摘要:

SUMMARYCentral parenteral nutrition can cause serious complications, particularly in association with the feeding catheter, previously in relation to nutrient provision, and occasionally in other organ systems, notably disease of the liver and abnormalities of bone composition.Developments in catheter design, the introduction of catheter care protocols based on an understanding of the common routes of catheter infection, and the identification of factors associated with central vein thrombosis have all reduced dramatically the incidence of complications. Furthermore, problems such as catheter occlusion, catheter infection and central vein thrombosis can now be treated effectively in many patients without the loss of the feeding catheter.This review summarizes the common and important complications of parenteral feeding with emphasis on their practical prevention and management.

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00490.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYHypergastrinaemia induced by potent inhibitors of acid secretion is thought to occur as a result of the elimination of the inhibitory effects of intragastric acid on gastrin release. The present study was designed to determine if the mechanisms responsible for feedback inhibition of gastrin release and acid secretion by intragastric acid are preserved during four weeks of varying degrees of drug‐induced acid inhibition. Forty‐eight healthy male volunteers were randomly assigned to one of four treatments for four weeks: 10 mg omeprazole o.m., 20 mg omeprazole o.m., 40 mg omeprazole o.m. or 150 mg ranitidine b.d. Gastrin release and acid secretion in response to peptone meals maintained at pH 2.5 and pH 5.5 by intragastric titration, and 24‐hour gastrin profiles in response to standard meals were determined before treatment, at the fourth week of treatment and two weeks after discontinuing treatment. As expected, omeprazole produced dose‐related effects on acid secretion and gastrin concentrations that were largely reversed after treatment was discontinued. Gastrin release in response to pH 5.5 peptone meals remained significantly greater than gastrin release in response to pH 2.5 meals during treatment with all doses of omeprazole. The ratio of pH 5.5/pH 2.5 peptone meal‐stimulated gastrin release was approximately 1.5, and remained constant for all treatment groups throughout the study period. These data indicate that four weeks of drug induced hypochlorhydria causes an apparent increase in overall G‐cell function, but it does not interfere with normal feedback inhibition of gastrin release and acid secretion mediated by intragas t

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00491.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYSixty infants were randomly assigned to one of three groups on admission to hospital with a diagnosis of gastroenteritis. After rehydration, Group A received a low‐lactose, low‐fat feed (HN25) in full strength; Group B were regraded on to a conventional formula (SMA); Group C received a hydrolysed soya and collagen feed (Prejomin) in full strength. All feeds were continued for 5 days. The median duration of loose stools from starting the feed was 24 hours in Group A, compared to 119 hours and 95 hours in Groups B and C, respectively. Group A showed a mean percentage increase in weight of 2.34%, Group B showed a mean loss of 1.45%, and Group C a mean increase of 0.15%. These differences were statistically significant. Recovery from gastroenteritis is hastened by the use of a low‐lactose, low‐fat feed in the initial post‐rehydration phase of th

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00492.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYStimulation of mucosal alkaline secretion represents an opportunity for discovering novel drugs of potential benefit in maintenance therapy of duodenal ulcer disease. We screened over 200 agents representing the full spectrum of pharmacological categories in order to characterize stimulatory pathways and identify mechanistic leads. A variety of eicosanoids, phospho‐diesterase inhibitors and adrenoreceptor agonists together with forskolin, 6–hydroxy‐dopamine, 2–chloroadenosine, diazepam, testosterone, dipyridamole and dihydropyridazinone caused a reproducible increase in the metabolism‐dependent component of alkaline secretion in bullfrog proximal duodenum. PGE2(ED500.02 μg/ml) was the most potent agent in vitro and was also the most effective stimulant of duodenal alkalinization in vivo in an anaesthetized cat preparation. Agents without effect on spontaneous alkaline secretion by amphibian duodenum included agonists and antagonists of histamine, 5–hydroxy‐tryptamine, γ‐aminobutyric acid, dopamine, muscarinic and nicotinic receptors, inhibitors of amine uptake, monoamine oxidase and cholinesterase, plus various corticoids, diuretics, oestrogens, chemotherapeutic (anticancer) and antimicrobial agents. The major mechanism of stimulating alkaline secretion in the isolated duodenum is by increasing intracellular cyclic AMP levels. This may occur by either inhibiting metabolism of the nucleotide or by stimulat

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00493.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYWe studied the effects of prostaglandin (PG) E2, carbenoxolone, cholecystokinin‐octapeptide (CCK‐OP), and the thromboxane‐mimetic U46619, all known to stimulate gastric mucus secretionin vivo, on protein and glycoprotein synthesis in and release from isolated and enriched pig gastric mucous cells, as measured by the incorporation of [3H]L‐leucine and N‐acetyl‐[14C]D‐glucosamine respectively into cellular and released acid insoluble material. PGE2stimulated glycoprotein and protein synthesis (EC507 and 30 nmol/L, respectively) and release (EC5050 and 140 nmol/L, respectively) in a concentration‐dependent manner, whereas carbenoxolone, CCK‐OP and U46619 failed to enhance the incorporation of the tracers. We conclude that stimulation of mucus secretion by PGE2is related to direct effects on protein and glycoprotein production of gastric non‐parietal cells, whereas indirect effects may be involved in the stimulation by carbenoxolone,

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00494.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYCombined oesophageal and gastric 24‐hour pH monitoring and oesophageal manometry were performed in 19 patients with resistant reflux oesophagitis after short‐term therapy with omeprazole (40 to 60 mg daily) or during maintenance treatment with omeprazole (20 to 80 mg daily). Omeprazole's effects on acidity were analysed as well as any possible influence on oesophageal motility. A pH in the stomach of below 4 was present during considerable periods of time (in 27 of 29 measurements), particularly during the night. As a consequence, pathological gastro‐oesophageal reflux occurred, particularly in the supine period. Insuficiency of the lower oesophageal sphincter was present in all but one patient; decreased or virtually absent motility of the oesophagus was found in 63 % of the patients. Combined intragastric and intra‐oesophageal pH monitoring, with oesophageal manometry, may contribute to the management of patients with reflux disease resistant to treatment with omeprazole. The present study emphasizes the need to individualize therapy in patients with refractory gastro‐ oesophageal reflu

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00495.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYAn Eudragit‐L coated oral 5‐aminosalicylic acid (5‐ASA; mesalazine) product (Mesasal), has been formulated to deliver 5‐ASA to the distal small bowel and colon for the treatment of inflammatory bowel disease. The purpose of this study was to compare the pharmacokinetic profile of this drug between two patient groups, with either inflamed small or large bowel and with volunteers.Two carefully selected patient groups (one with nine patients suffering from Crohn's disease restricted to the small intestine, and one with ten patients suffering from total ulcerative colitis) and a group of ten volunteers received two 250 mg Mesasal tablets in the morning, on a fasting stomach. Plasma 5‐ASA and acetyl‐5‐ASA concentrations were followed for 48 h, and urine and faecal excretion for 72 h. There was a great variation in most pharmacokinetic parameters within each group. Numerically, however, the data suggests a somewhat higher systemic absorption in patients with Crohn's disease than in healthy volunteers or patients with ulcerative colitis. The location of the inflammatory process might have some influence on the pharmacokinetics of 5‐ASA in inflammator

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00496.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

ABSTRACTPlatelet activating factor, a potent inflammatory mediator, has been reported to induce gastrointestinal damage, whereas its inhibition or antagonism is associated with mucosal protection. The aim of the present study was to elucidate the association between acute experimental gastric damage and mucosal platelet activating factor generation in the rat, and to evaluate the protective effect of sucralfate in relation to mucosal platelet activating factor formation. Gastric damage in the rat was induced by either subcutaneous injection of indomethacin 30 mg/kg or intragastric administration of aspirin 100 mg/kg, hydrochloric acid 0.6 N, taurocholate 30 mM, ethanol 96%, or sodium chloride 25%. All agents induced a significant increase in mucosal platelet activating factor levels concomittently with induction of mucosal damage. Pretreatment with sucralfate 150 mg/rat provided a significant macroscopic and microscopic mucosal protection in all experimental models. This protection was associated with a significant decrease in mucosal platelet activating factor level in the hydrochloric acid, taurocholate, ethanol and hyperosmolar sodium chloride treated rats, whereas it remained unchanged in the aspirin and indomethacin treated rats. The data imply that platelet activating factor may have a limited role in the pathogenesis of indomethacin or aspirin induced damage, where other mechanisms such as cyclooxygenase inhibition dominate. In the damage induced by topical strong irritants, platelet activating factor may have a major pathogenetic role.

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00497.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYHelicobacter pyloriis now recognized as a frequent cause of histological chronic gastritis, and this has radically changed our understanding of this common condition. In the light of these developments, the traditional view that non‐steroidal anti‐inflammatory drugs are one of the common ‘environmental’causes of chronic gastritis has been re‐examined.Gastric mucosal biopsies have been studied from 430 patients undergoing routine upper gastrointestinal endoscopy, 99 of whom had recently been taking non‐steroidal anti‐inflammatory drugs. No significant association was found between the use of these drugs and either the presence of chronic gastritis or the frequency of colonization withH. pylori, although there was a strong association (P<0.0001) betweenH. pyloriand gastritis. Non‐steroidal anti‐inflammatory drugs appear, however, to modify the inflammatory process in the gastric body, leading to a lower frequency of atrophic gastritis (P<0.05). The majority of peptic ulcers were associated withH. pyloriirrespective of non‐steroidal anti‐inflammatory drug use, but there was a higher frequency of H. pylori negative ulceration in the patients who had used these agents (P<0.04). Peptic ulceration was uncommon in the absence of either H. pylori or recent non‐steroidal ant

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00498.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

SUMMARYThe bioavailability of three pure 5‐aminosalicylic (5‐ASA) preparations (Asacol, Claversal, and Pentasa) was studied in 8 ileostomy patients and 12 normal subjects after 6 days of treatment with 2000 mg 5‐ASA. The local bioavailability, reflected by the 5‐ASA concentration was thereby measured at two clinically relevant areas of the gut: at the entrance to, and the exit from the colon. Estimates of the systemic bioavailability were obtained from the urinary excretions and the plasma values of 5‐ASA and Acetyl‐5‐ASA (Ac‐5‐ASA) during the three regimens. The three preparations studied are designed to release 5‐ASA at different levels in the intestine, but there was no significant difference in the 5‐ASA concentrations in the ileostomy effluents (Asacol 1.8 mmol/L, Claversal 3.4 mmol/L, Pentasa 2.0 mmol/L, median values). However, we found a smaller urinary excretion of 5‐ASA and Ac‐5‐ASA (5.2%vsClaversal 27.9% and Pentasa 23.0%, median values of ingested daily dose) and a lower concentration of Ac‐5‐ASA in the ileostomy effluents after Asacol treatment (0.8 mmol/L, median value) which indicates a more distal release from this preparation compared with Claversal (2.4 mmol/L, median value) and Pentasa (5.5 mmol/L, median value). In normal subjects a higher faecal water concentration of 5‐ASA was found after Asacol (9.8 mmol/L, median value) compared with Claversal (5.0 mmol/L, median value), whereas no difference between the faecal water concentrations of Ac‐5‐ASA was found (Asacol 21.5 mmol/L, Claversal 21.6 mmol/L, median values). This can be explained by a larger systemic absorption of 5‐ASA from Claversal, and accordingly Claversal treatment resulted in the largest urinary excretion of 5‐ASA and Ac‐5‐ ASA (43.7% us Asacol 35.6% and Pentasa 31.6 %, median values of ingested daily dose). The high Ac‐5‐ASA concentration in the ileostomy effluents and in the faeces after Pentasa, and the low plasma values, indicate a slow 5‐ASA release from this preparation throughout the small and large intestine. The results of the study indicate that Asacol is released in the distal part of the small intestine, that Pentasa is gradually released in the small and large intestine, and t

ISSN:0269-2813    

DOI:10.1111/j.1365-2036.1990.tb00499.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY