Leukotriene receptor antagonists as potential steroid sparing agents in a patient with serosal eosinophilic gastroenteritis.
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Biomedical subjects
Publications and source records attributed to M Banić.
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OBJECTIVE: The aim of this study was to determine the prevalence and risk factors for peptic ulcer disease (PUD) in dyspeptic patients with ischemic heart disease (IHD), and to assess whether the healing of PUD before coronary artery bypass grafting (CABG) could reduce the need for urgent postoperative endoscopy. PATIENTS AND METHODS: A series of 894 patients referred to Dubrava University Hospital in Zagreb for elective CABG during the period from May 1998 until April 2001 was prospectively analysed. Dyspepsia was assessed by a questionnaire, PUD by upper gastrointestinal endoscopy, and H. pylori status by histology/Giemsa staining and the rapid urease test. The need for urgent postoperative endoscopy (hematemesis and/or melena, sudden onset of anemia or unexplained epigastric pain) was compared between the prospective study group of 894 patients and a series of 463 patients referred for CABG to Dubrava University Hospital during the period from January 1997 until April 1998. RESULTS: Gastroduodenal dyspepsia predominated in 184 (20.6 %) patients, 142 (77.2 %) of them with Helicobacter (H.) pylori infection and 69 (37.5 %) with verified PUD. Univariate analysis indicated the increased risk of multiple PUD to be related to a previous diagnosis of PUD (OR 3.61, 95 % CI 1.32 - 9.82), H. pylori infection (OR 18.86, 95 % CI 2.31 - 153.98), use of aspirin (OR 5.70; 95 % CI 1.80 - 18.03) and left coronary artery occlusions (3.10, 95 % CI 1.00 - 9.59). Multivariate analysis pointed to H. pylori infection (OR 16.30, 95 % CI 1.57 - 168.53) and left coronary artery occlusions (OR 4.84, 95 % CI 1.05 - 22.30) as independent risk factors for multiple PUD. The OR for urgent postoperative endoscopy due to a major gastrointestinal event was 9.9 (95 % CI 2.2 - 45.1) and the OR for active peptic ulcer with stigmata of recent bleeding was 6.9 (95 % CI 1.4 - 33.1) in the group of patients with IHD who were not submitted to evaluation for dyspepsia prior to elective heart surgery. CONCLUSIONS: In areas with a high prevalence of H. pylori infection, endoscopy and a "search and treat" strategy for IHD patients with dyspepsia before elective cardiac surgery should significantly reduce the need for urgent postoperative endoscopy due to major gastrointestinal events.
Prospective investigation has been undertaken with the aim to study the frequency, location and age and sex distribution of various histological types of benign gastric epithelial polyps. Histological type--adenomatous, hyperplastic and fundic gland polyps--was diagnosed on the basis of at least three histological samples taken from the polyp. Biopsy samples were also taken from the antrum and the body of the stomach so that gastritis could be graded and classified, and the presence of H. pylori could be determined by histology. All 6,700 patients, who had undergone upper gastrointestinal endoscopy in a one-year period, participated in this study. Among them 42 benign gastric epithelial polyp were found in 31 patients: adenomatous gastric polyps in 7 patients, hyperplastic gastric polyp in 21 and fundic gland polyp in 3 patients. All patients with hyperplastic polyps had chronic active superficial gastritis, whereas most of the patients with adenomatous polyps had a chronic atrophic gastritis with high prevalence of intestinal metaplasia. Among 21 patients with hyperplastic gastric polyps, 16 (76%) patients were positive for H. pylori infection in contrast to only 2 patients (29%) with adenomatous gastric polyps and 1 patient (33%) with fundic gland polyp. Presented data indicates that hyperplastic gastric polyps are the most common and they are associated with the presence of chronic active superficial gastritis and concomitant H. pylori infection. Adenomatous polyps are rarer and they tend to be associated with chronic atrophic gastritis and intestinal metaplasia. Fundic gland polyp is the rarest type of gastric polyps.
The aim of the study was to demonstrate the effects of dopaminergic drugs on 2,4-dinitrofluorbenzene (DNFB) induced experimental inflammatory bowel disease (IBD) in previously sensitized BALB/c mice. The number and extent of ulcerations and erosions, the intensity of haemorrhages, oedema, and accumulation of neutrophils and eosinophils within colonic lamina propria and submucosa were scored and statistically evaluated. The 180 BALB/c mice, were allocated into three equal groups. The mice in the first experimental group were treated with domperidone (DP), a peripheral dopamine (DA) antagonist. The mice from the second experimental group were treated with bromocriptine (BC), a dopamine agonist. The mice from the control group were treated with an equivalent volume of normal saline in the same manner. Ten animals from each group were killed on days 1, 2, 3, 5 and 10, subsequent to the challenge enema of DNFB solution. Gross and microscopic examination of the colon was performed. Treatment with BC resulted in clinical improvement and decreased mortality rate by 2 of 60 (3%), while domperidone treatment increased mortality rate to 12 of 60 (20%) compared with the controls [4 of 60 (6%)]. The analysis of the microscopic lesions indicated that the beneficial effects of BC were the result of maintenance of vascular integrity.
Histopathologic and clinical data strongly suggest a causal relation between Helicobacter pylori infection and gastritis, peptic ulcer disease, or both. However, little has been written about the potential association between H. pylori infection and Brunner's gland adenoma. Therefore, we carried out a prospective study to determine the presence of H. pylori infection among patients with Brunner's gland adenoma. From November 1996 till October 1999, 19100 patients who had undergone upper gastrointestinal endoscopy at two clinical centers in Zagreb, Croatia, were candidates for participation in the study. Brunner's gland adenoma was diagnosed on the basis of histologic samples taken from the polyp (four patients) or after the entire polyp was made available upon endoscopic removal (three patients). When all endoscopic examinations had been performed, biopsy samples were taken from the antrum and body of the stomach, so that gastritis could be classified and H. pylori determined by histology. Biopsy samples were also taken from the duodenal bulb to verify duodenitis. Two other samples were taken from the antrum for rapid urease test. The patients were considered positive for H. pylori when both histology and rapid urease test were positive. Brunner's gland adenoma was diagnosed in seven patients (five women and two men; median age, 49 yrs). Five (71%) patients with diagnosed Brunner's gland adenoma had concurrent H. pylori infection. Duodenitis associated with gastric metaplasia was observed in six patients. Complete eradication of H. pylori was achieved in only two patients. Symptoms disappeared or markedly diminished in all patients with significant improvement during therapy or immediately upon endoscopic removal of the polyp. Although limited by a very small number of patients, our results suggest that concurrent H. pylori infection is very common in patients with Brunner's gland adenoma. However, the role of H. pylori infection in the pathogenesis and development of Brunner's gland hyperplasia remains unclear.
Spigelian hernia is a very rare anterior abdominal wall hernia with uncharacteristic symptoms and challenging diagnosis. The case of a 76-year-old male patient with colicky pain and vomiting lasting for 24 hours before admission to the hospital is presented. Physical examination of the patient revealed abdominal tenderness and a round-shaped tumefaction of 3 cm in size, located in the left lower abdominal quadrant. X-ray examination of the abdomen, obtained in left lateral position of the patient, showed small bowel ileus with distended jejunal loops. The abdominal ultrasound examination, followed by duplex ultrasonography, revealed a spigelian hernia with ischemic changes of strangulated bowel segment indicating incarceration of the herniated jejunal loop. Preoperative findings were confirmed by intraoperative diagnosis of spigelian hernia and incarcerated jejunal loop with ischemic changes and deserosation, followed by resection of the bowel segment involved and plastic surgical reconstruction of anterior abdominal wall. This case report highlights the role of duplex ultrasonography in the evaluation of circulatory status of potentially incarcerated bowel segment within hernial sac.
OBJECTIVE: Histopathological and clinical data strongly suggest that Helicobacter pylori is the cause of chronic gastritis and peptic ulceration. However, little has been written about the potential causal relation of H. pylori infection to hyperplastic and adenomatous gastric polyps. We therefore carried out a prospective study to determine the effect of eradicating H. pylori infection on the course of hyperplastic and adenomatous gastric polyps. METHODS: From November 1996 to December 1997, 6700 patients who had undergone upper gastrointestinal endoscopy at the two centres in Zagreb, Croatia, were candidates for participation in the study. Hyperplastic and adenomatous polyps were diagnosed on a basis of at least three histological samples taken from the polyp. In seven patients endoscopy had to be repeated because forceps biopsy sampling either provided inadequate tissue for correct histological diagnosis, or accurate characterization of gastric polyp histology was not possible. Upon completion of all endoscopic examinations before and after treatment, biopsy samples were taken from the antrum (two) and the body of the stomach (two) so that gastritis could be graded and classified, and the presence of H. pylori sought by histology. Two other samples were taken from the antrum for a rapid urease test. Follow-up examinations were performed by using endoscopy. Control endoscopy was performed at least 4 weeks after the treatment of H. pylori infection had been completed, and then every 3-4 months. The follow-up ranged from 4 to 17 months, with a median of 14 months. The treatment of H. pylori infection consisted of a 1-week course of either omeprazole (20 mg twice daily) or pantoprazole 40 mg twice daily), and a 1-week course of amoxicillin 2g twice daily) and metronidazole (400 mg three times daily), and clarithromycin (500 mg twice daily). Eradication of H. pylori infection was assessed by repeated histology and rapid urease test. RESULTS: Twenty-one patients (nine women, 12 men; median age 52 years) with histologically proven hyperplastic gastric polyps, and seven patients (two women, five men; median age, 67 years) with adenomatous gastric polyps were included in the study. Among 21 patients with hyperplastic gastric polyps, 16 patients (76%) were positive for H. pylori infection. Only two patients (29%) with adenomatous gastric polyps were positive for the infection. Complete eradication of H. pylori was initially achieved in all patients positive for H. pylori. Total regression of the gastric polyps was observed only among the patients with hyperplastic gastric polyps in whom H. pylori had been eradicated. Complete regression of the hyperplastic gastric polyps was observed in seven of the 16 evaluable patients (44%; 95% CI, 19-68%) after H. pylori eradication. The endoscopic snare polypectomy was carried out in nine patients with hyperplastic polyps and two patients with adenomatous gastric polyps in whom regression of the polyps was not observed after H. pylori eradication, as well as in five patients with hyperplastic and four with adenomatous gastric polyps who were negative for H. pylori. Exploratory laparotomy and gastrotomy with polyps excision were carried out in one patient with multiple adenomatous gastric polyps. In only one patient who was not positive for H. pylori recurrence of hyperplastic gastric polyp was recorded during follow-up, and no re-infection with H. pylori has been detected. CONCLUSIONS: Our results suggest that the development of hyperplastic gastric polyps may be directly related to chronic active gastritis and concomitant H. pylori infection. Cure of H. pylori infection associated with hyperplastic gastric polyps resulted in complete polyp regression in more than 40% of patients. Therefore, for patients with hyperplastic gastric polyps and concurrent H. pylori infection an antibiotic treatment designed to eradicate H. pylori appears to be recommended before further therapeutic options are consi
BACKGROUND: A low-sodium diet and diuretics, although widely used, are not always the most satisfactory therapy for treatment of ascites in nonazotemic patients with liver cirrhosis. The objective of this investigation was to analyze various predictive factors influencing the therapeutic response to diuretic treatment of ascites in these patients. METHODS: Twenty-seven patients with nonazotemic liver cirrhosis and ascites were initially treated with spironolactone, 200 mg/day. If no response was observed, furosemide was added at 40-120 mg/day. Before and during the diuretic therapy 30 clinical and laboratory variables were investigated as possible predictive factors influencing the therapeutic response to diuretics. The renal arterial resistive index (RI) (reflecting renal vascular resistance) was estimated with duplex Doppler ultrasonography. RESULTS: Sixteen of the 27 patients (59%) responded to spironolactone alone, whereas 6 patients (22%) responded to combined diuretic therapy with spironolactone and furosemide. Five patients (19%) did not respond to diuretic treatment. Eight of the 30 variables analyzed were statistically significant as possible predictive factors influencing the diuretic response: previous episodes of ascites and gastrointestinal hemorrhage, the presence of peripheral edema, the amount of ascites, plasma renin activity, plasma aldosterone concentrations, urinary sodium excretion, and renal interlobar arterial RI. In all patients who had diuretic-resistant ascites, renal interlobar arterial RI was greater than 0.70. Only 9% of patients who responded satisfactorily to diuretic therapy had interlobar arterial RI greater than 0.70. CONCLUSIONS: According to our results, consideration for combining the clinical findings with noninvasively measured renal arterial RI using duplex Doppler ultrasonography would be mandatory in identifying a subgroup of cirrhotic patients with ascites who are at high risk for diuretic unresponsiveness.
The aim of the study was to reveal the histopathologic features of intestinal inflammation as demonstrated in BALB/c mice, using the challenge of 2,4-dinitrofluorobenzene (DNFB) with or without previous sensitization. Forty mice were randomized into 5 groups. Two groups of animals were treated with rectal enema of 0.2% or 1.0% of 2,4-dinitrofluorobenzene solution. Third group was pretreated with 2 sensitizing doses of DNFB. Two control groups were treated with PBS or acetone and vehicle enema only (acetone and olive oil). In order to assess the extent of colonic inflammation and damage, a histopathologic score scale was developed. In contrast to scanty superficial ulcerations and mild edema observed in the control group of animals, edema, ulcerations, hemorrhage, necrosis and infiltration of inflammatory cells were observed in experiment groups treated with enema of DNFB. Total score of lesion as well almost all inflammatory parameters of injury observed were highest in previously sensitized animals. The results of this study clearly demonstrated the pattern of colonic inflammation induced with DNFB using the histopathologic scoring scale system.
The aim of this article was to reveal the major biologic features of intestine that predispose the intestinal mucosa to numerous inflammatory conditions, especially in regard to experimental models of inflammatory bowel disease. The need for the greater understanding of the etiology of intestinal inflammation and the search for more effective and novel therapy for the treatment of the disease has led to the development of variety of experimental models of inflammatory bowel disease. There is a growing number of animal models of inflammatory bowel disease, either naturally occurring in several mammalian species or inducible in various species of experimental animals by using physical, chemical and biologic agents including the embryonic stem cell technology for specific gene targeted defects. Despite some serious objectives in regard to clinical aspects of human intestinal bowel disease, animal models of intestinal inflammation have advantages and being complementary to clinical approach indicate the clear need for experimental studies to be continued.
The aim of the study was to investigate the serum selenium concentration in patients with liver cirrhosis and hepatocellular carcinoma. A total of 59 patients, 49 with liver cirrhosis and 10 with liver cirrhosis and coexistent hepatocellular carcinoma, as well as 202 healthy volunteers entered the study. In the patients with liver cirrhosis and in those with liver cirrhosis and coexistent hepatocellular carcinoma, serum selenium concentrations were significantly lower (39.28 +/- 13.99 and 42.00 +/- 10.59 g/L, respectively), when compared to the group of healthy volunteers (66. 79 +/- 9.13 g/L) (p < 0.001). There was no significant difference in serum selenium concentrations between the two patient groups. In the group of patients with liver cirrhosis positive correlation was found between serum selenium and albumin concentrations, and negative correlation between serum selenium and bilirubin (p < 0.05 and p < 0.01, respectively). There was no correlation of serum selenium concentration with fibrinogen and prothrombin time. Results of the study suggested the possible important nutritive and protective role of selenium in the patients with liver cirrhosis and coexistent hepatocellular carcinoma, as well as the potential need of selenium supplementation in these patients.
The most relevant clinical presentations of duodenal ulcer disease are pain and acute bleeding. The purpose of this study was to investigate the relevance of dyspepsia in patients with bleeding duodenal ulcer, and to compare the clinical and epidemiological characteristics of bleeding patients with and without dyspepsia. A total of 82 patients with isolated duodenal ulcer and bleeding were included in this study. There were 48 (58.5%) dyspeptic and 34 (41.5%) nondyspeptic patients. The patients with and without dyspepsia were almost identical with regard to their age (52.9 +/- 11.9 vs 53.4+/- 10.2 years, p > 0.05). In the dyspeptic group, significantly more patients had duodenitis and a deformed bulb (chi 2 = 4.05, p < 0.05 and chi 2 = 3.99, p < 0.05, respectively). Patients with bleeding duodenal ulcers and dyspepsia were more likely to have taken non-steroidal anti-inflammatory drugs (45.8 vs 8.8%; chi 2 = 11.18, p < 0.001), whereas significantly more patients in the nondyspeptic group have taken histamine H2 antagonists (85.3 vs 8.3%; chi 2 = 45.87, p < 0.01). No significant difference was found between the dyspeptic and nondyspeptic groups with regard to the previous diagnosis of peptic ulcer bleeding, the presence of environmental stress, gastritis, and alcohol or tobacco consumption. Furthermore, there was no significant difference in regard to the rebleeding, the need for urgent operation or hospital stay. The results of this study support the evidence that in patients with bleeding duodenal ulcers the dyspeptic symptoms were more often associated with objective signs of duodenal pathology, and the use of non-steroidal anti-inflammatory drugs and maintenance treatment with histamine H2 antagonists was associated with silent duodenal ulcer bleeding.
The aim of the study was to assess the diagnostic value of transrectal ultrasonography (TRUS) in detecting the depth of tumor infiltration as well as the involvement of lymph nodes in patients with rectal carcinoma diagnosed after rectoscopy and proven by examination of the biopsy specimen. TRUS was performed on thirty-three patients with rectal carcinoma prior to surgery, the first assessment of tumor growth, and extension by pathological examination of the operative specimen. TRUS correctly assessed perirectal growth in 18 out of 22 cases proven by pathology (two understaged, accuracy 86 percent), while in 12 cases with no perirectal growth proven by pathology this method was correct in 9 cases (three overstaged, accuracy 75 percent). The results of this study indicate that TRUS, combined with endoscopy and biopsy, is a useful procedure in the preoperative staging of malignant rectal lesions and provides valuable data for the therapeutic planning of patients with rectal carcinoma.
The aim of this study was to evaluate the influence of methylprednisolone (1 mg/kg, i.p.) on inflammatory lesions in the small bowel, liver (pericholangitis) and spleen (lymphofollicular proliferation), in a model of inflammatory bowel disease induced by 2.4-dinitrofluorobenzene in previously sensitized BALB-c mice. As a parameter of corticosteroid anti-inflammatory and immunosuppressive action, we simultaneously investigated its effects on mononuclear cell accumulation within the ileal lamina propria and submucosa during the observed time period (1-30 days). We noted a significant decrease in accumulation of mononuclear cells within the lamina propria (P < 0.001). An effect on mononuclear cell infiltration within the ileal submucosa was also noted but was not statistically significant. In addition, pericholangitis in the liver and lymphofollicular proliferation in the spleen were not observed in the experimental group during treatment with methylprednisolone. The results of this study indicate that the previously described model of intestinal inflammation could be used in further research of present and new therapeutic modalities for inflammatory bowel disease.
Prolactin inhibitory tests (bromocriptine in a single dose 2.5 mg orally) as well as stimulatory tests (metoclopramide in a single dose of 10 mg intravenously) were performed in 33 patients with endoscopically proven duodenal ulcer and in 32 healthy volunteers. Delayed response in inhibition of prolactin release as well as in stimulation of prolactin release was observed in duodenal ulcer patients compared to healthy volunteers (P < 0.01). The results implicate the role of the dopamine-prolactin axis in the pathogenesis of duodenal ulcer disease.
The aim of this study was to develop a model of inflammatory bowel disease (IBD) induced by colonic application of 2,4-dinitrofluorobenzene in previously sensitized BALB-c mice. During the follow-up period of 30 days we observed ulcerations, haemorrhage, necrosis, and mononuclear infiltration in the colonic mucosa of previously sensitized (experimental) and, to a lesser extent, nonsensitized (control) animals. In addition, the animals in the experimental group developed adhesions, thickening of colonic segments, stenosis, and dilatation of the colon, and some animals also developed megacolon. Oedema, mononuclear infiltration, and superficial ulcerations were observed in the ileum of experimental animals and, to a lesser extent, in the control group. In addition, the animals in the experimental group developed extraintestinal changes in the liver and spleen (that is, pericholangitis and lymphofollicular proliferation). We suggest that this model of IBD may have some value for the study of early pathogenetic mechanisms of IBD and for developing new therapeutic modalities for this condition.
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The aims of the study were to compare the results of endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous cystopancreatography (PCP) in the detection of the communication between the pancreatic pseudocyst and the pancreatic duct, and to assess the reliability of the increased amylase concentration in the pseudocyst content as an indicator of the existence of communication between the pancreatic pseudocyst and the pancreatic duct system. Forty-three patients were included in the study. Pseudocystic fluid content was obtained by percutaneous aspiration. Twenty-four patients had pseudocyst amylase concentrations above 64 Wolgemuth units (WU), and 19 patients had less than 64 WU. The communication between pseudocyst and the pancreatic duct was determined in 22 patients by ERCP and in 13 patients by PCP, all in the group with increased pseudocyst amylase concentration. Due to high sensitivity and specificity of pseudocyst amylase concentration for the existence of pseudocyst communication with the pancreatic duct, we conclude that guided percutaneous aspiration of the pancreatic pseudocyst with the determination of amylase concentration in the fluid can replace ERCP as a method of choice for the detection of pseudocyst communication with the pancreatic duct.