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Biomedical subjects

A Lanas

Publications and source records attributed to A Lanas.

At least 19 recordsLinked to original sources
PubMed1997

Evidence of aspirin use in both upper and lower gastrointestinal perforation.

BACKGROUND & AIMS: Current studies lack appropriate data on aspirin and other risk factors for gastrointestinal perforation. The aim of this study was to obtain the best estimate on aspirin and nonaspirin nonsteroidal anti-inflammatory drug (NSAID) use in these patients. METHODS: In 76 consecutive patients with gastrointestinal perforation and 152 matched controls, a detailed clinical history supplemented with an objective test of current aspirin use (platelet cyclooxygenase activity) was obtained. RESULTS: Of the 76 cases, 78.9% were upper and 21% lower gastrointestinal perforations. Evidence of NSAID use was found in 71% of cases (70% upper, 75% lower) vs. 26.9% of controls (odds ratio, 6.64; 95% confidence interval, 3.6-12.2; P < 0.0001). The objective test showed 12.7% more aspirin users than clinical history alone. NSAID use was aspirin (alone or combined) in 66.6% of cases, and 59.25% was nonprescription. Other independent risk factors were smoking, alcohol, and a history of arthritis or peptic ulcer but not a positive Helicobacter pylori serology. Age, but not NSAID use, affected perforation-associated mortality. CONCLUSIONS: NSAID use is strongly associated with an increased risk of both upper and lower gastrointestinal perforation. The high prevalence of aspirin (over-the-counter) use suggests that future introduction of new NSAIDs may not have a major impact on decreasing gastrointestinal complications if other measures are not taken. Concomitant NSAID use, smoking, and alcohol use is a pervasive association.

Aged↗
PubMed1997

Superoxide anions produced by inflammatory cells play an important part in the pathogenesis of acid and pepsin induced oesophagitis in rabbits.

BACKGROUND: Reactive oxygen metabolites have been associated with gastrointestinal injury. OBJECTIVE: To investigate whether mucosal reactive oxygen metabolites are involved in acid and pepsin induced oesophagitis, and if so, which specific metabolites. METHODS: The effects of free radical scavengers and the anti-inflammatory drug ketotifen on rabbit oesophagitis induced by acidified pepsin were studied. Isolated oesophageal cells were obtained before and after oesophageal injury and the generation of superoxide anion and hydrogen peroxide was analysed by flow cytometry. The presence of inflammatory cells was determined by indirect immunofluorescence with a mouse antirabbit CD11b antibody. RESULTS: Of the free radical scavengers tested, superoxide dismutase, which reacts with the superoxide anion, significantly reduced oesophagitis, whereas catalase, which reacts with hydrogen peroxide, had only a mild effect and dimethylsulphoxide had no effect. Ketotifen significantly reduced the inflammation and also prevented the induction of oesophagitis. Isolated cells obtained from the oesophageal mucosa after acidified pepsin exposure generated increased amounts of superoxide anions, which were mainly produced by CD11b positive cells. CONCLUSIONS: Reactive oxygen metabolites, especially superoxide anion, produced by inflammatory cells play a significant part in the genesis of oesophagitis induced by acid and pepsin in rabbits and might be a target for future medical therapy.

Animals↗
PubMed1996

Reversible prolonged skin bleeding time in acute gastrointestinal bleeding presumed due to NSAIDs.

The purpose of this research was to look for a possible mechanism whereby NSAIDs, and particularly ASA, might cause gastrointestinal bleeding. A total of 34 hospitalized GI bleeders and 29 age- and sex-matched controls were studied. Skin bleeding time (SBT) was measured within 6 h of coming to hospital and before any blood products were given. All patients and controls were questioned regarding current NSAID use. This history was supplemented by estimation of serum salicylate and of platelet cyclooxygenase activity to detect unreported current aspirin (ASA) use. Various aspects of platelet function were also tested by lumiaggregation in 28 controls and, after recovery, in 27 of the bleeders. Of 34 bleeders, 26 bled from the upper GI tract, (13 from peptic ulcer) and eight from the lower GI tract, 30 (88%) had a current intake of NSAIDs and of these 22 (73%) used ASA, some in combination with other NSAIDs, whereas 12 of 29 controls were using NSAID's, 11 of which were ASA. SBT in the bleeders was 9.0 +/- 1.02 min versus 4.8 +/- 0.42 min in the controls (p < 0.001). SBT measured 6.6 days later in 28 bleeders was 4.7 +/- 0.22 min (p < 0.0006), and of those tested after recovery all but one had fallen to 6.5 min or less. None had any residual constitutional platelet abnormalities as tested by lumiaggregation. By logistic regression, NSAID intake was strongly associated with prolonged SBT to > 6 min (odds ratio [OR], 16.7; p < 0.0002), whereas NSAID intake (OR 14.6; p < 0.0003) and SBT > 6 min (OR 1.8; p < 0.005) contributed to a bleeding outcome. Almost 90% of GI bleeders had recently consumed NSAIDs, mostly ASA, on an average 15 h before onset of bleeding. Although most of the nonbleeders who had used NSAIDs did not have a prolonged SBT, most of the bleeders who used NSAIDs had an abnormal elevation of SBT, suggesting a possible mechanism for GI bleeding. Retesting approximately 7 days after recovery from bleeding showed normalization of the SBT, indicating that the defect was transient and spontaneously reversible.

Acute Disease↗
PubMed1996

[Evaluation of intravenous ranitidine and omeprazole effect on the 24-hour gastric ph-metry in duodenal ulcer hemorrhage].

BACKGROUND: The pharmacotherapy of bleeding peptic ulcer is directed to improve the environment of the bleeding point by keeping the gastric pH above the proteolytic range for pepsin. OBJECTIVE: To evaluate the best pharmacological approach to inhibit gastric acid secretion with current antisecretory drugs in patients with bleeding duodenal ulcers. METHODS: Forty-seven patients with bleeding duodenal ulcers were randomized to receive I.V.: I) Omeprazole: an initial bolus of 80 mg + perfusion of 3.3 mg/h; II) Omeprazole: an initial bolus of 80 mg + 40 mg/12 h; III) Omeprazole: 40 mg/8 h; IV) Ranitidine: perfusion of 12.5 mg/h; V) Ranitidine: 50 mg/4 h. Gastric acidity was measured and recorded by 24 h gastric pH monitoring. RESULTS: All types of treatment with omeprazole were superior to either continuous perfusion or intermittent bolus of ranitidine in increasing the pH for 24 h and reducing the % of time the gastric pH was below 4 and 6, and the number of time the gastric pH was below 4 for more than 5 min. There were no statistical differences between the different regimens of omeprazole, but continuous perfusion of ranitidine was superior to intermittent ranitidine bolus. CONCLUSIONS: Parenteral omeprazole is better than parenteral ranitidine in keeping the intragastric pH above the proteolytic range for pepsin in patients with bleeding duodenal ulcers.

Adolescent↗
PubMed1995

Effect of parenteral omeprazole and ranitidine on gastric pH and the outcome of bleeding peptic ulcer.

The pharmacotherapy of bleeding peptic ulcer is directed at attempting to keep the gastric pH above the proteolytic range for pepsin. In this randomized, prospective, open clinical trial we have compared the effects and outcome of omeprazole versus ranitidine in patients with bleeding peptic ulcer. Of 219 consecutive patients with upper gastrointestinal bleeding, 51 (23.2%) had an ulcer with endoscopic predictors of rebleeding at the time of diagnosis. These 51 patients were selected at random to receive either omeprazole (80 mg bolus and 40 mg/12 h i.v.) or ranitidine (50 mg/4 h i.v.). No endoscopic therapy was performed at the time of diagnosis. Twenty of these patients with duodenal ulcer (n = 10 omeprazole, n = 10 ranitidine) underwent 24-h gastric pH monitoring. Both groups were homogeneous in all clinical and endoscopic parameters. No differences in blood transfusion units, time of hospitalization, the lowest hematocrit measured, and mortality rates were observed between the groups. However, omeprazole reduced the number of rebleeding episodes (p = 0.1) and the need for surgery (3.8% vs. 22.7%; p = 0.05). Omeprazole also reduced the amount of time the gastric pH was < 6 (15.3 +/- 5.9% vs. 61.8 +/- 5.6%, p < 0.0001). We conclude that parenteral omeprazole is much more effective than ranitidine in keeping the gastric pH above the proteolytic range for pepsin in bleeders and that this might explain a better outcome in a subset of patients with bleeding peptic ulcers treated with parenteral omeprazole.

Adult↗
PubMed1995

Increased gastric acid secretion after massive small bowel resection is related to a decrease in enterogastrones.

The reported increase of gastric secretion after small bowel (SB) resection is controversial. To determine the effect of SB resection on gastric acid secretion we studied basal and dose step pentagastrin-stimulated gastric acid secretion as well as basal serum gastrin, secretin, neurotensin and postprandial gastrin levels in 12 dogs, before and after resection of 60% of the intestine representing both proximal (n = 6) and distal (n = 6) SB. Rat bioassay was also performed to rule out the presence of unknown gastric secretagogues in the blood. Proximal SB resection produced a significant increase in basal and low dose (100 ng/kg/h) pentagastrin-stimulated gastric acid secretion (ED50 = 1,110 vs. 720 ng/kg/h after resection). However, no significant changes in gastric secretion were observed after distal SB resections. Neither proximal nor distal SB resection altered basal or postprandial serum gastrin levels. Proximal SB resection reduced serum secretin levels (229 +/- 38 vs. 134 +/- 16 pg/ml, p < 0.05) but did not alter neurotensin levels. Rat bioassay failed to reveal a circulating secretagogue after SB resections. We conclude that proximal but not distal SB resection increases basal and submaximally stimulated gastric acid secretion. Such an effect may be due to the observed decrease in circulating secretin levels.

Animals↗
PubMed1994

Ingestion of aspirin prevents platelet-induced human fibroblast growth. Implications for peptic ulcer healing.

Because aspirin (ASA) may affect peptic ulcer healing through actions on platelets (for example, by inhibiting release of growth factors), human foreskin fibroblast mitogenesis was used for two bioassays (24-h growth with 3H-thymidine incorporation and 5- to 6-day cell proliferation) for serum derived from collagen-aggregated platelet-rich plasma (PRP) or platelet-poor plasma (PPP) or from clotted whole blood (WBS). Blood was taken from five normal subjects before and 6 h after ingestion of ASA. After ASA ingestion serum (WBS or PRP) was less mitogenic (p < 0.01) by both bioassays, whereas PPP serum was not mitogenic either before or after ASA. In vitro, neither ASA nor salicylic acid alone at levels normally found in plasma with ASA use inhibited fibroblast growth. We conclude that ASA ingestion inhibits the mitogenic action of platelets on fibroblast culture by inhibiting the release of putative growth factors. Such an effect might explain the adverse effects of ASA on ulcer healing.

Aspirin↗
PubMed1994

[Favorable response to cisapride in acute colonic pseudo-obstruction (Ogilvie's syndrome)].

Acute pseudobstruction of the colon (Ogilvie's syndrome) has been treated by different surgical, endoscopic and radiological procedures, but a high proportion of recurrences has been reported. Here, we report two cases that showed a fast and favorable response to oral cisapride, a prokinetic agent that may become the treatment of choice for these patients.

Acute Disease↗
PubMed1994

[Diarrhea, protein-losing enteropathy and sarcoidosis].

A case of inactive sarcoidosis associated with protein-losing enteropathy, severe hypoalbuminemia and diarrhea is reported. 99mTc-labeled human serum albumin was performed to show protein loss. There was no abnormal upper gastrointestinal mucosa as shown by peroral duodenal and jejunal biopsies. However, a CT scan showed the presence of multiple calcified intra and retroperitoneal lymph nodes, which might explain the presence of lymphatic ectasia and protein-losing enteropathy in this case. A brief literature review of gastrointestinal sarcoidosis is included.

Biopsy↗
PubMed1992

Objective evidence of aspirin use in both ulcer and nonulcer upper and lower gastrointestinal bleeding.

To obtain the best evidence for nonsteroidal anti-inflammatory drug (NSAID) use in gastrointestinal (GI) bleeding, a detailed patient history was supplemented with objective tests of aspirin use, i.e., high-performance liquid chromatography of plasma and platelet cyclo-oxygenase inhibition, which detect aspirin intake within 24 and 120 hours, respectively. Seventy-one patients consecutively admitted for upper or lower GI bleeding and 138 age- and sex-matched controls were studied. Five bleeders were excluded for confounding factors, e.g., warfarin. Of the other 66 bleeders, 45 had upper GI bleeding (28 from peptic ulcer, 14 from duodenal ulcer, and 14 from gastric ulcer) and 21 lower GI bleeding. Evidence of current NSAID use (of which 89% was aspirin) was found in 80% of bleeders vs. 24.3% of controls (P less than 0.0001), for an odds ratio of 13.7 (95% confidence interval, 6.39-27.27). The cyclo-oxygenase test uncovered 21.5% more aspirin users than history alone. Severity of bleeding was not different in acetylsalicylic acid users. The surprisingly high association of current intake of NSAIDs, especially aspirin, with nonulcer GI bleeding including colonic bleeding, changes the conventional view of the following hierarchy of the risk: NSAID----peptic ulcer----bleeding to: NSAIDs----GI bleeding. This view has important implications for current ulcer cotherapy prophylactic strategies, which could fail to prevent greater than 50% of GI bleeding episodes.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Influence of smoking on basal and on vagally and maximally stimulated gastric acid and pepsin secretion.

Published data show that smokers have greater basal or peak acid and pepsin outputs, but the mechanisms underlying these effects are unknown. To confirm this and to determine whether these findings extend to, and implicate, any vagal overactivity, gastric secretions collected for 1 h basally, 1 h after 15 min of modified sham feeding (MSF), and 1 h after pentagastrin (6 micrograms/kg subcutaneously) were analyzed for acid and pepsin content in 204 subjects, 104 with duodenal ulcer (66 smokers) and 101 without (57 smokers). Maximal acid outputs (MAO, mu eq/kg/h, means +/- SEM) were higher in smokers than in non-smokers in both duodenal ulcer (DU) (623 +/- 35 versus 491 +/- 35, p less than 0.005) and non-DU (502 +/- 32 versus 376 +/- 20, p less than 0.005). Basal and MSF secretions were generally increased in smokers but, when expressed as a percentage of MAO, were not different in smokers and non-smokers (18% versus 17% and 43% versus 39%, respectively, in DU, and 13% versus 16% and 40% versus 36% in non-DU). Maximal pepsin outputs (units x 10(-2)/kg/h) were also higher in smokers than in non-smokers (DU, 129 +/- 7.9 versus 105 +/- 9.5, p = 0.05, and non-DU, 101 +/- 7.5 versus 77 +/- 10, p = 0.05). Basal and MSF secretions as a percentage of maximal pepsin output were not different in smokers versus non-smokers. Multivariate logistic regression shows that smoking was most strongly associated with MAO and sham feeding outputs, but the duration-intensity (pack-years) of smoking was associated only with elevated MAO.(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenal Ulcer↗
PubMed1992

[Gastric emptying of solids, acid secretion and tobacco in duodenal ulcer].

We study in a group of patients with endoscopically diagnosed duodenal ulcer (19; 17 males) and controls (11; 7 males) the gastric emptying of solids through scintigraphy and gastric acid secretion by standard tests. In the same way we investigated prospectively some clinical data, specially smoking habits. As a whole, patients with duodenal ulcer showed an emptying of solids slightly faster than controls (T 1/2-minutes-: 85.4 +/- 28.6 in patients with duodenal ulcer versus 116.9 +/- 46.5 in controls, p less than 0.03). However, most of our patients (15 of 19 or 79%) were found to have a normal emptying rate. No correlation was found between secretory outputs and gastric emptying. Smokers with duodenal ulcer had a faster emptying that non-smokers with duodenal ulcer (T 1/2 74.8 +/- 30.05 vs. 99.91 +/- 19.86; p = 0.05).

Adult↗
PubMed1991

Significant role of aspirin use in patients with esophagitis.

This study determines objectively the extent of nonsteroidal anti-inflammatory drug (NSAID) use in upper gastrointestinal (GI) mucosal acid-peptic diseases by supplementing the conventional interview with two tests of current aspirin (ASA) use--high-performance liquid chromatography (HPLC) for the presence of salicylates in serum and platelet cyclooxygenase activity, which detects ASA use within 5 days of testing. Of 186 consecutive patients undergoing upper endoscopy, 62% of 55 patients with esophagitis had evidence of current NSAID use, vs. 26% of 42 control patients with normal endoscopy (p less than 0.001), 12% of 17 patients with recently healed peptic ulcer (p less than 0.001), and 36% of 25 patients who had an active peptic ulcer (p less than 0.05), five of whom had concomitant esophagitis. Another 52 patients were ineligible for this analysis. Testing for platelet cyclooxygenase activity uncovered 26% more ASA users than history alone. In considering age, sex, smoking and drinking habits, arthritis, and ASA use by logistic regression, ASA use was the only factor contributing to esophagitis; ASA could not be further associated with severity, stricture or symptoms, however. In these patients, 95% of NSAID use was chronic, and 84% of that was ASA. These data show a previously unreported, strong association of ASA use with esophagitis, which suggests that ASA may be a significant factor in the resistance of esophagitis to current therapies as well as the frequently rapid relapse after therapy is withdrawn.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

NSAID association with gastrointestinal bleeding and peptic ulcer.

This paper reviews recent data describing the increased risk of bleeding and peptic ulcer with NSAID use in arthritis and non-arthritis populations. We briefly report personal studies on both aspects. By objective testing in 66 GI bleeders the use of NSAIDs, especially ASA, was more strongly associated with GI bleeding from both ulcer and non-ulcer sources, including colonic, than previously reported (82% vs. 21% in controls). ASA abuse, often surreptitious, may account for many, if not most, treatment-resistant peptic ulcers. We report 29 such patients. Adverse effects of NSAID use add considerably to economic cost, excess morbidity and mortality, especially in the elderly. Bleeding and peptic ulcer are separate risks of NSAID use. This conclusion carries major implications for prophylaxis strategies.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

[Smoking and serum gastrin and pepsinogen I levels in patients with duodenal ulcers].

At present the mechanisms by which the use of tobacco produces a damaging effect on duodenal ulcerous disease are not clearly understood. This paper reports the results of a study of basal and postprandial gastrin and pepsinogen I (PG I) levels of 74 duodenal ulcer (DU) patients and 18 controls in relation to their smoking habits. There was no difference between the UD group and the control group as far as basal gastrin levels were concerned, but there was in the PG I levels (107 +/- 54 ng/ml in UD vs. 69 +/- 30 ng/ml in control) (p less than 0.05). The postprandial gastrin and PG I responses in 34 UD subjects only differed in relation to smoker/non-smoker status; there was no correlation with age less than greater than 35, positive family history or duration of illness. Patients who had had UD less than 10 years showed higher postprandial PG I levels; however, this group included the 83.3% smokers with UD. It was concluded that chronic smoking is clearly related to the existence of hyperpepsinogenemia I, and probably also to postprandial hypergastrinemia in UD sufferers.

Adult↗
PubMed1989

[Primary biliary cirrhosis in Navarra].

50 cases of PBC registered in Navarra during 1974-1987 were studied retrospectively. 38% of the diagnosis were carried out in the non-symptomatic period. There were no histological differences between symptomatic (2.24 +/- 1.16) periods. In the first group the delay in diagnosis was very high: 28.21 months, the jaundice being followed by itching of 11.65 months duration. The rate of PBC has increased progressively, rising to a global incidence of 25.15/million and 78.03/million for women over 25 years old. There figures are 3 and 9 times higher than those published in spanish and most foreign literature. We did not find any significant differences between the several health service areas in Navarra, nor between rural or urban areas. Our paper brings to the fore this question: is Navarra an area of especial prevalence of PBC or does it simply offer better diagnosis conditions?

Adult↗
PubMed1989

[Effectiveness of emergency endoscopic sclerosis in the control of digestive hemorrhage caused by gastroduodenal ulcer].

An investigation was made of the effect of emergency endoscopic sclerotherapy on the evaluation of digestive hemorrhage (HDA) secondary to gastroduodenal ulcer disease in two consecutive groups of patients. The control group included 92 patients and the sclerotherapy group contained 63. Both groups had the same management and basic treatment of hemodynamic stabilization, anti-H2 agents and alkaline . The sclerotherapy group also received a local injection of 1/10,000 (5-12 ml) adrenaline and 1% polydocanol (5-12 ml) if direct signs of hemorrhage (active bleeding, red clot, visible vessel) were seen at the time of early endoscopy. Surgery was indicated in the presence of persistent, recurrent or massive digestive hemorrhage. Thirty-two percent of the control group and 34% of the sclerosis group presented direct signs of hemorrhage at the time of endoscopy. Both groups were homogeneous with respect to sex distribution, NSAID intake, hemoglobin, presence of shock and etiology (33.3% and 36.3%, respectively, had duodenal ulcer). The average age was significantly higher in the control group than in the sclerotherapy group. Neither the presence of any endoscopic sign nor etiology contributed to the evolution of digestive bleeding. It is concluded that emergency endoscopic sclerotherapy with injection of adrenaline and polydocanol has a clearly favorable effect on the evolution of bleeding secondary to gastrointestinal ulcer disease evidencing direct signs on endoscopy.

Acute Disease↗