Helicobacter pylori in alcohol induced acute pancreatitis.

BACKGROUND AND AIMS: The objective of this study was to measure the association of Helicobacter pylori infection with alcoholic acute pancreatitis. MATERIAL AND METHODS: This study comprised of 50 patients with their first alcoholic pancreatitis and 50 alcoholic controls with no history of pancreatitis but similar alcohol use recruited from an alcohol rehabilitation center. Helicobacter infection was measured using Enzygnost EIA IgG-test. Complications and length of hospital stay were also recorded in patients with alcoholic pancreatitis. RESULTS: The seroprevalence of Helicobacter pylori was 10/50 (20%) in the pancreatitis group and 15/50 (30%) in the control group (p = NS). The median length of hospital stay of pancreatitis patients was 7 days, 11 days for those tested positive (range 6-25) and 6 days for those tested negative (range 3-47) for Helicobacter pylori, p = 0.013. As determined with the Atlanta criteria, seropositive patients tended to have more often severe pancreatitis, 4/10 (40%) vs. 6/40 (15%), OR 3.78 (95% CI 0.815-17.52), p = 0.097. CONCLUSIONS: This study suggests that Helicobacter pylori infection is not associated clinically significantly with the development of alcoholic pancreatitis. However, Helicobacter pylori infection may be associated with longer hospital stay due to more severe disease, which needs to be studied in a larger series of patients.

Late postoperative quality of life following pancreatic head resections.

BACKGROUND/AIMS: To evaluate health-related quality of life (HRQoL) in patients that have undergone pancreatic resection and compare the results with representative population samples in early and late stage evaluations. Also, this study aims to observe possible associations with postoperative complications. METHODOLOGY: Twenty-seven single-institute patients operated on during a 3-year period due to a benign or malignant process of the periampullary region. HRQoL was measured by the 15D instrument. Data were compared with those obtained from representative Finnish general population samples. RESULTS: Twenty-five patients were interviewed in the early stage (24 months postoperatively). Fifteen had a benign and 12 a malignant disease. No differences were found in the postoperative HRQoL when the nature of the disease or the postoperative complications were considered. When compared with the general population in the early stage, HRQoL was lower in the study group in whole, and also when sleep, elimination (bladder or bowel function) and sexual activity were considered separately. In the late stage evaluation (110 months postoperatively) the study group consisted of 15 surviving patients. There were no differences in comparison to the general population. Also when comparing the same patients in 2 evaluation points (24 and 110 months), we did not find any difference in any of the 15D parameters. CONCLUSIONS: Postoperative HRQoL deteriorated in comparison to general population in the early stage but there were no differences in the late stage. This study encourages us to continue the use of the 15D at least as a part of HRQoL evaluation, because it allows comparisons between different diseases and the general population.

The differentiation between pancreatic neoplastic cysts and pancreatic pseudocyst.

The number of small and often asymptomatic cystic lesions detected in pancreas has increased during the last decade. Historically the vast majority of the pancreatic cystic lesions were considered pseudocysts, but in recent series the incidence of various neoplastic cysts, such as intraductal papillary mucinous neoplasm, serous cystadenomas and cystic endocrine tumours, has increased. The possible malignant potential in these cystic neoplasms warrants careful diagnostic workup to choose the optimal treatment for each patient. Patient's age, symptoms and a possible history of acute or chronic pancreatitis with known aetiology together with high quality imaging studies are important in the differential diagnosis between pseudocysts and neoplastic cysts. Endoscopic ultrasound, cyst fluid analysis and positron emission tomography may be used in selected patients, but the accuracy of these methods needs further investigation.

The profile of leg symptoms, clinical disability and reflux in legs with previously operated varicose disease.

PURPOSE: It is difficult to assess the severity and location of venous insufficiency in legs with recurrent varicose disease. This present purpose was to evaluate the distribution of reflux and the diagnostic role of current classifications in a consecutive series of legs with previously operated varicose disease. METHODS: A total of 90 legs in a cohort of 66 patients were included. The examination comprised CEAP clinical class, clinical disability score (CDS) and leg symptoms. Colour-flow duplex imaging (CFDI) was used to observe reflux in deep and superficial veins. Details of prior surgery were assessed. RESULTS: The site of superficial reflux was at the groin in 58% (recurrent or residive vein trunk or unoperated great saphenous vein), and the rate in the popliteal fossa was 11% (unoperated short saphenous vein). In 58% of the legs presenting superficial reflux at groin level, previous surgery at the saphenofemoral junction was noted. A sensation of pain was observed in 74% of the legs, sensation of oedema in 64%, itching in 26 %, and night cramps in 8%, respectively. Only itching was significantly infrequent in uncomplicated (CEAP C 2-3) legs, and in legs with local reflux was restricted to vein tributaries. Higher CDS (classes 2-3) were significantly more frequent among complicated legs (CEAP clinical class C2-3: 22% versus CEAP clinical class C4-6: 77%; p < 0.005). A similar situation was noted when legs with only local reflux were compared to those with more severe reflux (local reflux: 7% versus severe reflux: 48%; p < 0.005). CONCLUSIONS: Superficial reflux is frequently detected at groin level despite prior surgery. Unstructured evaluation of leg symptoms is not beneficial. Clinical disability scores associate well with the severity of the venous disease.

Progesterone-independent avidin in chick oviduct fibroblast culture.

The production of avidin was studied in chick oviduct cell cultures derived from immature chicks or from chicks with 4, 8, or 14 days of estrogen priming in vivo. Cells were grown for 5--7 weeks, and the monolayers formed were composed of collagen-producing fibroblasts. In some cultures, epithelial cells were also found, but only in the original explants. Two-day avidin production of cultures was measured in the media weekly. Cultures produced avidin spontaneously, the amount being fairly stable during the 7-week culture period. No difference was found in avidin production or cell morphology when estrogen-containing medium was used. Cultures from 4- to 8-day-estrogen-primed chick oviducts produced the same amount of avidin as cultures from immature oviducts, whereas further estrogen pretreatment seemed to reduce avidin production. Progesterone did not enhance avidin production with or without estrogen priming but, due to its inhibition of growth, clearly inhibited avidin when it was continuously in the culture medium. It is concluded that chick oviductal fibroblasts have an inherent capacity for avidin production and that this is independent of progesterone.

Control of vascular tone in isolated mesenteric arterial segments from hypertensive patients.

1. Experimental hypertension is associated with several functional alterations of vascular endothelium and smooth muscle, but relatively few studies have examined the control of arterial tone in isolated vascular preparations from patients with essential hypertension. Therefore, we compared functional characteristics in vitro of distal ring segments of the mesenteric artery from 17 hypertensive and 22 normotensive humans. 2. Arterial constrictor responses induced by cumulative addition of Ca(2+) in the presence of noradrenaline (NA) were more effectively inhibited by the Ca(2+) entry blocker nifedipine (0.5 nM) in hypertensive than normotensive subjects (by 55.4+/-4.9, n=17 and 35.0+/(-5.2%), n=22, respectively). Also the contractions elicited by high concentrations of KCl were more effectively inhibited by nifedipine in arterial rings from hypertensive than normotensive patients (by 38.9+/(-3.7), n=17 and 20. 2+/(-4.6%), n=22, respectively). However, the concentration-response curves of contractions to NA, serotonin and KCl in the absence of nifedipine were similar between the study groups. 3. The concentration-response curves of endothelium-dependent relaxations to acetylcholine and Ca(2+) ionophore A23187, as well as of endothelium-independent relaxations to the nitric oxide donor nitroprusside, beta-adrenoceptor agonist isoprenaline and K+ channel opener cromakalim did not show any differences between the groups. Moreover, the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (0.1 mM) almost abolished the relaxations to acetylcholine and Ca(2+) ionophore in both groups, indicating that these responses were largely mediated by nitric oxide. The function of arterial sodium pump was evaluated by relaxations elicited by the return of K+ upon contractions induced by K+-free solution. The rate of K+-relaxation was similar in hypertensive and normotensive arteries (for all these responses n=20 - 22 in the normotensive and 15 - 17 in the hypertensive group). 4. These results suggest abnormal function of voltage-dependent Ca(2+) channels in arterial smooth muscle of hypertensive patients, whereas vascular responses to endothelium-dependent and -independent vasodilators and classical contractile agents were similar between hypertensive and normotensive subjects. The present findings support the view that blockade of voltage-dependent Ca(2+) channels is an effective means of reducing arterial tone in essential hypertension.

Effects of glucocorticoids and disodium cromoglycate on avidin production in chick tissues.

The effects of anti-inflammatory glucocorticoids and a membrane stabilizer (disodium cromoglycate) on avidin induction were studied. Chicks were primed for 0, 3 or 7 days with diethylstilboestrol (DES; 0.5 mg/day per animal, s.c.). Actinomycin D (0.2 mg/kg, i.p.) stimulated avidin production in the oviduct, intestine, lung and wing muscle of both DES-primed and unprimed chicks. Prednisolone (5 mg/animal, i.m.) given 1 h before actinomycin D reduced the avidin amounts to control levels in the unprimed oviducts and in non-oviductal tissues. The signs of inflammation (ascites, oedema) in chicks receiving actinomycin D also disappeared with prednisolone premedication. Cortisol (50 mg/animal, i.m. or 1, 5 or 50 microgram/ml medium), prednisolone (5 mg/animal, i.m. or 0.5, 5, 10 or 50 microgram/ml medium) and dexamethasone (1 mg/animal, i.m. or 0.05 or 0.5 microgram/ml medium) stimulated avidin production in DES-primed oviducts in vivo and in vitro. Culture in vitro induced avidin production in lung and oviduct but not in wing muscle. This avidin production in culture was not inhibited by cortisol, prednisolone or disodium cromoglycate. It is concluded that actinomycin D induces avidin production through its inflammatory effect and that the induction can be prevented by anti-inflammatory glucocorticoids. It is proposed that the 'spontaneous' avidin production in culture is not the effect of trauma during tissue preparation but rather a new form of avidin induction.

Clinical pathology of acute necrotising pancreatitis.

Seventy nine pancreatic specimens were obtained from patients treated with pancreatic resection for acute necrotising pancreatitis. The necrotising process had started in the periphery of the gland, so that eight of seventy nine cases contained peripancreatic (mainly fat) necrosis only without any parenchymal necrosis. Peripheral parenchymal necrosis was characterised by a severe inflammatory reaction, with multinucleated leucocytes and microabscess. In the deep parts of the pancreas coagulation necrosis was found. Vascular changes (thrombosis, vessel necrosis) correlated with postoperative haemorrhagic complications, but they did not seem to have any important role in the necrotising process. The vascular changes seemed to be a secondary phenomenon. In clinical practice the most important aspects in reporting the histology of acute necrotising pancreatitis are the extent of parenchymal necrosis, because the surgeon may overestimate its extent, and the existence of vascular changes, because of the correlation with postoperative recovery.

The mechanism of conversion of xanthine dehydrogenase to xanthine oxidase in acute pancreatitis in the canine isolated pancreas preparation.

Four models of acute pancreatitis have been previously developed that use the ex vivo perfused isolated canine pancreas preparation. The four models include the intraarterial infusion of oleic acid (FFA) that mimics hyperlipemic pancreatitis, partial obstruction of the pancreatic duct with secretin stimulation (POSS) that mimics gallstone pancreatitis, a 2-hour period of ischemia before perfusion (ISCH 2) that mimics shock pancreatitis, and the infusion of cerulein at supramaximal stimulatory doses (CER), which lacks an obvious clinical counterpart. In the FFA, POSS, and ISCH 2 pancreatitis, but not in the CER pancreatitis, toxic oxygen metabolites, generated by the enzyme xanthine oxidase (XO), have been shown to be important mediators in the early pathogenesis. Ordinarily XO primarily occurs as xanthine dehydrogenase (XD) but can be converted to XO, which is the form that generates toxic oxygen metabolites. This conversion of XD to XO may take place either reversibly by way of sulfhydryl group oxidation or irreversibly by means of proteolytic cleavage of XD. This study was undertaken to investigate the mechanism of conversion of XD to XO in the FFA-, POSS-, and ISCH 2-induced pancreatitis models. CER pancreatitis was studied for comparison. After 4 hours of perfusion, pancreatitis was manifest by edema, weight gain, and hyperamylasemia in all four models. Dithiothreitol, a sulfhydryl group protector, ameliorated the weight gain in the FFA (40 +/- 14 gm to 18 +/- 13 gm; p < 0.05), POSS (28 +/- 10 gm to 9 +/- 3 gm; p < 0.05), and ISCH 2 pancreatitis (30 +/- 13 gm to 15 +/- 3 gm; p < 0.05), and ameliorated the hyperamylasemia in the POSS pancreatitis (12,062 +/- 4304 units/dl to 5877 +/- 2659 units/dl; p < 0.05). The CER pancreatitis was not ameliorated with dithiothreitol. A serine protease inhibitor of low molecular weight, phenylmethylsulfonyl fluoride, ameliorated only the CER pancreatitis (weight gain from 28 +/- 10 gm to 17 +/- 10 gm, p < 0.05; amylase activity from 38,116 +/- 6491 units/dl to 23,372 +/- 11,654 units/dl, p < 0.05), and not the FFA, POSS, or ISCH 2 pancreatitis. We conclude that in the three models of pancreatitis (FFA, POSS, and ISCH 2) that are mediated by toxic oxygen metabolites, XD is converted to XO reversibly by way of sulfhydryl group oxidation rather than irreversibly by way of proteolysis. In the CER pancreatitis, where XO does not play a role in the pathogenesis, proteolytic enzymes may be important mediators in the injury.

Second primary lesions in the biliary tree after successful resection of ampullary carcinoma.

Two patients are described who had an adenocarcinoma at the site of the hepaticojejunostomy 5 and 15 years after pancreaticoduodenectomy for an ampullary adenocarcinoma. Both patients had symptoms and signs of biliary obstruction. Both tumors were identified by upper endoscopy and resected at laparotomy. In both patients the tumor was considered a new primary carcinoma rather than a recurrent or metastatic carcinoma. Evidence to support this was the finding of an intraepithelial component of the tumor in the resection specimens of both patients, the fact that the tumors were on the luminal side of the distal bile duct in both cases, lack of other evidence of recurrent or metastatic tumor, and the time interval between the pancreaticoduodenectomy and the development of the new tumor.

The role of cholecystokinin in the pathogenesis of acute pancreatitis in the isolated pancreas preparation.

In a variety of animal models of acute pancreatitis, cholecystokinin-receptor antagonists have ameliorated the injury response. These results suggest that cholecystokinin may play a primary role in the pathogenesis of pancreatitis initiated by multiple stimuli. In an effort to test this theory, a sensitive and high affinity cholecystokinin-receptor antagonist L364,718 was administered to four different models of acute pancreatitis that were produced in the ex vivo perfused canine pancreas preparation. The four models of pancreatitis were initiated by cerulein infusion, partial duct obstruction with secretin stimulation, oleic acid infusion, and a 2-hour period of ischemia. In each model, pancreatitis was manifest by edema formation, weight gain, and hyperamylasemia during a 4-hour perfusion. In cerulein infusion-induced pancreatitis L364,718 inhibited edema formation and weight gain (31 +/- 5 gm versus 7 +/- 6 gm; p less than 0.05) and significantly decreased plasma amylase activity (36,605 +/- 21,216 U/dl versus 9421 +/- 5149 U/dl; p less than 0.05). The acute pancreatitis induced by the other three stimuli was not ameliorated by L364,718 treatment. We conclude that in the ex vivo-perfused canine pancreas preparation cerulein-induced pancreatitis is mediated at least in part by the cholecystokinin receptor. Early blockade of the cholecystokinin receptor was of no benefit in treating the other models of pancreatitis, suggesting that cholecystokinin is not involved in the early pathogenesis.

Amount of alcohol is an important determinant of the severity of acute alcoholic pancreatitis.

BACKGROUND: Does the amount of recently consumed alcohol correlate with the severity of acute alcoholic pancreatitis? METHODS: One hundred one consecutive episodes of acute pancreatitis (AP) were prospectively studied. Seventy-three were alcoholic AP episodes; 40 patients had their first alcoholic AP episode. A standard personal interview was used to determine the alcohol consumption during 2 months and during 1 week before AP. The severity of AP was evaluated according to the Ranson criteria, the serum C-reactive protein (CRP) concentration measured 24 to 48 hours after admission, the length of the hospital stay, the development of complications, and the mortality rate. RESULTS: In the 40 patients having their first alcoholic AP episode, the reported 2-month alcohol consumption correlated significantly with the number of positive Ranson criteria (correlation coefficient r = 0.44, p < 0.01), serum CRP concentration (r = 0.51, p < 0.001), and the length of the hospital stay (r = 0.45, p < 0.01). Complications occurred in eight of 14 patients with 2-month alcohol consumption of more than 5000 gm as compared with one of 14 patients with consumption of less than 2000 gm (p < 0.05). In the same 40 patients the 1-week alcohol consumption correlated with the number of positive Ranson criteria (r = 0.40, p < 0.05) and serum CRP concentration (r = 0.37, p < 0.05). Of the 12 patients who had consumed more than 1000 gm alcohol during the last week before admission, two died and complications developed in six (50%), as compared with none (p < 0.05) and six (21%), respectively, of those who had consumed less than 1000 gm. No significant correlations were observed between the reported alcohol consumption and any of the severity parameters in the 33 patients with recurrent episodes of alcoholic AP. CONCLUSIONS: The amount of alcohol consumed may be an important determinant of the severity of the first alcoholic AP episode but not of recurrent alcoholic AP.

Detailed characterization of experimental acute alcoholic pancreatitis.

BACKGROUND: With the ex vivo perfused canine pancreas preparation, the infusion of acetaldehyde, the primary metabolite of ethanol oxidation, plus a short period of ischemia to convert xanthine dehydrogenase to xanthine oxidase, results in the physiologic injury response of acute pancreatitis (edema, weight gain, hyperamylasemia). The free radical scavengers superoxide dismutase and catalase and a xanthine oxidase inhibitor, allopurinol, ameliorate this injury response, suggesting that toxic oxygen metabolites generated by xanthine oxidase play an intermediary role. METHODS: The isolated ex vivo canine pancreas preparation was perfused for 4 hours, and weight gain of the preparation and amylase activity in the perfusate were monitored. Changes in pancreatic acinar cell architecture were characterized by light and electron microscopy, and intracellular phosphate metabolism was followed by magnetic resonance spectroscopy in control preparations and in glands simulating alcoholic pancreatitis. RESULTS: Control preparations and preparations with a 1-hour period of ischemia before perfusion gained little weight (7 +/- 3 gm and 8 +/- 1 gm), amylase activity in the perfusate remained normal (933 +/- 513 units/dl and 1537 +/- 553 units/dl), and no changes in architecture were observed. Weight gain (5 +/- 6 gm) and amylase activity (1188 +/- 173 units/dl) were also normal in the preparations receiving acetaldehyde without preceding ischemia, but mild vascular and islet cell injury were observed on electron microscopy. One hour of ischemia followed by acetaldehyde infusion resulted in edema, increased weight gain (21 +/- 12 gm [p < 0.05]), and amylase activity (2487 +/- 1484 units/dl [p < 0.05]). Microscopy showed mild acinar cell damage and greater injury to the capillaries and the islets. The capillary and islet cell changes were reduced by superoxide dismutase and catalase. Intracellular adenosine triphosphate levels remained at baseline levels in the control preparations. Adenosine triphosphate decreased during ischemia but quickly recovered during perfusion without a significant difference whether acetaldehyde was infused after ischemia. An iron chelator desferoxamine ameliorated the injury response in the preparations simulating acute pancreatitis (weight gain, 13 +/- 6 gm [p = 0.09] and amylase activity, 1198 +/- 471 units/dl [p = 0.08]), but a cholecystokinin receptor antagonist L364,718 did not have an effect. A sulfhydryl group protector, dithiothreitol, decreased weight gain (10 +/- 7 gm [p = 0.06]), and amylase activity was not significantly increased over that of the control group (1582 +/- 641 units/dl), but a serine protease inhibitor phenylmethylsulphonylfluoride was ineffective. CONCLUSIONS: In this model simulating acute alcoholic pancreatitis, both the early physiologic injury response and the early morphologic changes are mediated at least in part by free radicals, which are generated by xanthine oxidase converted reversibly from xanthine dehydrogenase. In addition to the superoxide radical, the hydroxyl radical may also be an important early intermediate step, but the cholecystokinin receptor is not.

Clinical assessment compared with cyst fluid analysis in the differential diagnosis of cystic lesions in the pancreas.

BACKGROUND: In adults 80% to 90% of cystic lesions in the pancreas are pseudocysts and the remainder are mostly neoplastic cysts. To choose optimal treatment for an individual patient, exact nonoperative diagnosis would be preferable. This study was done to assess the value of cyst fluid analysis, compared with clinical and radiologic findings, in the differential diagnosis of pancreatic cystic lesions. METHODS: Twenty-two patients with a cystic lesion in the pancreas underwent operation, cyst wall biopsy, and aspiration of cyst fluid. Carcinoembryonic antigen (CEA), CA 19-9, pancreatitis-associated protein (PAP), and total protein concentration, amylase activity, and cytologic findings were studied. Final diagnosis was pseudocyst in 14 patients, serous cystadenoma in two, mucinous cystadenoma in two, and mucinous cystadenocarcinoma in four patients. RESULTS: Clinical and radiologic judgment correctly differentiated pseudocysts and neoplastic cysts. Cyst fluid aspiration did not succeed in two patients with mucinous cystadenocarcinomas because of the high fluid viscosity. Cyst fluid amylase activity was high (greater than 16,000 IU/ml) in all but one pseudocyst and low (less than 83 IU/ml) in all but one neoplastic cyst. CEA level was lower in pseudocysts than in neoplastic cysts, but with an overlapping value between the groups. Mean CA 19-9 concentration was higher in pseudocysts than in neoplastic cysts, but with wide overlap between the groups. Pancreatitis-associated protein and total protein concentration and cystic fluid cytologic findings did not differ between various types of cysts. CONCLUSIONS: Clinical judgment including careful history and radiologic studies seems to be the most reliable method of differentiating neoplastic pancreatic cysts from pseudocysts. Amylase and CEA levels give suggestive information, but cyst fluid analysis may be misleading in an individual patient.

Unresectable hilar cholangiocarcinoma: percutaneous versus operative palliation.

BACKGROUND: Several nonoperative and operative options are available for palliation of patients with unresectable hilar cholangiocarcinoma. This retrospective analysis compares the results of nonoperative percutaneous stenting and operative palliation in 65 patients. METHODS: Twenty-one patients were managed with percutaneous biliary stents (group A), and 44 patients underwent laparotomy (group B) with placement of large-bore silicone rubber transhepatic stents in 33. The two groups were similar with respect to age, gender, mean laboratory data, and cholangiographic extent of tumor. RESULTS: Group A and group B patients were comparable in hospital morbidity (67% vs 61%), hospital mortality (14% vs 7%), and mean initial hospital stay (27 vs 31 days). Survival was greater in group B laparotomy patients at 1, 3, and 6 months (p < 0.01), and median survival was 5 months for group A compared with 8 months for group B patients (p = 0.06). Group A patients who were managed with percutaneous stents required more stent changes per month of survival (0.5 vs 0.3, p = 0.06). However, group B patients who underwent operative palliation were more likely to undergo a second operation (0% vs 21%, p = 0.05), most often for duodenal or small-bowel obstruction. CONCLUSIONS: Operative placement of large-bore transhepatic stents may reduce cholangitis, delay hepatic failure, and prolong survival. We conclude that patients with unresectable hilar cholangiocarcinoma who are fit for surgery may benefit from operative palliation.

Hyperamylasemia after cardiopulmonary bypass: pancreatic cellular injury or impaired renal excretion of amylase?

BACKGROUND: Postoperative hyperamylasemia and even acute pancreatitis are associated with coronary artery bypass grafting (CABG). The mechanism of hyperamylasemia and pancreatic acinar cell damage was studied in 20 patients undergoing CABG. METHODS: Serial blood and urine samples at eight time points before, during, and 24 hours after the CABG were collected. Salivary and pancreatic isoamylases, the fractional clearance of isoamylases (i.e., relative to creatinine clearance), pancreatic phospholipase A2 (a specific serum marker of pancreatic acinar cell injury), and cystatin C (a sensitive marker of glomerular filtration rate) were measured. RESULTS: Mild serum hyperamylasemia (300 to 1000 units/L) was found in 11 of 20 (55%) and severe (> 1000 units/L) in 6 of 20 (30%) patients with no signs of clinical acute pancreatitis. Hyperamylasemia occurred from 6 to 24 hours after the CABG and was mainly caused by pancreatic isoamylase. Serum pancreatic phospholipase A2 concentration remained unchanged, which excludes acinar cell damage. Although renal glomerular filtration was normal during CABG as measured by serum cystatin C and creatinine clearance, the fractional clearance of isoamylases decreased. CONCLUSIONS: The decreased rate of excretion into urine, rather than pancreatic cellular damage, is the major source of hyperamylasemia after CABG.

Pretreatment with antioxidants and allopurinol diminishes cardiac onset events in coronary artery bypass grafting.

Oxygen-derived free radicals constitute one part of the etiologic factors for cardiac onset harmful events. Allopurinol is able to reduce the generation of free radicals. Vitamins E and C scavenge radicals after their formation. Eighty-one patients with coronary artery disease were randomized into four study groups: Group 1 (n = 20) patients had stable disease and received oral vitamin E for 4 weeks, and vitamin C and allopurinol 2 days before and 1 day after coronary artery bypass grafting. Group 2 (n = 25) consisted of their controls. Group 3 patients (n = 17) had more unstable disease and received the same medications as group 1, except that vitamin E was given only 2 days before the operation. Group 4 (n = 19) was their controls. Groups 1 and 3 had fewer ischemic electrocardiographic events and required less dopamine perioperatively than corresponding control groups 2 and 4. Group 3 had fewer perioperative infarctions and less creatine kinase-MB release than the respective controls (group 4). Plasma levels of vitamins E and C, urate, and total free radical trapping ability were considered to support the theory about the role of free radicals in reperfusion injury. Especially the unstable patients, but also patients with stable coronary artery disease requiring coronary artery bypass grafting benefit from perioperative allopurinol and vitamin E and C treatment.

Bile flow to the duodenum is reduced in hypothyreosis and enhanced in hyperthyreosis.

Disturbances in sphincter of Oddi (SO) function may prevent normal bile flow and thus enhance probability of common bile duct stone (CBDS) formation. We have previously shown increased prevalence of diagnosed hypothyroidism in CBDS patients, which may be explained by thyroxine-induced inhibition of SO contractility, in addition to previously suggested changes in bile composition and hepatocytic excretion. The aim of this study was to investigate biliary dynamics in relation to altered thyroid gland function in rat, a rodent without a gallbladder. Euthyroid, hypothyroid or hyperthyroid Spraque-Dawley rats were anaesthetized with i.p. urethane, and exsanguinated at 15, 45, or 60 min after intravenous 99mTc HIDA injection. At these timepoints, the bile flow to intestine was determined by measuring the relative intestine vs. liver radioactivity. At 45 min this was 44% lower in hypothyroid rats and at 60 min 73% higher in hyperthyroid rats compared to euthyroid rats, while hepatic radioactivity at 15 min and blood pressure at injection were similar in the groups. We conclude that the bile flow to duodenum is reduced in hypothyreosis and enhanced in hyperthyreosis.

Histamine in the control of porcine and human sphincter of Oddi activity.

Histamine decreases sphincter of Oddi (SO) contractility in vivo in opossum, but increases contractility in vitro in guinea-pig. In resistor-like SO, such as in pig and man, the histamine effect is poorly known. We investigated the effect of histamine on pig SO in vivo and in vitro and on human SO in vitro. Perfusion manometry catheter and two silver electrodes for simultaneous pressure and electromyography registration were inserted into the SO transduodenally by laparotomy in six anaesthetized pigs weighing for 25-28 kg. Histamine (5-10 microgram kg-1) was infused intra-arterially (i.a.) into the pancreaticoduodenal artery with and without diphenhydramine (75 microgram kg-1) i.a. premedication. Acetylcholine (4 microgram kg-1) i.a., a potent SO stimulator, was used as positive control. After these experiments, the SO was removed and, together with seven human SO from Whipple specimens, were cut into 1.0-1.5 mm thick transverse sections (rings). The rings were placed between two hooks in oxygenated organ bath solution at 37 degrees C. The SO contraction force was measured with isometric force-displacement transducers and registered on a polygraph. SO rings were incubated with histamine (10-100 micromol L-1) and acetylcholine (100 micromol L-1) with or without diphenhydramine (10 micromol L-1), cimetidine (10 micromol L-1), or atropine (1 micromol L-1). Acetylcholine induced huge electrical bursts, and basal SO pressure increased by 20 +/- 10 mmHg. Histamine (10 microgram kg-1) induced strong SO contraction and the SO remained oedematous for over 10 min. Histamine (5 microgram kg-1) resulted in electromyographic burst activity with phasic SO contractions and increase in basal SO pressure by 34 +/- 19 mmHg for over 15 min. Diphenhydramine did not alter acetylcholine-induced SO motility, but significantly decreased histamine-induced contractions and almost abolished electrical activity. In vitro, acetylcholine induced SO contractions in pig (335 +/- 111 mg) and in man (323 +/- 54 mg). Histamine did not change SO tone in man, but in pig it induced dose-dependent contractions in the same way as acetylcholine. These contractions could be inhibited by diphenhydramine, but not by cimetidine or atropine. We conclude that histamine has a stimulatory effect, mediated by H1-receptor, on the pig SO motility. The SO response to histamine is different in adult humans from that observed in young pigs.

Intracystic hemorrhage in pancreatic pseudocysts: initial experiences of a treatment protocol.

The treatment recommendations for intracystic hemorrhage in pancreatic pseudocysts are various. We have used a defined treatment protocol in these difficult cases. The experiences gained are reported here. Patients with clinical signs of ongoing bleeding and with hemorrhagic pancreatic pseudocyst in ultrasonography and computed tomography (CT) were studied with urgent angiography. Patients showing a pseudoaneurysm were treated with immediate embolization and delayed elective surgery whenever candidates for surgery. During a 5-year period 10 patients were treated according to the protocol. Pseudoaneurysm was demonstrated and subsequent embolization performed in six. Angiography was negative in four patients. During the study period two additional patients were treated conservatively without angiography because the bleeding had stopped 2 weeks prior to the referral to our institution. Two patients were electively operated on and the remaining 10 patients were treated conservatively. Fever and elevated transaminases developed in one of the six patients after the embolotherapy. One of the four embolized patients who were not operated on developed pseudocyst infection 4 months after the embolization. One of the 10 conservatively treated patients died (1/10 = 10%; total mortality, 1/12 = 8%) during the follow-up for infection complications of necrotizing pancreatitis 2 months after the initial bleeding. Another conservatively treated patient with negative angiography had recurrent bleeding during the follow-up but could not be operated on due to severe liver cirrhosis. In the remaining eight patients pseudocysts resolved during the 3-month to 3.5-year follow-up as confirmed by CT. The low rates of mortality and rebleeding support a fairly conservative approach for hemorrhagic pancreatic pseudocysts.