in accelerating small bowel adaption and preventing the development of short gut syndrome.

Evaluation of a carboxymethylcellulose sponge for prevention of postoperative adhesions.

BACKGROUND: A novel lyophilized carboxy-methylcellulose (CMC) sponge has been developed for prevention of surgical wound adhesions. One potential mechanism for preventing abdominal adhesion is suppression of the cytokine transforming growth factor beta (TGF-beta) and other macrophage derived fibroblast stimulating factors that partially mediate adhesion formation. METHODS: To study the efficacy and mechanisms of action of the CMC sponge, we performed standard cecal denudation and abdominal wall apposition on rats. A CMC sponge or a commercially available adhesion preventive barrier (Interceed) was placed on the denuded surface. After 14 days, adhesion severity was graded blindly on a scale ranging from 0 (no adhesion) to 5 (severe adhesion). TGF-beta expression was determined by immunocytochemical staining. To assess the secretion of macrophage derived fibrogenic factors in control and CMC rats, labeled thymidine and proline uptake and hydroxyproline production were measured in NRK rat fibroblasts cultured with conditioned medium of peritoneal macrophages. RESULTS: The severity of adhesions in the CMC sponge group (0.7 +/- 0.3) was significantly lower than in the Interceed or control groups (2.2 +/- 0.3; 4.6 +/- 0.1). In control animals TGF-beta expression in endothelium and fibroblasts was maximal on day 3. Neither CMC nor Interceed reduced this expression. Conditioned media derived from sponge-exposed postsurgical peritoneal macrophages did not inhibit fibroblast growth or collagen formation. CONCLUSIONS: In this model the CMC sponge was more effective than Interceed in preventing postoperative adhesions. Its action was not due to inhibition of TGF-beta expression or macrophage derived fibrogenic factors. These data highlight the primary importance of local barrier effect in adhesion prevention.

Transduodenal sphincteroplasty and transampullary septotomy for primary sphincter of Oddi dysfunction.

We examined 29 patients without stone disease or pancreatic ductal ectasia who underwent transduodenal sphincteroplasty and transampullary septotomy for symptoms of biliary colic or pancreatitis. The combination of biliary symptoms and a fibrotic ampulla of Vater portends a favorable surgical outcome in virtually all such patients. Patients with pancreatitis did worse overall, perhaps due to the existence of unappreciated subclinical parenchymal disease not related to sphincter dysfunction. Although endoscopic retrograde cholangiography was sensitive in demonstrating abnormalities of the pancreaticobiliary system, its specificity as a predictor of good results was poor. It seems prudent to temper one's enthusiasm for sphincteroplasty in the patient with pancreatitis, whereas patients with biliary symptoms, the postcholecystectomy syndrome, or both will usually benefit significantly from this procedure.

Extrapelvic endometriosis: diagnosis and treatment.

BACKGROUND: Young women with nondescript abdominal pain can be difficult to diagnose. Although extrapelvic endometriosis is infrequent, we have treated 7 patients over the past 3 years with endometriosis in the abdominal wall, inguinal canal, or surgical incisions as the etiology of their symptoms. PATIENTS AND METHODS: We reviewed the medical records of patients whose final pathology report confirmed a diagnosis of extrapelvic endometriosis. Seven women who were treated at the University of Rochester Strong Memorial Hospital from May 1, 1991 through April 30, 1994 were identified. RESULTS: All patients were premenopausal with no history of pelvic endometriosis. In 4 patients, symptoms were cyclical. Surgical excision was initially curative in 5 patients. Two women required reexcision. The diagnosis of endometriosis was established at exploration by gross appearance and by frozen section. CONCLUSIONS: Endometriosis should be included in the differential diagnosis of a symptomatic mass in a celiotomy scar, the abdominal wall, or the inguinal canal. Principles of management include obtaining an accurate diagnosis and performing an adequate excision to prevent recurrence.