Biomedical subjects

W Bielański

Publications and source records attributed to W Bielański.

At least 19 recordsLinked to original sources

PubMed2005

Variable effect of ghrelin administration on pancreatic development in young rats. Role of insulin-like growth factor-1.

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been primarily isolated from the human and rat stomach. Ghrelin has been shown to stimulate appetite and fat deposition in adult rats and humans. The aim of this study was to investigate the effect of ghrelin administration on pancreatic growth in suckling, weaned and peripubertal seven week old rats. Rats were treated with saline or ghrelin (4, 8 or 16 nmol/kg/dose) intraperitoneally twice a day: suckling rats were treated for 7 or 14 days starting from the first postnatal day, three week old weaned rats and seven weeks old rats were treated for 5 days. Treatment with ghrelin did not affect animal weight in suckling or weaned rats, whereas in young seven week old rats, ghrelin caused a significant increase in body weight. Ghrelin decreased food intake in weaned rats; whereas in seven week old rats, food intake was enhanced. In suckling rats, ghrelin decreased the pancreatic weight, pancreatic amylase content, DNA synthesis and DNA content. In contrast, ghrelin increased pancreatic weight, DNA synthesis, DNA content and amylase content in weaned or young seven week old rats. Pancreatic blood flow was not affected by ghrelin in any group of rats tested. Ghrelin increased serum level of growth hormone in all rats. This effect was weak in suckling rats, higher in weaned and the highest in seven week old animals. Ghrelin did not affect serum level of insulin-like growth factor-1 (IGF-1) in suckling rats. In weaned and in seven week old rats, treatment with ghrelin caused increase in serum level of IGF-1. We conclude that ghrelin reduces pancreatic growth in suckling rats; whereas in weaned and young seven week old animals, treatment with ghrelin increases pancreatic growth. This biphasic effect of ghrelin in young animals on pancreatic growth seems to be related to age-dependent changes of the release of anabolic IGF-1.

Amylases↗

PubMed2004

Association of the presence of Helicobacter pylori in the oral cavity and in the stomach.

UNLABELLED: Helicobacter pylori is a gram-negative, microaerophilic rod-shaped bacteria that lives beneath the gastric mucous layer, on the surface of epithelial cells. Stomach infection with this organism causes inflammation of the gastric mucosa, which can lead to gastritis, duodenal or gastric ulcer and even in rare cases to gastric carcinoma or MALT lymphoma. Approximately 50% of the world's population is believed to be infected with H. pylori. Most infections is probably acquired in childhood, but the exact route of transmission is unknown. It has been speculated that dental plaque might harbour Helicobacter pylori and, therefore, might be a source of gastric infection. In order to address this issue we studied the relationships between oral and gastric infections with H. pylori in 100 subjects. METHODS: Gastric H. pylori infection was determined by (13)C-urea breath test (UBT) and the presence of the bacteria in oral cavity was monitored by the culture from the saliva and from dental plaque. RESULTS: H. pylori was found in the stomach in 51% of studied individuals, while oral H. pylori was found in 54% (in saliva) and in 48.3% (in gingival pockets), the difference was not statistical significant (p=NS). Interestingly, anti-Hp IgA was found in 84% of studied individuals. No relationship was found between the presence of the bacteria in the oral cavity and the H. pylori gastric infection. 54.9% of subjects with stomach infection showed concomitant presence of H. pylori in saliva. 52.3% of examined subjects with negative UBT-test revealed the presence of H. pylori in culture from the saliva. The X(2) value of relationship between UBT and culture H pylori in saliva was 0.029 (p=0.9). Similarly, no relationship was found between the presence of H. pylori in the stomach and in the dental plaque (X2=0.6); p=0.4). As expected, the presence of H. pylori in the dental plaque was significantly correlated with the presence of bacteria in the saliva (X2=18.4; p=0.0002). We also compared the presence of H. pylori in the saliva of patients with and without teeth. The cultured H. pylori was found in 63.7% of patients without teeth and in 52.9% of patients with teeth. This indicates that the presence of teeth does not seem to affect the occurrence of H. pylori in saliva. We conclude that oral activity contamination with of H. pylori occurs at similar degree to that in the stomach. However, there was no significant correlation between the occurrence of H. pylori in the stomach and in the oral cavity indicating that other factors, like susceptibility to infection due to acid environment in the stomach may be the major factor in gastric infection with that bacteria, while oral cavity may serve only as transient food-related contamination without clear relation to gastric infection.

Adult↗

PubMed2003

Helicobacter pylori, non-steroidal anti-inflammatory drugs and smoking in risk pattern of gastroduodenal ulcers.

BACKGROUND: Helicobacter pylori, NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. METHODS: 5967 dyspeptic patients underwent 13C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. RESULTS: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. CONCLUSIONS: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).

Adult↗

PubMed2001

Leptin in the control of gastric secretion and gut hormones in humans infected with Helicobacter pylori.

BACKGROUND: Leptin, a protein product of obese gene expressed primarily by adipocytes, provides feedback information on the size of energy stores to central OB receptors controlling the food intake, energy expenditure and body weight homeostasis. It has recently been detected in the rat stomach, especially after cholecystokinin (CCK) administration and in human stomach infected with Helicobacter pylori, but its role in gastric secretory functions in humans has not been revealed. This study was designed to determine the involvement of leptin in the control of basal, CCK- and meal-induced gastric H+ secretion and plasma gastrin and CCK levels in humans before and after an eradication of H. pylori. METHODS: Two groups (A and B) of subjects were used; group A (n = 7), for comparison of the effects of CCK and leptin on basal gastric H+ and plasma hormone (leptin, gastrin and CCK) levels, and group B (n = 6), for studies on the involvement of leptin in gastric secretory and plasma hormonal responses to vagal stimulation and gastric peptone meal before and after H. pylori eradication. RESULTS: In H. pylori-positive subjects, CCK (12-200 pmol kg(-1) h(-1)) given i.v. caused a dose-dependent increase of gastric H+ accompanied by a dose-dependent rise in plasma CCK and leptin levels. In contrast, leptin administered i.v. in graded doses (5-80 pmol kg(-1) h(-1)) resulted in a gradual inhibition of basal gastric H+ secretion and in adose-dependent increment in plasma leptin accompanied by an increase in plasma gastrin without alteration of plasma CCK level. Following eradication of H. pylori by 1-week triple therapy in group B patients, the infusion of CCK produced a significantly smaller increase in gastric H+ secretion and significantly smaller rise in plasma leptin as compared to those before the eradication. Cephalic phase stimulation of gastric secretion induced by modified sham-feeding in group B H. pylori-positive subjects increased gastric H+ secretion to about 40% of pentagastrin maximum without affecting plasma leptin, gastrin, or CCK level, while gastric peptone meal resulted in the increase in gastric H+ response reaching about 70% of pentagastrin maximum accompanied by a marked rise in plasma leptin, gastrin and CCK. The treatment with a standard dose of leptin (20 pmol kg(-1) h(-1)) failed to affect sham-feeding-induced gastric H+ secretion but reduced significantly the peptone meal-stimulated H+ secretion, while raising plasma gastrin in response to this meal. Plasma CCK under basal conditions and after sham-feeding was not affected, but plasma CCK response to gastric meal was significantly reduced by leptin infusion. Eradication of H. pylori did not affect basal or sham-feeding-induced H+ secretion but resulted in a significant fall in gastric meal-induced H+ and plasma leptin, gastrin and CCK levels. CONCLUSIONS: 1) The gastric meal and CCK enhance the release of leptin in H. pylori-positive patients and this leptin is capable of inhibiting basal and meal-stimulated gastric H+ secretion, while raising plasma gastrin and reducing the plasma CCK levels, and 2) the eradication of H. pylori reduces the postprandial gastric H+ and plasmagastrin responses as well as the release of leptin in response to CCK and meal.

Adult↗

PubMed2001

Involvement of cyclooxygenase-derived prostaglandin E2 and nitric oxide in the protection of rat pancreas afforded by low dose of lipopolysaccharide.

Prostaglandins (PG), the products of arachidonate metabolism through cyclooxygenase (COX) pathway, protect the pancreas from the acute damage. The existence of two isoforms of COX was documented including: COX-1, present in normal tissues and COX-2, expressed at the site of inflammation, such as induced by bacterial lipopolysaccharide (LPS). Pretreatment with low dose of LPS and activation of nitric oxide (NO) synthase (NOS) has been shown to prevent the injury caused by caerulein-induced pancreatitis (CIP) in the rat. The aim of this study was to investigate the role of COX-1 and COX-2 in the LPS-induced protection of the pancreas against CIP and the involvement of NOS in the activation of COX-PG system in the rats with CIP. CIP was produced by subcutaneous (s.c.) infusion of caerulein (5 microg/kg-h for 5 h) to the conscious rats. Protective dose of LPS, from Escherichia coli, (1 mg/kg) was given intraperitoneally (i.p.) 15 min prior to the start of CIP. Nonselective inhibitor of COX; indomethacin (5 or 10 mg/kg), selective inhibitor of COX-1: resveratrol, or a highly selective inhibitors of COX-2: rofecoxib or NS-398 (2 or 10 mg/kg) were injected i.p. 15 min prior to the administration of LPS. COX-1 or COX-2 mRNA was determined by reverse transcription-polimerase chain reaction (RT-PCR) in the pancreatic tissue. Pancreatic blood flow (PBF) was measured by a laser Doppler flowmetry. PGE2 content in the pancreas was measured by radioimmunoassay. CIP was manifested by an increase of pancreatic weight and plasma amylase activity (by 500% and 700%, respectively) and it was confirmed by histological examination. CIP slightly increased pancreatic PGE2 generation (by 12%) and diminished PBF (by about 40%). LPS (1 mg/kg i.p.), given prior to the start of CIP, increased PGE2 generation in the pancreas (by 45%), reversed the histological manifestations of pancreatitis, reduced the rise in amylase blood level and improved PBF. Administration of nonselective inhibitor of COX; indomethacin (5 or 10 mg/kg i.p.) prior to the injection of LPS abolished its protective effects on CIP and reduced pancreatic PGE2 generation. Selective inhibitor of COX-1; resveratrol (10 mg/kg i.p.) given prior to the injection of LPS reversed its protective effects against CIP. Pretreatment with a selective inhibitors of COX-2: rofecoxib or NS-398 (10 mg/kg) attenuated LPS-induced pancreatic protection in the CIP rats. COX-1 expression was detected in the intact pancreas and was not significantly changed by CIP, LPS, indomethacin, NS-389 and their combination, while COX-2 mRNA expression appeared in the pancreas of ratssubjected to CIP and was significantly increased after LPS injection to these rats. Addition of selective COX-2 inhibitor; NS-389, or nonselective inhibitor of COX; indomethacin, enhanced COX-2 mRNA expression in the rats with CIP pretreated with LPS. Pretreatment of the rats with inhibitor of NOS; L-NNA (20 mg/kg i.p.), given together with LPS, 15 min prior to the start of caerulein overstimulation, resulted in complete reversion of LPS-induced pancreatic protection and decreased PGE2 generation stimulated by LPS. Addition to L-NNA of the substrate for NOS; L-arginine (100 mg/kg i.p.), restored pancreatic protection afforded by low dose of LPS and increased pancreatic PGE2 level in the rats with CIP. We conclude that: 1. increased pancreatic PGE2 generation, induced by low dose LPS pretreatment, contributes to the pancreatic resistance to acute damage produced by caerulein overstimulation and 2. the NO-system is involved in above stimulation of PGE2 generation and pancreatic protection against acute damage.

Acute Disease↗

PubMed2000

Water extracts of Helicobacter pylori suppress the expression of histidine decarboxylase and reduce histamine content in the rat gastric mucosa.

BACKGROUND: Acute Helicobacter pylori (Hp) infection in humans may be associated with markedly reduced gastric acid secretion, but the mechanism of this hypochlorhydria has not been fully explained. AIMS: This study was designed to investigate how water extracts (WE) of Hp applied on rat gastric mucosa affect gastric secretion and mucosal histamine concentration as well as the gene expression for histamine decarboxylase (HDC), the key enzyme converting histidine to histamine and for interleukin-1beta (IL-1beta), the important proinflammatory cytokine. MATERIALS AND METHODS: Wistar rats were surgically equipped with small cannulas to form gastric fistulas (GF). Four weeks after formation of GF, rats received either saline (control group) or WE obtained from type I Hp strain expressing CagA/VacA proteins and from type II Hp strain negative for CagA/VacA. Hp-WE was applied intragastrically (i.g.) in a volume of 1 ml at days 0, 2, 4 and 6 (total 4 times). At days 7 and 14, the secretory tests were performed during which basal gastric acid and pepsin secretion was examined and acid and pepsin outputs were measured. After secretory tests, the rats were sacrificed, the stomachs removed and the damage to the gastric mucosa was assessed by measuring the lesion area planimetrically and by histology, the gene expression in gastric mucosa for HDC and interleukin-1beta (IL-1beta) was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) and Southern blot. Additionally, somatostatin concentration in gastric juice, gastric mucosal histamine content and plasma gastrin and IL-1beta levels were determined using radioimmunoassay (RIA). RESULTS: Administration of Hp-WE failed to induce gross mucosal damage but microscopic examination revealed partial denudation of gastric surface epithelium without causing deep necrosis. In secretory tests, Hp-WE produced marked hypochlorhydria but type I Hp-WE induced significantly stronger inhibition of acid and pepsin secretion than type II Hp-WE, both at days 7 and 14. Both, type I and type II Hp-WE suppressed significantly the gene expression for HDC mRNA and lowered significantly gastric mucosal histamine content as compared to respective values in vehicle-treated control gastric mucosa. Furthermore, Hp-WE, resulted in a significant increase in expression of IL-1beta mRNA and a significant fall in luminal somatostatin concentration as well as a insignificant elevation of plasma gastrin level, the type I Hp-WE being more effective in these alterations than type II Hp-WE. CONCLUSIONS: (1) Ability of Hp-WE to induce superficial damage, the reduction in HDC mRNA and accompanying fall in gastric histamine release, contribute, at least in part, to marked hypochlorhydria observed in the stomach exposed to repeated Hp-WE treatments, and (2) the deleterious effect of Hp-WE on the gastric mucosa involves an impairment of gastrin-somatostatin link possibly resulting from the action of Hp-derived toxins and the induction in mucosal cells of proinflammatory cytokine such as IL-1beta.

Animals↗

PubMed2000

The effects of ammonia on pancreatic enzyme secretion in vivo and in vitro.

BACKGROUND: Recent studies clearly demonstrate that Helicobacter pylori (H. pylori) infection of the stomach causes persistent elevation of ammonia (NH3) in gastric juice leading to hypergastrinemia and enhanced pancreatic enzyme secretion. METHODS: The aim of this study is to evaluate the influence of NH4OH on plasma gastrin level and exocrine pancreatic secretion in vivo in conscious dogs equipped with chronic pancreatic fistulas and on secretory activity of in vitro isolated acini obtained from the rat pancreas by collagenase digestion. The effects of NH4OH on amylase release from pancreatic acini were compared with those produced by simple alkalization of these acini with NaOH. RESULTS: NH4OH given intraduodenally (i.d.) in increasing concentrations (0.5, 1.0, 2.0, 4.0, or 8.0 mM/L) resulted in an increase of pancreatic protein output, reaching respectively 9%, 10%, 19%, 16% and 17% of caerulein maximum in these animals and in a marked increase in plasma gastrin level. NH4OH (8 x 0 mM/L, i.d.) given during intravenous (i.v.) infusion of secretin (50 pmol/kg-h) and cholecystokinin (50 pmol/kg-h) reduced the HCO3 and protein outputs by 35% and 37% respectively, as compared to control obtained with infusion of secretin plus cholecystokinin alone. When pancreatic secretion was stimulated by ordinary feeding the same amount of NH4OH administered i.d. decreased the HCO3- and protein responses by 78% and 47% respectively, and had no significant effect on postprandial plasma gastrin. In isolated pancreatic acini, increasing concentrations of NH4OH (10(-7)-10(-4) M) produced a concentration-dependent stimulation of amylase release, reaching about 43% of caerulein-induced maximum. When various concentrations of NH4OH were added to submaximal concentration of caerulein (10(-12) M) or urecholine (10(-5) M), the enzyme secretion was reduced at a dose 10(-5) M of NH4OH by 38% or 40%, respectively. Simple alkalization with NaOH of the incubation medium up to pH 8.5 markedly stimulated basal amylase secretion from isolated pancreatic acini, whereas the secretory response of these acini to pancreatic secretagogues was significantly diminished by about 30%. LDH release into the incubation medium was not significantly changed in all tests indicating that NH4OH did not produce any apparent damage of pancreatic acini and this was confirmed by histological examination of these acini. CONCLUSIONS: 1. NH4OH affects basal and stimulated pancreatic secretion. 2. The excessive release of gastrin may be responsible for the stimulation of basal pancreatic enzyme secretion in conscious animals, and 3. The inhibitory effects of NH4OH on stimulated secretion might be mediated, at least in part, by its direct action on the isolated pancreatic acini possibly due to the alkalization of these acini.

Alkalies↗

PubMed1999

Leptin in gastroprotection induced by cholecystokinin or by a meal. Role of vagal and sensory nerves and nitric oxide.

Leptin, detected recently in the stomach, is a product of the ob gene released by cholecystokinin (CCK) and plays an important role in the control of food intake but its influence on gastroprotection against the damage caused by noxious agents has not been studied. This study was designed to compare the effects of leptin and cholecystokinin-8 (CCK-8) on gastric mucosal lesions induced by topical application of 75% ethanol or acidified aspirin. Four series of Wistar rats (A, B, C and D) were used to determine the effects of: (A) suppression of prostaglandin biosynthesis by indomethacin (5 mg/kg i.p.); (B) inhibition of nitric oxide (NO)-synthase by nitro-L-arginine methyl ester (L-NAME) (5 mg/kg i.v.); (C) blockade of sensory nerves by capsaicin (125 mg/kg s.c.) and (D) bilateral vagotomy, on the gastric lesions induced by intragastric (i.g.) application of ethanol with or without pretreatment with CCK-8, a known gastroprotective substance or leptin. CCK-8 (1-100 microg/kg i.p.) and leptin (0.1-50 microg/kg i.p.) dose dependently attenuated gastric lesions induced by 75% ethanol; the dose reducing these lesions by 50% being about 10 microg/kg and 8 microg/kg, respectively. The protective effects of CCK-8 and leptin were accompanied by a significant rise in gastric blood flow (GBF) and luminal NO concentration. Leptin was also effective to attenuate aspirin-induced damage and the accompanying fall in the GBF, whereas CCK-8 dose dependently worsened aspirin damage and failed to influence GBF. CCK (1-100 microg/kg i.p.), given in graded doses, produced a dose-dependent increase in the plasma leptin level and a rise of the expression of ob messenger RNA (mRNA) in gastric mucosa, the maximum being reached at a dose of 100 microg/kg. Pretreatment with CCK-8 (10 microg/kg i.p.) or with 8% peptone, that is known to stimulate CCK release, also produced a significant rise in plasma leptin levels and up-regulation of ob mRNA while reducing significantly the gastric lesions induced by 75% ethanol to the same extent as that induced by exogenous leptin (10 microg/kg i.p.). Indomethacin, which suppressed prostaglandin generation by approximately 90%, failed to influence leptin- or CCK-8-induced protection against ethanol, whereas L-NAME attenuated significantly CCK-8- and leptin-induced protection and hyperemia but addition to L-NAME of L-arginine, but not D-arginine, restored the protective and hyperemic effects of both hormones. The ob mRNA was detected as a weak signal in the intact gastric mucosa and in that exposed to ethanol alone but this was further enhanced after treatment with graded doses of CCK-8 or peptone meal applied prior to ethanol. We conclude that: (1) exogenous leptin or that released endogenously by CCK or meal exerts a potent gastroprotective action depending upon vagal activity, and involving hyperemia probably mediated by NO and sensory nerves but unrelated to endogenous prostaglandins; (2) leptin mimics the gastroprotective effect of CCK and probably mediates the protective and hyperemic actions of CCK in the rat stomach.

Animals↗

PubMed1999

Role of Helicobacter pylori infection in extragastroduodenal disorders: introductory remarks.

Numerous studies initiated by Warren and Marshall in 1982 confirmed the crucial role of H. pylori infection in the pathogenesis of gastritis, peptic ulcer and possibly also gastric cancer leading to reappraisal of fundamental concept of gastric pathophysiology. These topics were covered, in part, by our previous H. pylori-related symposium I (1995), II (1997) and III (1999) organized in Cracow. H. pylori is one of the most frequent causes of gastroduodenal infection worldwide, resulting in the release of various bacterial and host dependent cytotoxic substances including ammonia, platelet activating factor (PAF), cytotoxins and lipopolysaccharides (LPS) as well as cytokines such as interleukins (IL)-1-12, tumor necrosis factor alpha (TNF(alpha), interferon gamma (INFgamma) and reactive oxygen species (ROS). Recently, several extradigestive pathologies have been linked to H. pylori infection including cardiovascular, cutaneous, autoimmune, esophageal and other diseases such as sideropenic anemia, growth retardation, extragastric MALT-lymphoma etc. The potential role of H. pylori infection in the pathogenesis of these extradigestive disorders has been based on facts that 1) local gastric inflammation may exert systemic effects, 2) chronic infection of gastric mucosa induces immune responses that are able to cause the lesions remote to primary site of infection and 3) H. pylori eradication improves the extradigestive disorders. The aim of present III International Symposium is to provide critical reviews based on personal experience and the available literature about extragastric manifestations of H. pylori infection. The ultimate goal of this symposium is to foster interdisciplinary research and exchange of opinion about the possible involvement of H. pylori in extradigestive pathologies.

Animals↗

PubMed1999

Helicobacter pylori associated gastric pathology.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.

Animals↗

PubMed1999

Epidemiological study on Helicobacter pylori infection and extragastroduodenal disorders in Polish population.

UNLABELLED: An association between Helicobacter pylori (H. pylori) infection and extragastroduodenal disorders (EGDD) is still not clear. The aim of the study was to investigate the relationship between H. pylori infection and the symptoms of coronary artery disease (CAD), facial dermatological changes (FDC), gastroesophageal reflux diseases (GERD), and periodontal diseases (PD) in Polish population. The study was performed between 1996-1999 year on 7,060 adult inhabitants of municipal area of Krakow (aged 18-76, mean 46.3 year; 55.8% female, 44.2% male): 2,204 subjects with EGDD and 4,856 without symptoms of EGDD. Each patient responded to a detailed questionnaire under supervision of medical staff. The H. pylori status was assessed non-invasively using urea breath test (UBT) with capsulated low-dose 13C-UBT (38 mg). Exclusion criteria were: recent H. pylori eradication, treatment with PPI, bismuth and/or antibiotics in the last 4 weeks. Four groups of cases with EGDD symptoms were selected. Within each group exclusively only one of studied symptoms was recorded. The study included 328, 138, 688, and 1,050 patients with CAD, FDC, GERD and PD, respectively. For each studied group an age and sex-matched asymptomatic controls were selected (897, 387, 1,083, and 2,489 control patients). RESULTS: Overall H. pylori infection rate was 69,9% (in 71.4% of 2,204 cases and in 69.31% of 4,856 controls). In CAD group: 68% of 328 cases were H. pylori (+ve) vs. 70% H. pylori (+ve) of 897 controls. An association was not significant: OR = 0.93 (95% CI, 0.72-1.20). In 138 of FDC cases, 59% were H. pylori (+ve) vs. 71% H. pylori (+ve) in 387 controls showing the lack of positive association; OR = 0.60 (95% CI, 0.42-0.87). In GERD, 69% of 688 cases were H. pylori (+ve) vs. 73% of 1,083 H. pylori (+ve) controls and negative association was observed; OR=0.80 (95% CI, 0.65-1.00). In 1,050 of PD cases 75% were H. pylori (+ve) vs. 68% H. pylori (+ve) of 2,489 controls; positive association was significant; OR = 1.4 (95% CI, 1.16-1.68). We conclude that in the studied Polish population, no positive association exists between H. pylori positivity and CAD, FDC or GERD possibly due very high overall H. pylori infection rate. The only positive link observed between H. pylori infection and periodontal disease may reflect direct "in situ" H. pylori pathological action of H. pylori in oral cavity. It is not excluded that periodontal diseases may facilitate the H. pylori oro-gastric transmission and colonisation of the bacteria in the digestive tract.

Adolescent↗

PubMed1999

Helicobacter pylori and its eradication in rosacea.

Rosacea is a common condition of unknown etiology usually accompanied by gastrointestinal symptoms and favorably responding to the treatment with antibiotics. This study was designed to examine the prevalence of gastric Helicobacter pylori (Hp) infection verified by 13C-UTB-test, CLO, Hp culture and serology (IgG) in patients with rosacea. Gastroduodenoscopy was combined with pentagastrin secretory test and antral and fundic biopsy samples were taken for histological evaluation (the Sydney system). Blood samples were also taken for the determination of plasma gastrin using RIA and plasma interleukin (IL)-8 and tumor necrosis factor alpha (TNFalpha) using ELISA. This study was performed in 60 patients, 31-72 year old, with visible papules and pustules associated with erythema and flushing on the face and on 60 age- and gender-matched patients without any skin diseases but with similar as in rosacea gastrointestinal symptoms but without endoscopic changes in gastroduodenal mucosa (non-ulcer dyspepsia - NUD). The Hp prevalence in rosacea patients was about 88 % as compared to 65% in control NUD patients. Among rosacea patients, 67% were cytotoxin associated gene A (CagA) positive, while in NUD patients only 32% were CagA positive. Rosacea patients showed gastritis with activity of about 2.1 in antrum and 0.9 in the corpus of the stomach while those with NUD only mild gastritis with activity of approximately 1.0) confined to the antrum only. Following initial examination, typical 1 wk anti-Hp therapy including omeprazole (20 mg bd.), clarithromycin (500 mg bd.) and metronidazol (500 mg bd.) was carried out. After eradication, 51 out of 53 treated rosacea patients became Hp negative. Within 2-4 weeks, the symptoms of rosacea disappeared in 51 patients, markedly declined in 1 and remained unchanged in 1 other subject. A dramatic reduction in activity of gastritis (to 0.3 in antrum and to 0.1 in corpus) was observed. Basal plasma gastrin decreased from 48 +/- 5 pM before to 17+/-3 pM after eradication, while pentagastrin-induced maximal (MAO) declined, respectively, from about 16.6 +/- 4.2 to 8.5 +/- 1.8 mmol/h. Plasma TNFalpha and IL-8 were reduced after the therapy by 72% and 65%, respectively. We conclude that: 1) Rosacea is a disorder with various gastrointestinal symptoms closely related to gastritis, especially involving the antrum mucosa, with Hp expressing cagA in the majority of cases and elevated plasma levels of TNFalpha and IL-8; 2) The eradication of Hp leads to a dramatic improvement of symptoms of rosacea and reduction in related gastrointestinal symptoms, gastritis, hypergastrinemia and gastric acid secretion; and 3) Rosacea could be considered as one of the major extragastric symptoms of Hp infection probably mediated by Hp-related cytotoxins and cytokines.

Adult↗

PubMed1997

Gastric mucosal expression and luminal release of growth factors in gastric carcinoma and duodenal ulcer patients before and after eradication of Helicobacter pylori.

Epidemiological studies have consistently shown an association between infection of Helicobacter pylori (Hp) and duodenal ulcer (DU) and gastric cancer. The mechanism of the ulcerogenic effect of Hp has been related to excessive gastrin release, gastric acid hypersecretion and gastric metaplasia in duodenum. The implication of Hp in gastric carcinogenesis has not been explained. In this study, mucosal expression of EGF and TGF alpha and luminal release of EGF as well as basal and pentagastrin-stimulated acid secretion and plasma gastrin levels have been determined in healthy subjects, gastric carcinoma and DU patients. It was found that Hp positive DU patients show excessive gastrin release and gastric acid secretion combined with increased expression and luminal release of EGF and TGF alpha. These changes returned to normal values two years after the eradication of Hp. Gastric cancer patients also showed increased expression of EGF and TGF alpha and highly increased plasma gastrin but their gastric acid secretion was markedly reduced possibly due to atrophy of oxyntic mucosa. This study indicates that overexpression of growth factors in gastric mucosa may be implicated in the pathogenesis of both duodenal ulcer and gastric cancer and that Hp positive hypochlorhydric and hypergastrinemic patients may be predisposed to development of gastric cancer.

Adult↗

PubMed1997

[Hormonal changes and secretion and stomach mucosal microstructure in the course of H. pylori in patients with duodenal ulcer].

We designed this study to follow exocrine, endocrine and microstructural changes in duodenal ulcer patients with H. pylori infection in the course and after quadruple eradication regimen. Quadruple therapy appeared to be highly effective method of both ulcer healing and H. pylori eradication. We observed enhanced regeneration of gastric mucosa in the course of treatment. Almost immediate decrease of plasma gastrin and increase of plasma somatostatin and EGF concentration in gastric juice were noticed.

Amoxicillin↗

PubMed1997

[Endocrine and exocrine gastric mucosal secretion in the course of H. pylori eradication in patients with non-ulcer dyspepsia].

Microstructural, endo- and exocrine changes in gastric mucosa of Non-Ulcer Dyspepsia patients with H. pylori infection in the course of eradication has been studied. Before, during and after anti H. pylori therapy plasma gastrin and somatostatin levels, EGF and somatostatin concentration in gastric juice and basal and pentagastrin stimulated gastric acid secretion were measured. Moreover microstructure of gastric mucosa specimens has been studied. Maximal Acid Output initially higher in NUD patients than in healthy volunteers increased slightly in the course of eradication. Plasma gastrin decreased while EGF and somatostatin concentration in gastric juice increased. After treatment the ratio of patients with pronounced features (activity) of gastritis was significantly reduced.

Amoxicillin↗

PubMed1996

Oral cavity as permanent reservoir of Helicobacter pylori and potential source of reinfection.

Recent studies in developed countries showed that neither dental plaques nor dentures are important reservoir for Helicobacter pylori (Hp), whereas studies in developing countries revealed a high prevalence of Hp in dental plaques, though elsewhere the culture of bacterium or its DNA analysis by polymerase chain reaction in the material obtained from oral cavity were not successful. This study was designed to compare the incidence of Hp in oral cavity (saliva, dental plaques and gingival pockets) using Campylobacter-like organism (CLO) test and culture and in the presence of Hp in the stomach using 14C-urea breath test (UBT), CLO-test and culture (antral biopsy specimens). Hundred dyspeptic subjects with endoscopically normal gastro-duodenal mucosa and 55 symptomatic patients with active duodenal peptic ulcer (DU) were tested for the presence of Hp. Thirty of these DU patients were also examined for presence of Hp in oral cavity and the stomach just before the start and 4 weeks after the termination of one week triple therapy (Omeprazole 20 mg bd, Clarithromycin 500 mg bd and Tinidazole 500 mg bd) when the DU was found endoscopically healed. In the group of 100 dyspeptic subjects, the Hp was detected by CLO-test in saliva, dental plaques and gingival pockets in 84%, 100% and 100% of cases and by the culture in 55%, 88% and 100%, respectively. The presence of Hp, as determined by UBT in the stomach in these subjects was 60%. Using CLO-test and culture, all (100%) out of 55 DU patients, were found to be Hp positive in the oral cavity and in 95% in the stomach. Following one week triple therapy in 30 DU patients, the Hp was still detected in oral cavity by CLO-test in all patients (100%) and by culture in 27 patients (90%), whereas in the stomach, the Hp was found by UTB and culture only in one of these patients (97% Hp eradicated). We conclude that the Polish population including dyspeptic and DU patients, the mouth is permanent reservoir of Hp and that the successful Hp eradication from the stomach by systemic therapy fails the Hp status in the oral cavity that might be a potential source of gastric reinfection in these patients.

Adult↗

PubMed1996

Eradication of Helicobacter pylori and gastrin-somatostatin link in duodenal ulcer patients.

Helicobacter pylori (Hp) infection may be associated with duodenal ulcer (DU) and accompanied by increased release of gastrin and deficiency of somatostatin (S-S) but the mechanisms of these changes in DU patients after eradication of Hp have been little studied. Cholecystokinin (CCK) has been implicated in the feedback control of gastric acid secretion in healthy subjects but its contribution to secretory disorders in DU patients has been little examined. This study, therefore, investigated whether CCK participates in the impairment of postprandial gastrin release and gastric acid secretion in active DU patients. Tests were undertaken in 10 DU patients without or with elimination of the action of endogenous CCK using loxiglumide (LOX), a selective CCK-A receptor antagonist, before and 4 wk. after eradication of Hp with triple therapy (omeprazole, amoxycillin and bismuth). In Hp positive DU patients, the postprandial acid secretion (measured by continuous intragastric pH monitoring) was accompanied by a pronounced increment in plasma gastrin with negligible increase of intraluminal release of S-S. The administration of LOX in these patients did not affect significantly the postprandial pH profile and the rise in plasma gastrin. After eradication of Hp the median postprandial intragastric pH increased to about 4.3 (compared to 3.5 before the Hp eradication); the postprandial gastrin concentration was reduced by about 40%, while luminal release of S-S was increased 2 folds. The administration of LOX resulted in significantly greater decrease in median pH (3.1) and higher rise in postprandial plasma gastrin in these patients. Also the postprandial plasma S-S showed a small, but significant decline (by about 25%) as compared to that in placebo treated patients. This study provides evidence that: (1) Hp infection in DU patients is accompanied by enhanced gastrin release and the reduction in luminal release of S-S; (2) The failure of LOX to affect gastric secretion and plasma gastrin DU Hp infected patients could be attributed, at least in part, to the failure of endogenous CCK to control gastric acid secretion via release of S-S; (3) Hp infected patients appear to exhibit a deficiency of S-S release that can be reversed by the eradication of Hp indicating that both peptides may contribute to the acceleration of the ulcer healing following Hp eradication in DU patients; (4) The test with LOX and gastric luminal S-S assay may be useful in identification of Hp positive DU patients with CCK-mediated impaired feedback control of gastric secretion and deficiency of S-S caused by Hp infection.

Adult↗

PubMed1996

One week treatment with omeprazole, clarithromycin and tinidazole or lansoprazole, amoxicillin and metronidazole for cure of Helicobacter pylori infection in duodenal ulcer patients.

We defined optimal Helicobacter pylori (Hp) treatment as Hp eradication rate about 90%, well-tolerated with few side-effects. Two centers carried out randomized trials including 90 patients (74% men, 26% women, ages ranging from 18 to 65, mean age 42 +/- 8) with active duodenal ulcers (DU). Patients were treated with the combination of Omeprazole (O) 20 mg bd + Clarithromycin (C) 250 mg bd + Tinidazole (T) (500 mg bd) or with Lansoprazole (L) 15 mg bd + Amoxicillin (A) 750 mg bd + Metronidazole (M) 500 mg bd administered for one week. The DU healing rate was evaluated by endoscopy and the Hp status by rapid urease CLO-test and 14C-urea breath test (UBT). The healing rate of the DU in a group treated with the combination of O + C + T was 91% and in group treated with L + A + M was 93%. The eradication of Hp in group O + C + T and L + A + M averaged 91% and 87%, respectively. There was no statistically significant difference in the DU healing rate and the Hp eradication rate between these two groups. Both treatments were accompanied by a marked rise in the basal and postprandial plasma gastrin levels and the rise in the intragastric pH but these alterations returned to the pre-treatment values 4 weeks after the termination of the therapy. Both treatments were well tolerated and the only side effect was the taste disturbance observed in few patents treated with O + C + T. None of patients discontinued the treatment because of the adverse events. We conclude that one week treatment using O + C + T or L + A + M are highly and equally effective in the healing of DU and in the eradication of Hp.

2-Pyridinylmethylsulfinylbenzimidazoles↗