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tom 67
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nr 1
13-22
EN
INTRODUCTION Peptic ulcers affect a large part of the general adult population. The associated risk factors and symptoms seem to be widely known. Nevertheless, deaths due to complications of undiagnosed or inappropriately treated peptic ulcers remain relatively frequent. The aim of this study was to assess the level of Upper Silesia inhabitants' knowledge of the disease. MATERIAL AND METHODS The survey was conducted among 203 randomly selected adult Upper Silesians. The questionnaire assessed the general knowledge about ulcers. The respondents were asked to indicate the definition, predisposing factors, direct causes and characteristic symptoms of the disease. They also had to choose the applicable diagnostic methods and therapies. RESULTS Only 7.9% of respondents defined peptic ulcers correctly. There were no statistically significant differences in the frequencies of correct answers between the group of sex, age, education level or place of living. Every seventh person claimed that the complications of peptic ulcers cannot lead to death. Helicobacter pylori infection was recognized as a main pathogenetic factor only by 42.9% of respondents. Instead, respondents chose inappropriate diet, chronic stress and alcohol abuse as the main causes of peptic ulcers. CONCLUSIONS Few respondents are able to identify the correct definition of a peptic ulcer. Less than half of the respondents recognize the direct contribution of Helicobacter pylori infection to gastric ulcer formation. The majority is aware of the risks posed by the complications of peptic ulcers.
PL
W S T Ę P Choroba wrzodowa dotyka znacznej części społeczeństwa, a czynniki ryzyka oraz objawy schorzenia wydają się powszechnie znane. Wciąż zdarzają się jednak zgony spowodowane powikłaniami choroby u pacjentów, którzy nie zostali zdiagnozowani lub nie poddali się terapii. Celem pracy była ocena poziomu wiedzy mieszkańców Śląska na temat tego schorzenia. M A T E R I A Ł I M E T O D Y Przeprowadzono badanie ankietowe wśród 203 przypadkowo wybranych, pełnoletnich mieszkańców Śląska. Kwestionariusz oceniał ogólną wiedzę na temat choroby wrzodowej. Badano umiejętność dopasowania prawidłowej definicji, wskazania czynników predysponujących, bezpośrednich przyczyn powstawania oraz charakterystycznych objawów schorzenia. Ankietowani byli również proszeni o wskazanie sposobów diagnostyki i terapii. WYNIKI Zaledwie 7,9% ankietowanych wskazało prawidłową definicję wrzodu trawiennego. Nie wykazano istotnej statystycznie różnicy między częstością udzielania prawidłowych odpowiedzi zależnie od płci, grupy wiekowej, wykształcenia lub miejsca zamieszkania. Co siódmy badany uznaje, że powikłania choroby wrzodowej nie mogą doprowadzić do śmierci. Zakażenie Helicobacter pylori (H. pylori) jest uważane za czynnik patogenetyczny schorzenia przez 42,9% ankietowanych, częściej wymieniane są natomiast: przewlekły stres, dieta i nadużywanie alkoholu. WNIOSKI Niewielki odsetek ankietowanych wskazuje prawidłową definicję wrzodu trawiennego. Mniej niż połowa respondentów dostrzega bezpośredni wpływ zakażenia H. pylori na powstawanie wrzodów żołądka. Większość ankietowanych zdaje sobie sprawę z ryzyka, jakie niosą ze sobą powikłania choroby wrzodowej.
EN
Solcoseryl, a deproteinized extract of calf blood, protects the gastric mucosa against various topical irritants and enhances the healing of chronic gastric ulcerations but the mechanisms of these effects have been little studied. This study was designed to elucidate the active principle in Solcoseryl and to determine the role of prostaglandisn (PG) and polyamines in the antiulcer properties of this agent. Using both, the radioimmunoassay and radioreceptor assay, EGF-like material was detected in Solcoseryl preparation. Solcoseryl given s. c. prevented the formation of stress-indused gastric lesions and this was accompanied by an increase in the generation of PGE2 in the gastric mucosa. Similar effects were obtained with EGF. Pre treatment with indomethacin, to suppress mucosal generation of prostaglandins (PG), greatly augmented stress- induced gastric ulcerations and antagonized the protection exerted by both Solcoseryl and EGF. Solcoseryl, like EGF, enhanced the healing of chronic gastroduodenal ulcerations. This effect was abolished by the pretreatment with difluoro- methylomithine, an inhibitor of ornithine decarboxylas, the key enzyme in the biosynthesis of polyamines. The healing effects of Solcoseryl and EGF was also reduced by prednisolone which decreased the angiogenesis in the granulation tissue in the ulcer area. These results indicate that Solcoseryl 1. contains EGF-like material, 2. displays the protective and ulcer healing effects similar to those of EGF and involving both PG and polyamines and 3. acts via similar mechanism as does EGF.
EN
The discovery of Helicobacter pylori (H. pylori) provided a possibility to cure effectively patients with peptic ulcers. Recent studies have shown varying susceptibility of H. pylori strains to antibiotics and increasing resistance to some of the recommended drugs. The purpose of the present study was to evaluate the efficacy of the currently recommended eradication schemes and to assess the increasing resistance of H. pylori strains to recommended antibiotics. Furthermore, the effect of probiotics (Lacidofil) on the efficacy of first-line treatment with amoxicillin and clarithromycin was analyzed. The study population consisted of 641 patients: 192 received amoxicillin with clarithromycin and proton pump inhibitor (PPI), 241 - tetracycline, tinidazole, bismuth and PPI, 53 - amoxicillin with clarithromycin and PPI supplemented with Lacidofil. The efficacy of eradication treatment was evaluated by the 13C-urease breath test. The microbiological examination included 111 samples of H. pylori. The present study demonstrated low efficacy of the tetracycline, tinidazole, bismuth and PPI scheme i.e. 71.4%, moderate efficacy of the amoxicillin with clarithromycin and PPI scheme i.e. 85.9%, whereas the supplementation with Lacidofil significantly increased the efficacy of eradication to 94.3%. The microbiological examination revealed a relatively high level of primary resistance to clarithromycin (22.2%) and a high level to metronidazole (46.7%), with no resistance to amoxicillin. However, the most important finding is the high level of secondary resistance to clarithromycin and metronidazole (more than 66% in both cases). The present findings suggest the need for modification of the recommended eradication schemes.
4
Content available Cost-effectiveness of H. pylori eradication
72%
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tom 47
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nr 1
EN
The current scientific literature is replete with investigations providing information on the molecular mechanisms governing the regulation of circadian rhythms by neurons in the suprachiasmatic nucleus (SCN), the master circadian generator. Virtually every function in an organism changes in a highly regular manner during every 24-hour period. These rhythms are believed to be a consequence of the SCN, via neural and humoral means, regulating the intrinsic clocks that perhaps all cells in organisms possess. These rhythms optimize the functions of cells and thereby prevent or lower the incidence of pathologies. Since these cyclic events are essential for improved cellular physiology, it is imperative that the SCN provide the peripheral cellular oscillators with the appropriate time cues. Inasmuch as the 24-hour light:dark cycle is a primary input to the central circadian clock, it is obvious that disturbances in the photoperiodic environment, e.g., light exposure at night, would cause disruption in the function of the SCN which would then pass this inappropriate information to cells in the periphery. One circadian rhythm that transfers time of day information to the organism is the melatonin cycle which is always at low levels in the blood during the day and at high levels during darkness. With light exposure at night the amount of melatonin produced is compromised and this important rhythm is disturbed. Another important source of melatonin is the gastrointestinal tract (GIT) that also influences the circulating melatonin is the generation of this hormone by the entero-endocrine (EE) cells in the gut following ingestion of tryptophan-containing meal. The consequences of the altered melatonin cycle with the chronodisruption as well as the alterations of GIT melatonin that have been linked to a variety of pathologies, including those of the gastrointestinal tract.
8
Content available remote Afferent signalling of gastric acid challenge
58%
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nr 4
43-53
EN
Gastric acid is a factor in the pain associated with peptic ulcer and other acid-related disorders including functional dyspepsia, given that antisecretory treatment is a mainstay in the treatment of upper abdominal pain. However, the molecular sensors, afferent pathways and central processing systems of gastric chemonociception are little known. This article reviews emerging evidence that vagal afferent pathways play a pivotal role in gastric chemonociception. Exposure of the rat gastric mucosa to backdiffusing concentrations of luminal acid is signalled to the brainstem, but not spinal cord, as visualized by functional neuroanatomy based on the rapid expression of c-fos. This observation is complemented by the finding that the visceromotor response to gastric acid challenge is suppressed by vagotomy, but not splanchnectomy. The gastric acid-induced expression of c-fos in the brainstem is reduced by inhibition of gastric acid secretion and enhanced by pentagastrin-evoked stimulation of gastric acid secretion. These data indicate that endogenous acid modulates the sensory gain of acid-sensitive vagal afferents. Further consistent with a role of these neurons in gastric nociception is the finding that exposure to proinflammatory cytokines and the induction of experimental gastritis or gastric ulceration sensitizes vagal afferent pathways to gastric acid. Taken together, these observations are of relevance to the understanding and treatment of gastric hyperalgesia and dyspeptic pain.
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Content available remote Helicobacter pylori and its involvement in gastritis and peptic ulcer formation
58%
EN
Modern gastroenterology started in early 19th century with the identification by W. Prout of the inorganic (hydrochloric) acid in the stomach and continued through 20th century with the discoveries by I.P. Pavlov of neuro-reflex stimulation of gastric secretion for which he was awarded first Nobel Prize in 1904. When concept of nervism or complete neural control of all digestive functions reached apogeum in Eastern Europe, on the other side of Europe (in United Kingdom), E. Edkins discovered in 1906 that a hormone, gastrin, may serve as chemical messenger in stimulation of gastric acid secretion, while L. Popielski revealed in 1916 that histamine is the most potent gastric secretagogue. K. Schwartz, without considering neural or hormonal nature of gastric secretory stimulation, enunciated in 1910 famous dictum; “no acid no ulcer” and suggested gastrectomy as the best medication for excessive gastric acid secretion and peptic ulcer. In early 70s, J.W. Black, basing on earlier L. Popielski’s histamine concept, identified histamine-H2 receptors (H2-R) and obtained their antagonists, which were found very useful in the control of gastric acid secretion and ulcer therapy for which he was awarded in 1972 second Nobel Prize in gastrology. With discovery by G. Sachs in 1973 of proton pumps and their inhibitors (PPI), even more effective in gastric acid inhibition and ulcer therapy than H2-R antagonists, gastric surgery, namely gastrectomy, practiced since first gastric resection in 1881 by L. Rydygier, has been considered obsolete for ulcer treatment. Despite of the progress in gastric pharmacology, the ulcer disease remained essentially “undefeated” and showed periodic exacerbation and relapses. The discovery of spiral bacteria in the stomach in 1983 by B.J. Marshall and R.J. Warren, Australian, clinical researches, awarded in 2005 the Nobel Prize for the third time in gastrology, has been widely considered as a major breakthrough in pathophysiology of gastritis and peptic ulcer, which for the first time can be definitively cured by merely eradication of germ infecting stomach. This overview presents the mechanism of induction of gastritis and peptic ulcer by the H. pylori infection and describes accompanying changes in gastric acid and endocrine secretion as well as the effects of germ eradication on gastric secretory functions and gastroduodenal mucosal integrity
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nr 3
99-126
EN
The common acid related diseases of the upper GI tract could be considered as primarily due to the defect in barrier function either of the gastric mucosal or duodenal epithelium leading to the formation of gastric or duodenal ulcers. An attempt was made in this chapter to discuss the history of peptic ulcer disease in humans and methods for the production of acute gastric lesions and ulcers in experimental animals with the special attention focused to the contribution of Polish scientists and investigators into this field. Early surgical advances in the management of peptic ulcers were emphasized that were then subsequently replaced by pharmacological treatment (histamine H2-receptor antagonists, proton pump inhibitors) and considered as the major strategy against the acid disorders. This included the immense body of work performed by numerous group of investigators, including Polish researchers, to identify the effects of acid, bile salts, aspirin and other non-steroidal anti-inflammatory drugs (NSAID), stress, Helicobacter pylori (H. pylori) infection, prostaglandins (PG) and nitric oxide (NO) on the integrity of the gastrointestinal mucosa, which all were discussed in this chapter. The concept of major defensive mechanism in the stomach called "cytoprotection", originally proposed by Andre Robert is recalled in the relevance to the great contribution of polish scientist working at the Jagiellonian University in Cracow. These experimental studies gave a new insight into the mechanism of action of arachidonate cascade products such as PGs, tromboxanes and leukotrienes and had opened the new therapeutic avenues for the gastroprotective treatment of the acute gastric mucosal damage. Detailed studies revealed, however, that PG-induced cytoprotection offers a short-term protection against gastric lesions induced by corrosive agents but unfortunately this phenomenon gives a little, if any, impact to the process of ulcer healing. The experimental studies on healing of gastric ulcers that become supportive for the clinical trial in humans, performed also by polish pioneers and the effect of numerous growth factors (EGF, TGFalpha), NO inhibitors, cyclooxygenase- (COX)-1 and COX-2 inhibitors and new safer derivatives of NSAID releasing NO in protection and ulcer healing are discussed. Finally, the major discovery by Warren and Marshall of H. pylori that have been studied world-wide in experimental animals including also Polish investigators, allowed for the better insight to the pathological consequences of this germ infection in the gastric mucosa and helped to establish the anti-H. pylori eradication therapy.
EN
Rapid progress in gastroenterological research, during past century, was initiated by the discovery by W. Prout in early 18th century of the presence of inorganic, hydrochloric acid in the stomach and by I.P. Pavlov at the end of 19th century of neuro-reflex stimulation of secretion of this acid that was awarded by Nobel prize in 1904. Then, J. W. Black, who followed L. Popielski's concept of histamine involvement in the stimulation of this secretion, was awarded second Nobel prize in gastrology within the same century for the identification of histamine H2-receptor (H2-R) antagonists, potent gastric acid inhibitors, accelerating ulcer healing. The concept of H2-R interaction with other receptors such as muscarinic receptors (M3-R), mediating the action of acetylocholine released from local cholinergic nerves, and those mediating the action of gastrin (CCK2-R) on parietal cells, has been confirmed both in vivo studies and in vitro isolated parietal cells. The discovery of H2-R antagonists by Black and their usefulness in control of gastric secretion and ulcer healing, were considered as real breakthrough both in elucidation of gastric secretory mechanisms and in ulcer therapy. Discovery of even more powerful gastric acid inhibitors, proton pump inhibitors (PPI), also highly effective in acceleration of ulcer healing was, however, not awarded Nobel prize. Unexpectedly, two Australian clinical researchers, R.J. Warren and B.J. Marshall, who discovered in the stomach spiral bacteria, named Helicobacter pylori, received the third in past century Nobel prize in gastrology for the finding that this bacterium, is related to the pathogenesis of gastritis and peptic ulcer. They documented that eradication of H. pylori from the stomach, using antibiotics and potent gastric inhibitors, not only accelerates healing of ulcer but also prevents its recurrence, the finding considered as greatest discovery in practical gastrology during last century. Thus, the outstanding achievements in gastroenterology during last century have been awarded by three Nobel prizes and appreciated by millions of ulcer patients all over the world.
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