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Biomedical subjects

J W Konturek

Publications and source records attributed to J W Konturek.

At least 19 recordsLinked to original sources
PubMed1999

Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.

BACKGROUND: Gastric adaptation to aspirin is well-documented. However, the mechanisms underlying the reduction of aspirin-induced mucosal damage despite continued ingestion of the drug remain poorly understood. METHODS: Eight healthy volunteers who received aspirin 1 g b.d. for 14 days were compared with eight placebo-dosed controls. Gastroscopy with mucosal biopsy was performed, and gastric mucosal blood flow was measured before and following 3, 7 and 14 days of aspirin treatment. At the same time points, tissue concentration and the content of prostaglandin E2 in the gastric juice were determined and expression of endothelial cell-derived nitric oxide synthase (eNOS) in mucosal biopsies was measured using Western blot analysis. RESULTS: Aspirin-induced mucosal damage that reached a maximum on day 3, declining significantly by day 14. Concomitantly, mucosal blood flow significantly increased on day 3 and returned to initial values on day 14. Aspirin intake led to a significant decrease in prostaglandin E2 concentration in the gastric mucosa and in gastric juice during the whole period of aspirin consumption. eNOS expression started to increase on day 7 in oxyntic mucosa and on day 3 in antral mucosa, reaching its highest values at the end of the consumption of aspirin. CONCLUSIONS: The human gastric mucosa adapts to prolonged aspirin intake, and this is accompanied by an increase in mucosal blood flow and reduced prostaglandin synthesis. Increase of mucosal eNOS expression might compensate for reduced prostaglandin synthesis and be responsible for gastric adaptation to chronic aspirin intake in humans.

Adult↗
PubMed1999

[Helicobacter pylori and gastric acid secretion].

Helicobacter pylori (H. pylori) infection leads to profound changes in gastric physiology. Several clinical and animal studies have been performed to clarify the influence of H. pylori on gastric acid secretion. Published data, however, are not consistent throughout. Infection of the gastric antrum, which can be observed mainly in duodenal ulcer patients, increases gastrin release and consecutively acid output. The net effect of corpus and antrum gastritis, such as in patients with gastric cancer, is to decrease acid secretion. Chronic H. pylori infection may finally promote gastric atrophy with irreversibly diminished acid secretion but in earlier stages of this infection eradication of H. pylori normalizes gastric secretory activity.

Animals↗
PubMed1998

Infection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans.

BACKGROUND & AIMS: Involvement of Helicobacter pylori in aspirin-induced gastropathy and adaptation to aspirin remains unclear. The aim of this study was to compare gastric damage and adaptation after repeated exposures to acetylsalicylic acid in the same subjects before and after eradication of H. pylori. METHODS: Before and after H. pylori eradication, 8 volunteers were given aspirin, 2 g/day during 14 days. Mucosal damage was evaluated by endoscopy and histological analysis of biopsy samples. Gastric microbleeding, DNA synthesis, prostaglandin E2 generation, and luminal contents of transforming growth factor alpha and its immunohistochemical expression were determined on days 0, 3, 7, and 14 of aspirin course. RESULTS: In all subjects, aspirin-induced gastric damage that reached maximum on day 3. In H. pylori-positive subjects, this damage was maintained at a similar level up to day 14. After H. pylori eradication, the damage was significantly lessened both in endoscopy and histology at day 14 and accompanied by increased mucosal expression and luminal release of transforming growth factor alpha. Prostaglandin E2 generation was significantly greater in H. pylori-positive subjects than after H. pylori eradication, but aspirin treatment resulted in >90% reduction of this generation independent of H. pylori status. CONCLUSIONS: Gastric adaptation to aspirin is impaired in H. pylori-positive subjects, but eradication of this bacterium restores this process.

Adaptation, Physiological↗
PubMed1998

Enhancement in the protective qualities of gastric mucus with combination therapy of ebrotidine and amoxicillin for H. pylori eradication.

1. Gastric mucus from Helicobacter pylori-positive patients with active chronic gastritis type B, before and after successful combination therapy consisting of the H2 receptor antagonist ebrotidine (400 mg) and amoxicillin (1,000 mg) administered b.i.d., in the morning and at bedtime for a period of 2 weeks followed by administration of ebrotidine alone for the subsequent 4 weeks, was assessed for the changes in physicochemical properties associated with the mucosal protective potential and anti-H. pylori activity. 2. The results of physicochemical measurements revealed that eradication of H. pylori associated with the successful therapy for active chronic gastritis type B with ebrotidine-amoxicillin was accompanied by a 36% increase in gastric mucus hydrogen ion retardation capacity, a 1.5-2.1-fold increase in mucus gel viscosity and a 2.4-fold increase in its hydrophobicity. 3. The beneficial changes brought about by the ebrotidine-amoxicillin therapy in the physical properties of gastric mucus were also manifest in a 2.7-fold enhancement in the proportion of the high-molecular-weight polymeric mucin form responsible for the maintenance of gastric mucus gel integrity. 4. Moreover, assays of H. pylori aggregating titer of gastric mucus revealed that the successful combination therapy with ebrotidine and amoxicillin led to a 3.8-fold increase in mucin anti-H. pylori activity. 5. The results demonstrate that combination therapy with ebrotidine and amoxicillin for H. pylori eradication leads to a marked improvement in the protective qualities of gastric mucus essential for the preservation of mucosal integrity and enhances the inherent mucosal defense against H. pylori infection.

Adult↗
PubMed1998

Helicobacter pylori-positive peptic ulcer patients do not adapt to aspirin.

BACKGROUND: Recent studies indicate that eradication of Helicobacter pylori might prevent peptic ulcer formation in patients treated with non-steroidal anti-inflammatory drugs (NSAIDs). On the other hand, gastric adaptation after repeated exposures to aspirin (ASA) is well documented but the influence of H. pylori on this process remains to be elucidated. AIM: To compare gastric damage and adaptation following repeated exposures to ASA in a group of patients with H. pylori infection, before and after eradication of the bacterium, and in H. pylori-negative controls. METHODS: Eight healthy volunteers without H. pylori infection and eight patients with duodenal ulcer (DU) history and H. pylori infection before and after H. pylori eradication were given ASA 2 g/day for a period of 14 days. Mucosal damage was evaluated by endoscopy and histology of biopsy samples. Gastric microbleeding, DNA synthesis in the gastric mucosa and mucosal expression, as well as luminal content of transforming growth factor-alpha (TGFalpha) were determined on days 0, 3, 7 and 14 of the ASA course. RESULTS: In all patients aspirin-induced gastric damage reached a maximum on day 3. In H. pylori-positive patients, this damage was maintained at a similar level up to day 14, whereas in H. pylori-negative controls and H. pylori-eradicated patients this damage significantly lessened on day 14 and was accompanied by elevated DNA synthesis as well as increased mucosal expression and luminal release of TGFalpha.

Adaptation, Physiological↗
PubMed1998

Physiological role of cholecystokinin in gastroprotection in humans.

OBJECTIVE: Cholecystokinin (CCK) is able to protect gastric mucosa against acute injury in experimental animals but little is known about the role of this hormone in maintaining mucosal integrity in humans. This double-blind, placebo controlled study was performed in 16 healthy volunteers. It describes the effects of CCK-8 infused intravenously (i.v.) at physiological doses and endogenous CCK released by intraduodenal (i.d.) oleate on gastric mucosal damage, as brought about by ethanol without or with pretreatment with loxiglumide, a selective CCK-A receptor antagonist. METHODS: CCK-8 was infused i.v. 30 min before and throughout the study or i.d. oleate was instilled through a separate duodenal tube. Thirty minutes after the start of i.v. infusion of CCK or i.d. oleate instillation, 100 ml of 50% ethanol spray was applied to the gastric mucosa using an endoscope. Gastroscopy was performed and mucosal lesions were quantified using modified Lanza score. Gastric biopsies were taken from oxyntic mucosa for histological evaluation and gastric content was aspirated for radioimmunoassay of somatostatin. RESULTS: In placebo-treated subjects ethanol caused endoscopic damage, with an average score of 2.8+/-0.2. Histologically, a widespread disruption of surface epithelium and deep hemorrhagic necrotic lesions were observed. Pretreatment with CCK or i.d. oleate markedly reduced the endoscopic lesion score to 0.7+/-0.1 and 0.3+/-0.1, respectively, and in both cases this reduction was accompanied by a significant rise in plasma CCK. Histologically, surface epithelium was still disrupted but deep necrotic lesions were absent. Gastric content collected before and after CCK or oleate showed a several-fold increase of luminally released somatostatin. CONCLUSIONS: Pretreatment with loxiglumide abolished the protective effects of i.v. CCK-8 and i.d. oleate on mucosal lesions induced by ethanol and prevented the rise in intragastric somatostatin, but failed to affect the increments in plasma CCK. Endogenous CCK plays a physiological role in the maintenance of mucosal integrity. This occurs through activation of CCK-A receptors and is associated with an increased gastric luminal release of somatostatin.

Adult↗
PubMed1998

Disturbed gastric motility and pancreatic hormone release in diabetes mellitus.

BACKGROUND AND AIMS: The influence of glucose metabolism and postprandial release of glucagon on gastric emptying in diabetes mellitus is still unclear. The aim of this study was to assess the relationship between glucose, insulin and glucagon and alterations of gastric motility in symptomatic diabetic subjects with delayed gastric emptying. METHODS: Scintigraphy for solids and liquids, 13C-acetate breath test, electrogastrography and antral manometry were assessed in 20 symptomatic subjects with diabetes mellitus type II and in 20 healthy controls. Simultaneously, serum glucose, glucagon and insulin levels were determined during the functional studies. RESULTS: Postprandial increase in antral motility and myoelectrical activity were seen in controls, but were missing in the group with diabetes mellitus. Moreover, in the fasting state the dominant frequency instability coefficient observed in healthy individuals and in subjects with diabetes of short (<5 years) duration was significantly reduced in subjects with longer duration of diabetes while the postprandial increase in dominant frequency instability coefficient was missing in all diabetics. Following the standard test meal, serum glucose and plasma glucagon in the diabetics increased to a significantly higher degree when compared to controls. CONCLUSIONS: Symptomatic subjects with delayed gastric emptying present abnormal patterns of gastric motor and electrical activity. Higher than normal postprandial plasma levels of glucagon may, at least in part, be responsible for disturbed gastric motility in non-insulin-dependent diabetic subjects.

Acetates↗
PubMed1997

[Intraductal ultrasound in the pancreaticobiliary duct system].

BASIC PROBLEM AND OBJECTIVE OF STUDY: The power of resolution of conventional imaging methods is too low for the diagnosis of very small pancreaticobiliary tumours. High-frequency ultrasound transducers (20 MHz), adapted to the dimensions of the pancreaticobiliary systems (2 mm diameter), make intraductal ultrasound examination possible during endoscopic retrograde cholangiopancreatography (ERCP). In a prospective study the invasiveness and diagnostic value of intraductal ultrasound (IDUS) was compared with ERCP, endosonography (ES) and computed tomography (CT). PATIENTS AND METHODS: During ERCP in 51 consecutive patients an intraductal ultrasound transducer was introduced into the pancreaticobiliary duct system, the results being compared with those obtained with the other imaging modalities and histopathological findings, if available. RESULTS: IDUS of the pancreatic and bile duct systems is a rapid, simple and reliable method during ERCP and provides valuable additional information on periductal tissues. In the diagnosis of carcinoma of the pancreas its sensitivity was 75% (six of eight cases), that of ERCP 37% (3/8), ES 50% (4/8) and CT 37% (3/8). In the diagnosis of biliary tract tumour the sensitivity of the different modalities (in the above order) was 89% (8/9), 78% (7/9), 33% (3/9) and 33% (1/3). Specificity was 67% (2/3), 67% (2/3), 67% (2/3) and 33% (3/9); predictability 89%, 88%, 75% and 60%. CONCLUSIONS: The use of small ultrasound catheter transistor system in the biliary and pancreatic ducts, introduced during ERCP, is technically simple and has few complications. It is a valuable addition to ERCP in the precise diagnosis of small pancreaticobiliary lesions.

Adult↗
PubMed1997

Role of endogenous nitric oxide in the control of exocrine and endocrine pancreatic secretion in humans.

BACKGROUND: Nitric oxide (NO) is an unstable vasodilator formed by NO synthetase (NOS) from L-arginine (L-Arg) in various cells but its role in the control of pancreatic secretion in humans has not been examined. AIMS: This study was designed to determine the role of endogenous NO in the control of exocrine and endocrine pancreas using NOS inhibitor, NG-monomethyl-L-Arg (L-NMMA). METHODS: Pancreatic secretion was stimulated by intravenous infusion of secretin (80 pmol/kg/h) plus caerulein (50 pmol/kg/h) and duodenal content was aspirated by gastroduodenal tube. Two series of tests with secretagogue infusion were performed, one, with addition of graded doses of L-NMMA and, another, with addition of a constant dose of L-Arg alone followed by L-NMMA alone and finally by a combination of L-Arg and L-NMMA. RESULTS: Addition of L-NMMA in graded doses (2-8 mumol/kg/h) reduced dose dependently the secretin-caerulein stimulated pancreatic enzyme secretion without alterations in the volume flow and bicarbonate outputs. The addition of L-Arg to L-NMMA reversed the inhibitory action of L-NMMA on protein enzyme response to secretin-caerulein in these subjects. Secretin-caerulein infusion caused significant increase in plasma insulin and pancreatic polypeptide levels but without changes in plasma glucagon or somatostatin levels. L-NMMA alone resulted in a significant fall in plasma insulin and pancreatic polypeptide levels, while L-Arg added to pancreatic secretagogue infusion caused a significant increase of plasma insulin and pancreatic polypeptide levels above those attained with secretagogues alone. After the addition of L-Arg to L-NMMA, both plasma insulin and pancreatic polypeptide levels rose significantly above the levels observed with L-NMMA plus secretin-CCK stimulation. CONCLUSION: This study provides evidence that the suppression of NOS reduces pancreatic enzyme secretion and the plasma insulin and pancreatic polypeptide levels suggesting that endogenous NO affects both exocrine and endocrine pancreatic secretion in humans.

Adult↗
PubMed1997

Physiological role of nitric oxide in gallbladder emptying in men.

This study was designed to determine the role of nitric oxide in gallbladder (GB) contractions in men. The studies were performed in 10 young healthy male volunteers. GB emptying was examined by ultrasonography under basal conditions and after intravenous infusion of cholecystokinin (CCK8; 12.5 pmol/kg x h) or yolk intake in tests without (saline) and with intravenous infusion of NG-monomethyl-L-arginine (L-NMMA; 4.0 micromol/kg x h) and/or L-arginine (1 mmol/kg x h). The plasma CCK level was determined by radioimmunoassay. It was found that the basal GB volume was about 27 +/- 3 ml, and after CCK8 infusion or yolk meal this volume was reduced within about 30 min by about 93 and 80%, respectively. Pretreatment with L-NMMA caused reduction of the baseline volume by about 15% and significantly augmented the GB emptying induced by CCK8 infusion and yolk intake. L-Arginine alone failed to affect basal or stimulated (CCK or yolk) emptying of the GB, but when combined with L-NMMA, it reversed the enhancement of GB contraction caused by L-NMMA. The basal plasma CCK level was 1.2 +/- 0.3 pmol/l and rose to 7.9 +/- 2.1 pmol/l with CCK8 infusion and to 4.7 +/- 1.8 pmol/l after yolk meal. No significant change in plasma CCK levels was observed in tests with L-NMMA and/or L-arginine. We conclude that under physiological conditions, the GB contractile activity is regulated predominantly by CCK, but endogenous nitric oxide has a tonic relaxing influence on this activity.

Adult↗
PubMed1997

Disturbed gastric motor activity in patients with human immunodeficiency virus infection.

BACKGROUND: Human immunodeficiency virus (HIV) infection is accompanied by a wide spectrum of disorders that affect the central and peripheral nervous system. Damage to the peripheral and central nervous system, including its autonomic division, may become manifest at any stage of the disease. METHODS: Twenty HIV-positive patients with abdominal complaints like dyspepsia, dysphagia, vomiting, and nausea underwent several function tests to determine oesophageal motility, gastric motor and electric activity, and gastric emptying rate. The CDC (Center for Disease Control) classification was used to determine the stage of the disease, which varied from B2 to C3. Before gastric motility examinations all patients underwent endoscopy of the upper gastrointestinal (GI) tract, and none of them showed any morphologic changes of the stomach or oesophagus. Biopsy specimens taken during upper GI endoscopy did not show any histologic alterations of the gastric or oesophageal mucosa. RESULTS: Manometry of the antrum showed an unchanged postprandial (after 200 ml liquid, caloric meal) motility index (MI) when compared with the fasting period (mean fed MI, 174 +/- 43; mean fasting MI, 136 +/- 51). The same was seen for frequency, amplitude, and duration of antral contractions. The electrogastrographic recordings showed basal rhythm of 3 cpm, and no significant changes of the electric pattern were observed postprandially. The amplitude of electric oscillations (power content) significantly increased postprandially when compared with the fasting period. The gastric emptying rate of liquids, measured by means of the 13C-acetate breath test, was faster in HIV patients than in healthy controls. On the other hand, in HIV patients the scintigraphically determined emptying rate of solids was significantly delayed compared with the normal values. There were no significant differences in the oesophageal motility pattern with regard to the amplitude, duration, and propagation of peristaltic waves when compared with the values obtained from healthy volunteers. CONCLUSION: Our results suggest that HIV-associated visceral neuropathy may present already in relatively early stages of infection and may contribute to abdominal symptoms that occur frequently in these patients.

Adult↗
PubMed1997

Epidermal growth factor in gastric ulcer healing by nocloprost, a stable prostaglandin E2 derivative.

BACKGROUND: The gastroprotective and ulcer-healing properties of prostaglandins, especially in gastric ulcers induced by non-steroidal anti-inflammatory drugs, are well established. Ulcer healing is an active process of filling the mucosal defect with migrating and proliferating epithelial cells combined with angiogenesis in granulation tissue at the ulcer bed. Growth factors, especially epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) are crucial in the regulation of the reconstruction of damaged mucosal structures. METHODS: In this double-blind, randomized, prospective study 40 patients with gastric ulcer were treated with nocloprost, a stable prostaglandin E2 derivative, or with ranitidine. All subjects underwent endoscopy before and after 4 and 8 weeks of anti-ulcer therapy. During endoscopy mucosal biopsies were performed for determination of EGF content in gastric mucosa at the ulcer margin and in the intact mucosa. Additionally, EGF output in saliva and its plasma concentrations were determined in all subjects before and during the treatment. RESULTS: The gastric ulcer healing rate after 4 weeks was significantly higher in patients treated with nocloprost than in those treated with ranitidine (63% versus 39%, respectively). At initial examination the EGF content in the gastric mucosa obtained from the ulcer edge was significantly higher than that in the intact mucosa. There was a significant increase in the EGF content in both the ulcer margin and the intact mucosa in subjects treated with nocloprost but not in patients under treatment with ranitidine. Similarly, patients treated with nocloprost had significantly higher EGF output in saliva and higher EGF concentration in plasma throughout the anti-ulcer therapy. CONCLUSION: Nocloprost is superior to ranitidine in the treatment of chronic gastric ulcers, and these effects could be due, at least in part, to higher expression and mucosal content of EGF in the ulcer area.

Adult↗
PubMed1997

Endogenous nitric oxide in the control of esophageal motility in humans.

Recent animal studies have suggested that nitric oxide (NO) plays an important role in the regulation of esophageal motility, being partly responsible for latency period and latency gradient between the onset of a swallow and contractions of esophageal circular smooth muscles. The aim of this study was to evaluate whether endogenous NO is responsible for physiological timing of forthcoming contractions in the human esophageal body after swallowing. Eight male volunteers (age 21-25 years, weight 67-82 kg) were involved in this placebo controlled study on the effects of increasing doses of the NO synthase blocker, NG-monomethyl-L-arginine (L-NMMA 1.0-4.0 mumol/min i.v.), and/or L-arginine (L-arg) (30 mumol/kg-min i.v.) on the peristalsis of esophageal body in response to wet swallows (5 ml of water) and lower esophageal sphincter (LES) resting pressure. The esophageal motor activity was determined manometrically using 3-channel electronic catheter. Additionally, during all examinations arterial blood pressure (BP) was measured every 5 min. L-NMMA resulted in a significant and dose-dependent reduction in the latency period between swallows and the onset of contractions which was most pronounced in the distal esophagus (control: 7.07 +/- 0.74 s vs. L-NMMA 4.0 mumol/min: 5.87 +/- 0.57 s), and this effect was partially reversed after addition of L-arg to the L-NMMA infusion (6.91 +/- 0.62 s). L-NMMA infusion significantly reduced the duration of contractions and increased the velocity of onset propagation but did not change the amplitude of contractions and again, these effects were reversed during simultaneous infusion of L-arg. The resting tone of LES increased significantly during infusion of L-NMMA and these effects were reversed by addition of L-arg. The mean BP significantly increased during infusion of L-NMMA (control 97.0 +/- 5.7 vs. L-NMMA 4.0 mumol/min: 116.4 +/- 3.1 mm Hg) and this was also reversed by L-arg. We conclude that in humans endogenous NO is involved, at least in part, in the physiological regulation of motility patterns of the distal esophageal body and LES.

Adult↗
PubMed1997

Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans.

The gastric irritant properties of nonsteroidal anti-inflammatory drugs (NSAID) are well established but the pathogenic mechanisms by which these agents damage the mucosa or delay its repair are poorly understood. The phenomenon of gastric adaptation after repeated exposures to ASA is well documented but the involvement of Helicobacter pylori (H. pylori) in NSAID-induced gastropathy and adaptation has not been elucidated. The aim of this study was 1) to compare the gastric damage in response to repeated exposures to ASA in the same subjects before and after eradication of H. pylori and 2) to examine the morphological and functional changes of gastric mucosa during the 14 day treatment with ASA in H. pylori-infected subjects before and after eradication of this bacteria: Eight healthy volunteers (age 19-28) with H. pylori infection were given ASA 1g bd during 14 days before and after H. pylori eradication. Mucosal damage was evaluated by endoscopy before and at 3, 7 and 14 days of ASA administration using modified Lanza score. During endoscopy mucosal biopsies were obtained for determination of DNA synthesis, by measuring 3H-thymidine incorporation into DNA. Prior to each endoscopy gastric microbleeding was determined in three consecutive gastric washings. Three months after successful eradication of H. pylori confirmed by 13C-urea breath test and mucosal rapid urease test, the same subjects received again 14 day treatment with ASA and underwent the same examinations as prior to the therapy. In all subjects, ASA administration induced acute gastric damage with endoscopic Lanza score reaching maximum at 3rd day. In H. pylori-positive subjects, this damage was maintained at similar level up to day 14th, whereas in H. pylori-eradicated subjects, this damage was lessened at day 14th by about 60-75%. Gastric microbleeding also reached its maximum at 3rd day of ASA treatment being significantly higher in H. pylori-eradicated subjects than in those with H. pylori infection. This microbleeding decreased to almost normal values by the end of the study in all H. pylori-negative subjects but remained significantly elevated in H. pylori-infected subjects. DNA synthesis before and following ASA administration was significantly higher in subjects after H. pylori eradication than in those with H. pylori infection. Moreover, this DNA synthesis showed significant increase at day 7 of ASA administration only in H. pylori-eradicated subjects. We conclude that: 1) gastric adaptation to ASA is impaired in H. pylori-positive subjects but eradication of H. pylori restores this adaptation, 2) the DNA synthesis and possibly also mucosal cell turnover in response to ASA are suppressed in H. pylori infection and this can be reversed by eradication of H. pylori.

Adaptation, Physiological↗
PubMed1996

Growth markers in the human gastric mucosa during adaptation to continued aspirin administration.

The mechanism of gastric mucosal adaptation to continued aspirin (ASA) administration is unknown. We have investigated growth and proliferation markers in healthy subjects under prolonged ASA treatment. In eight healthy volunteers, ASA treatment (2 g/day) was continued for 14 days. Endoscopy was performed before medication; at days 3, 7, and 14 of ASA treatment; and at days 16 and 18 (2 and 4 days, respectively, after medication was ceased). Gastric biopsies from oxyntic and antral mucosa were studied by histology and by histochemistry for proliferating cell nuclear antigen (PCNA), epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), and epidermal growth factor receptor (EGFr). ASA treatment did not change the expression of EGF and EGFr significantly. The PCNA index showed local inconsistent variations. However, increased TGF-alpha expression after ASA was noted, particularly in hyperplastic surface epithelium. Edema and teleangiectases were common in gastric mucosa after ASA. An increasing incidence of foveolar hyperplasia was also noted in the antral mucosa. Healthy subjects on prolonged ASA treatment gradually develop parameters of chronic reactive gastritis accompanied by increased TGF-alpha expression in gastric surface epithelial cells, especially in hyperplastic areas.

Adaptation, Physiological↗
PubMed1996

Endoscopic and histological appearance of pancreatic metaplasia in the human gastric mucosa: a preliminary report on a recently recognized new type of gastric mucosal metaplasia.

Recently a new type of gastric mucosal metaplasia referred to as pancreatic metaplasia (pancreatic acinar metaplasia) has been recognized. The difference is characterized by the presence of epithelial cells with the cytoplasm strongly basophilic in the basal compartment, whereas in the middle and apical portions it is acidophilic and finely granular. In contrast to intramuscular heterotopic pancreas, foci of pancreatic metaplasia are located in the lamina propria of the gastric mucosa. They form lobules, small clusters, or may be single. The present series included 13 cases of pancreatic metaplasia found in gastroscopic specimens obtained from seven women and six men. We investigated the histological pattern and endoscopic changes. Based upon clinical data it was found that in five patients the gastric mucosa was defined as 'dichromatic'. It is possible that studies involving greater numbers of patients will permit closer correlation between the histological pattern of pancreatic metaplasia and the corresponding endoscopic changes.

Adult↗
PubMed1996

Helicobacter pylori from duodenal ulcer patients expresses inducible nitric oxide synthase immunoreactivity in vivo and in vitro.

Helicobacter pylori is a major pathogenic factor in gastritis, ulcer disease and gastric cancer. Helicobacter pylori associated gastritis is of complex pathogenesis which is only partially elucidated. In the present study we investigated by immunohistochemical BSA method the expression of inducible nitric oxide synthase in the gastric wall and in vitro in Helicobacter pylori. In the gastric wall nitric oxide synthase immunoreactivity was found in macrophages, in endothelial cells and in neural elements. In Helicobacter pylori nitric oxide synthase was also expressed. In conclusion, we postulate a possibility of a direct toxic effect of Helicobacter pylori to gastric epithelial cells through the nitric oxide radical.

Adult↗