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INTRODUCTION AND OBJECTIVE Screening colonoscopy is a recommended tool, and the most sensitive and cost-effective method for reducing the incidence of colorectal cancer (CRC). OBJECTIVE The purpose of the study was to present the results of a 5-year screening for early detection of CRC carried out among the population of the central-eastern regions of Poland, primarily in Lublin Province. MATERIALS AND METHOD Screening colonoscopy was conducted in a group of 1,009 patients - 636 women and 373 men, aged 40-65 years. RESULTS Neoplastic polyps were found in 275 patients, advanced adenomas in 49 patients and adenocarcinoma in 13. 70.55% of neoplastic polyps was located in the distal colon, 18.9% in the proximal part and 10.55% in both regions, advanced adenomas in 79.59%, 8.16% and 12.25%, respectively. Adenocarcinoma was located in the proximal colon in 2 cases and in the distal region in 11 cases. Neoplastic polyps and advanced adenomas occurred significantly more frequently in smokers than in non-smokers. Neoplastic polyps were found statistically more frequent in males than in females, among the overweight and obese patients, than in subjects with normal BMI, and more frequently in the group of urban, compared to rural patients. However, the frequency of advanced adenomas and CRC was not statistically different in those groups. The incidence of CRC was statistically more frequent in males than in females. Smoking and male gender were significant risk factors for developing neoplastic polyps. Male gender seemed to predispose to CRC. Obesity was found to favour advanced adenomas. CONCLUSIONS The results of screening found neoplastic polyps in every third person (mean) who did not have any symptoms suggestive of colon pathology. Advanced adenomas were found in 5% of the examined and CRC was detected in 1.29% of participants. Smoking, male gender and overweight were significant risk factors for developing neoplastic polyps. No correlation was found between gender and the location of neoplastic polyps and advanced adenomas in the colon.

Summary Aim. The aim of the present study was to analyse the impact of education of patients with irritable bowel syndrome (IBS) on their quality of life. Methods. The study was carried out at the Gastroenterology Outpatient Clinic of the Independent Public Clinical Hospital No. 4 in Lublin and Gastroenterology Outpatient Clinic of the Cardinal Stefan Wyszynski Regional Specialist Hospital in Lublin in the years 2010–2011. The quality of life was analysed using the Quality of Life Questionnaire (QOL-Q R. Schalock, K. Keith). Material. The group of 83 patients with the diagnosis of irritable bowel syndrome, who gave their consent for inclusion in the study, was provided with information about the essence of the disease, disease-related diet and lifestyle, course of the disease, medications, and check-ups. Results. Our patients educated by the physician, nurse and those provided with written information had substantially higher scores in multi-dimensional aspects of the quality of life after education. Six months after education patients with IBS showed a significantly higher quality of life in all aspects, i.e. Satisfaction, Competence/productivity, Empowerment/ independence and Social inclusion/community integration. The understanding of the essence of their disease contributed to a decrease in anxiety associated with the neoplastic disease and worrying symptoms, which significantly reduced the incidence of complaints. Conclusions. 1. Quality of life of patients with irritable bowel syndrome is substantially reduced in all the examined spheres. 2. Education of patients with IBS resulted in enhanced quality of life and reduced disease-related complaints. 3. Education of patients with IBS plays a significant role in the entire therapeutic process.

There are some divergent data concerning the role of matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitor of MMP (TIMP)-2 in the pathogenesis of alcoholic cirrhosis (AC) and chronic pancreatitis (CP). Our objective was to evaluate the activity of MMP-2, MMP-9 and TIMP-2 serum levels in patients with AC and CP. Twenty-one patients with diagnosis of AC and twenty-two with CP admitted to the outpatient clinic for a control visit were enrolled. All results were compared with age and sex-matched control group (n=19). The sera obtained from venous blood were stored at -70°C for further analysis. Activity of MMP-2 and MMP-9 were evaluated with gelatin zymography, TIMP-2 serum level was analyzed with the usage of ELISA method. A significant decrease of serum MMP-2 activity was noted in sera of AC and CP patients in comparison with control. Activity of MMP-9 was elevated only in CP patients and TIMP-2 serum level was elevated only in AC patients. Decreased activity of MMP-2 in AC patients can contribute to cirrhosis development. The high level of MMP-9 in serum related to CP patients theoretically can exacerbate the inflammatory process within the pancreas.

Amyloidosis is characterised by the accumulation of poorly soluble fibrous proteins in the extracellular space of various bodily organs. Light chain amyloidosis (AL) is recognised as the most common form of systemic amyloidosis. Light chains are deposited in the majority of bodily organs, and accumulation of them in the liver produces hepatomegaly. We report a case of AL-systemic amyloidosis with liver involvement in a 71-year-old woman. Hepatomegaly, weight loss and general malaise were the first manifestations of the disease. Liver biopsy found amyloid deposits along the sinusoids as well as in the space of Disse, inside the vascular wall and in connective tissue of the portal tracts, which showed a positive reaction in Congo Red stain. Further diagnosis showed the presence of systemic amyloidosis. The patient was put on cyclophosphamide and steroid therapy.

Regulation of gene expression is essential for normal physiological functions; thus deregulation of gene expression is common in disease conditions. One level of regulation of gene expression is performed by noncoding RNAs, among which microRNAs (miRNA) are the best studied. Abnormal expression of these molecular players can lead to pathogenic processes such as heart disease, immune system abnormalities, and carcinogenesis, to name but a few. Of a length of 18–25 nucleotides miRNAs are involved in binding partial complementary sequences within the 3′-UTR (3′-untranslated region) of the target mRNAs. Depending on the type of neoplastic transformation, miRNAs can act both as oncogenes (oncomirs) or as tumor suppressors. Because of the great importance of miRNAs, most researches focus on either their role as biomarkers or their potential as therapeutic targets. Herein, we present the review of microRNA biology, function, and tumorigenic potential with emphasis on their role in lung cancer.

The role of adenosine A3 receptors and their distribution in the gastrointestinal tract have been widely investigated. Most of the reports discuss their role in intestinal inflammations. However, the role of adenosine A3 receptor agonist in pancreatitis has not been well established. The aim of this study is (Ed note: Purpose statements should be in present tense) to evaluate the effects of the adenosine A3 receptor agonist on the course of sodium taurocholate-induced experimental acute pancreatitis (EAP). The experiments were performed on 80 male Wistar rats, 58 of which survived, subdivided into 3 groups: C—control rats, I—EAP group, and II—EAP group treated with the adenosine A3 receptor agonist IB-MECA (1-deoxy-1-6[[(3-iodophenyl) methyl]amino]-9H-purin-9-yl)-N-methyl-B-d-ribofuronamide at a dose of 0.75 mg/kg b.w. i.p. at 48, 24, 12 and 1 h before and 1 h after the injection of 5 % sodium taurocholate solution into the biliary–pancreatic duct. Serum for α-amylase and lipase determinations and tissue samples for morphological examinations were collected at 2, 6, and 24 h of the experiment. In the IB-MECA group, α-amylase activity was decreased with statistically high significance compared to group I. The activity of lipase was not significantly different among the experimental groups but higher than in the control group. The administration of IB-MECA attenuated the histological parameters of inflammation as compared to untreated animals. The use of A3 receptor agonist IB-MECA attenuates EAP. Our findings suggest that stimulation of adenosine A3 receptors plays a positive role in the sodium taurocholate-induced EAP in rats.

Background and aims. There is growing evidence that white adipose tissue is an important contributor in the pathogenesis of alcoholic liver disease (ALD). We investigated serum concentrations of total adiponectin (Acrp30), leptin, and resistin in patients with chronic alcohol abuse and different grades of liver dysfunction, as well as ALD complications.Materials and Methods. One hundred forty-seven consecutive inpatients with ALD were prospectively recruited. The evaluation of plasma adipokine levels was performed using immunoenzymatic ELISA tests. Multivariable logistic regression was applied in order to select independent predictors of advanced liver dysfunction and the disease complications.Results. Acrp30 and resistin levels were significantly higher in patients with ALD than in controls. Lower leptin levels in females with ALD compared to controls, but no significant differences in leptin concentrations in males, were found. High serum Acrp30 level revealed an independent association with advanced liver dysfunction, as well as the development of ALD complications, that is, ascites and hepatic encephalopathy.Conclusion. Gender-related differences in serum leptin concentrations may influence the ALD course, different in females compared with males. Serum Acrp30 level may serve as a potential prognostic indicator for patients with ALD.

Background Non-alcoholic fatty liver disease (NAFLD) refers to a very wide clinical spectrum. Advanced fibrosis that accompanies disease leads to the development of cirrhosis and hepatocellular carcinoma. Thus, identification of patients with advanced fibrosis is essential. The aim of the present study was to compare the usefulness of NAFLD fibrosis and BARD scores in predicting fibrosis in NAFLD and to determine the risk factors of advanced fibrosis. Material/methods The study included 126 patients with NAFLD. Fibrosis in liver biopsy was scored on a 5-point scale. The BARD and the NAFLD fibrosis scores were compared with the biopsy findings. Results Liver biopsy revealed 27 patients with advanced and 99 with mild/moderate fibrosis. Advanced fibrosis was statistically significantly more common in older patients with obesity, AST/ALT ratio ≥0.8, diabetes mellitus, and thrombocytes ≤200 × 10³/L. Positive predictive value, negative predictive value and AUROC curve for BARD score, and NAFLD fibrosis score were 68.57%, 96.70%, 0.865 and 70.59%, 98.11%, 0.919, respectively. Conclusions Both scores are capable of ruling out advanced fibrosis and markedly reducing the need for liver biopsies in patients with NAFLD. Obesity, diabetes mellitus, thrombocytes ≤200 × 10³/L, advanced age and AST/ALT ratio ≥0.8 are the risk factors of advanced fibrosis.

INTRODUCTION Recent studies have shown the key role of genetic factors in the development of chronic pancreatitis. OBJECTIVES The aim of the study was to establish whether the frequency of the N34S mutation of serine protease inhibitor Kazal type 1 (SPINK1) gene differs between patients with alcoholic chronic pancreatitis, patients with nonalcoholic chronic pancreatitis, alcoholics without any digestive organ damage, and controls. We also sought to investigate whether the frequency of this mutation differs between women and men, and whether the mutation is associated with the age of patients at first diagnosis of chronic pancreatitis. PATIENTS AND METHODS The study included 207 patients: 67 with alcoholic chronic pancreatitis, 35 with nonalcoholic chronic pancreatitis, 43 alcoholics with no damage to digestive organs, and 62 healthy volunteers who served as controls. The N34S mutation of the SPINK1 gene was detected with the polymerase chain reaction. RESULTS The N34S mutation of the SPINK1 gene occurred in 15 of 207 patients (7.25%). The mutation was most frequent in patients with alcoholic chronic pancreatitis (10 patients, 16.39%) and was more frequent compared with the control group (2 patients, 3.23%) (P = 0.047). There were no statistically significant differences between the other groups: patients with nonalcoholic chronic pancreatitis (2 patients, 5.71%), alcoholics without digestive organ damage (1 patient, 2.33%), and controls. The mutation was more frequent in men than in women (P = 0.043). There were no differences between patients with and without the mutation in terms of the age at first diagnosis of chronic pancreatitis (P >0.05). CONCLUSIONS The N34S mutation of the SPINK1 gene seems to be significantly correlated with alcoholic chronic pancreatitis.

Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the gastrointestinal tract. They originate from the myenteric ganglion cells, termed the interstitial Cajal cells. The majority, i.e. 95% of GIST, show expression of the membrane receptor protein CD117 with a tyrosine kinase activity c‑kit. Gastrointestinal stromal tumors constitute less than 1% of all digestive tract tumors. They may be benign or malignant (30%), and occur in every part of the gastrointestinal tract, however the stomach is the most common localization. They develop with the same prevalence in men and in women, usually above the age of 50 years. The peak incidence is observed between the fifth and the sixth decade of life. Symptoms are not typical and depend on the localization and the tumor size. About 10–30% of GIST are completely asymptomatic, and are discovered accidentally during the endoscopy or X‑rays evaluation as well as during surgical interventions performed for various reasons. The malignant tumors metastasize most commonly to the liver and peritoneum. The metastases are rarely found in the lungs, pleura and bones. The detection of GIST is based on imaging, endoscopy, histological and immunohistochemical examinations. A useful and promising diagnostic procedure is positron emission tomography. The final diagnosis is mostly based on the pathologic findings of the removed tumor. The prognosis of GIST depends on its size, mitotic activity in 50 high power fields and mucosal infiltration. Radical surgery is the best treatment of GIST.Key words: diagnosis of gastrointestinal stromal tumors, epidemiology, prognosis, symptoms

Chronic pancreatitis (CP) is a necroinflammatory process characterized by loss of both exocrine and endocrine function. To date, the disease has been treated symptomatically. Real advances in CP management can be expected once the pathophysiology of the disease is elucidated and individual stages of its development are properly managed. A key role in the CP pathogenesis is played by activation of pancreatic stellate cells (PSCs) that cooperate with the remaining pancreatic cells. All these cells produce cytokines, growth factors, angiotensin and other substances, which paracrinally or autocrinally induce further, persistent activation of PSCs. The activated PSCs are capable of producing and modifying the extracellular matrix. An optimal therapeutic preparation should exert beneficial effects on all the above-mentioned phenomena observed in CP. The most promising treatment modalities include blocking of the renin-angiotensin system (RAS), activation of peroxisome proliferator-activated receptors gamma (PPAR-γ), influence on the remaining PSC signaling pathways, blocking of substances produced by activated PSCs, and antioxidants. The findings of many recent experimental studies are highly encouraging; however, their efficacy should be confirmed in well-designed clinical trials.

Purpose To assess the prevalence of spontaneous bacterial peritonitis (SBP) in asymptomatic patients with decompensated liver cirrhosis. Material and methods Patients (pts) with symptoms of decompensation of liver cirrhosis, ascites, and no signs indicating SBP were included to our study. Exclusion criteria include: 1/ clinical symptoms of infection, 2/ developing de novo or worsening hepatic encephalopathy, 3/ gastrointestinal bleeding within the last month, 4/ renal failure, 5/ antibiotic treatment or norfloxacin prophylaxis at admission. About 60 ml of ascitic fluid were drawn for lab examination. Pathologic assessment for atypical cells was also performed. Results 37 patients fulfilled inclusion criteria. Their mean age was 56.2 ± 12.1. The Child- Pugh classification revealed 13 (35.1%) patients of class B and 24 (64.9%) patients of class C. The mean Model for End-Stage Liver Disease score in this group was 16.6 ± 6.8. The mean ascitic protein content was 1.85 ± 1.09 g/dL and mean neutrophil count 144.8 ± 445.1/mm3. Ascitic fluid analysis revealed: signs of bacterascites in 6 of 37 (16.2%) pts; neutrocytic ascites in 1 of 37 (2.7%) pts; and 2 of 37 (5.4%) pts met criteria for SBP. C-reactive protein level was the best predictor of infection [SBP(+) 47.9 ± 40.9 versus SBP(-) 11.7 ± 5.1; p= 0.0005]. Conclusions The prevalence of SBP in asymptomatic cirrhotics with ascites is low. We observed the trend towards more frequent occurrence of the infection in patients suffered from severe liver disease (Child-Pugh C group).

Melatonin and L-tryptophan (Trp) are highly gastroprotective in humans, but no study has assessed their impact on healing of chronic gastroduodenal ulcers in humans. Three groups (A, B and C) of 14 idiopathic patients in each treatment group with gastroduodenal chronic ulcers were treated with omeprazole (20 mg twice daily) combined either with placebo (group A), melatonin (group B) or with Trp (group C). The rate of ulcer healing was determined by gastroduodenoscopy at day 0, 7, 14 and 21 after initiation of therapy. Plasma melatonin, gastrin, ghrelin and leptin were measured by RIA. On day 7, omeprazole by itself (group A) had not healed any ulcers, but four ulcers were healed with omeprazole plus melatonin and two with omeprazole plus tryptophan. At day 21, all ulcers were healed in patients treated with melatonin or Trp, but only 10-12 ulcers were healed in placebo-treated patients. After treatment with omeprazole plus melatonin (group B) or Trp (group C), plasma melatonin levels rose several-fold above initial values. Plasma gastrin level also rose significantly during treatment with omeprazole plus melatonin or Trp, but it was also significantly increased in patients treated with omeprazole plus placebo. Plasma ghrelin levels did not change significantly after treatment with melatonin or Trp, while plasma leptin increased significantly in patients treated with melatonin or Trp but not with placebo. We conclude that melatonin or Trp, when added to omeprazole treatment, accelerates ulcer healing and this likely depends mainly upon the significant increments in plasma melatonin.

Summary Background This study sought to define the mechanism by which PPAR-γ ligands affect the course of experimentally induced colitis in rats. Material/Methods Inflammation was induced in Wistar rats by a single rectal administration of 2,4,6,-trinitrobenzene sulfonic acid (TNBS). The antagonist of PPARγ antagonist, bisphenol A diglycidyl ether (BADGE), was administrated intraperitoneally 120 mg/kg 4 times every other day. Rosiglitazone 8 mg/kg was administrated by gastric tube 4 times. Body weight was measured daily. After killing, the large intestinal tissue was weighed and collected for histopathologic and immunoenzymatic tests. Levels of IL-6, IL-10, and myeloperoxidase (MPO) were determined in serum and in intestinal homogenates. Results Rats receiving rosiglitazone had higher body weight, whereas large intestine weight/length ratio was lower; histology showed fewer inflammatory markers. Rats receiving TNBS and TNBS along with BADGE had more intensive inflammatory changes. Rosiglitazone alone decreased expression of IL-6; used with TNBS it decreased expression of MPO in intestinal tissue, yet did not increase the expression of IL-10. Decreased levels of MPO indicate reduced neutrophil-dependent immune response. The antagonist of PPAR-γ increased IL-6 in serum and decreased IL-10 in intestinal homogenates. Bisphenol A diglycidyl ether administrated to healthy animals increases serum IL-6 levels. Conclusions Rosiglitazone inhibits experimental inflammation; administration of its selective antagonist abolishes this protective influence. Rosiglitazone inhibits expression of proinflammatory IL-6 and does not affect IL-10. Agonists of PPARs-γ are possibilities for inflammatory bowel disease prevention. Exogenous substances blocking PPARs-γ may contribute to development or relapse of nonspecific inflammatory bowel diseases.

The toxicity of non-steroidal anti-inflammatory drugs (NSAIDs) related to the upper gastrointestinal (GI) tract is well established. However, they may cause injury distal to the duodenum as well – to the small and large intestine and/or to other organs of the digestive system. Non-steroidal anti-inflammatory drugs induce small intestinal perforation, ulcers or strictures requiring surgery and inflammation with blood and protein loss called NSAID enteropathy. These drugs can exacerbate pre-existing large bowel disease (e.g. ulcerative colitis, diverticular disease) and precipitate relapse of inactive disease or the new onset of inflammatory bowel disease (IBD) with rapid resolution of symptoms on their withdrawal. They have been implicated in the development of microscopic colitis. Non-steroidal antiinflammatory drugs-associated toxicity of the small and large bowel is increasingly recognized in clinical practice, as enteroscopic procedures become more frequently used. Liver injury is an uncommon, but potentially lethal complication. It can occur with all NSAIDs, but diclofenac and sulindac seem to be most commonly associated with the problem. These drugs may contribute to acute fatty liver of pregnancy. Hepatotoxicity is likely due to an idiosyncratic reaction resulting from an immunological response or altered metabolic pathways. The major benefits of NSAIDs relate to reports of possible prevention, delay or regression of progress towards cancer of the colon, oesophagus, stomach as well as of cancer of the breast, lung, prostate and skin. Despite their promise, NSAIDs are not yet recommended for prevention or treatment of any cancer, because the balance of hazards and benefits from the treatment must be resolved in the designated patient population. Streszczenie Toksycznośc niesteroidowych lekow przeciwzapalnych (NLPZ) w stosunku do gornego odcinka przewodu pokarmowego jest dobrze udokumentowana. Mogą one jednak powodowac uszkodzenia rowniez dystalnie do dwunastnicy – w jelicie cienkim oraz grubym i/lub w innych narządach ukladu trawiennego. Niesteroidowe leki przeciwzapalne wywolują perforacje, owrzodzenia i przewezenia jelita cienkiego, ktore wymagają leczenia operacyjnego, oraz stan zapalny z utratą krwi i bialka, zwany enteropatią. Mogą zaostrzyc objawy podstawowej choroby jelita grubego (np. wrzodziejącego zapalenia jelita grubego, choroby uchylkowej), wtornie wzmagac aktywnośc choroby nieaktywnej lub indukowac pierwotny epizod nieswoistych zapalnych chorob jelit, z szybkim ustepowaniem objawow po odstawieniu leku. Sugeruje sie ich udzial w rozwoju mikroskopowego zapalenia jelita grubego. W praktyce klinicznej toksycznośc NLPZ w jelicie cienkim i grubym rozpoznaje sie coraz cześciej ze wzgledu na coraz powszechniejszą dostepnośc procedur endoskopowych. Uszkodzenie wątroby jest rzadkim, lecz potencjalnie śmiertelnym powiklaniem. Moze sie ono pojawic po uzyciu kazdego NLPZ, ale najcześciej problem ten wywolują diklofenak i sulindak. Niesteroidowe leki przeciwzapalne mogą brac udzial w ostrym stluszczeniu wątroby u kobiet w ciązy. Ich hepatoto ksycznośc jest prawdopodobnie reakcją idiosynkrazji w wyniku odpowiedzi immunologicznej lub zaburzen metabolicznych. Najwazniejsze korzyści z terapii NLPZ wykazaly raporty o mozliwej profilatyce, opoźnieniu lub regresji rozwoju raka w jelicie grubym, przelyku, zolądku, a takze raka piersi, pluc, gruczolu krokowego i skory. Mimo tych doniesien nie sformulowano dotychczas rekomendacji dla profilaktyki i leczenia NLPZ w przebiegu zadnego z tych nowotworow. Stosunek ryzyka do korzyści wynikający z takiego leczenia musi zostac oszacowany w badaniach w odpowiednich grupach chorych.

This investigation was designed to assess the effects of oral administration of melatonin (10 mg) and tryptophan (Trp) (500 mg) on fasting and postprandial plasma levels of melatonin, gastrin, ghrelin, leptin and insulin in 10 healthy controls and in age-matched patients with liver cirrhosis (LC) and portal hypertension. Fasting plasma melatonin levels in LC patients were about five times higher (102 +/- 15 pg/mL) than in healthy controls (22 +/- 3 pg/mL). These levels significantly increased postprandially in LC patients, but significantly less so in controls. Treatment with melatonin or L-Trp resulted in a further significant rise in plasma melatonin, both under fasting and postprandial conditions, particularly in LC patients. Moreover, plasma gastrin, ghrelin, leptin and insulin levels under fasting and postprandial conditions were significantly higher in LC subjects than in healthy controls and they further rose significantly after oral application of melatonin or Trp. This study shows that: (a) patients with LC and portal hypertension exhibit significantly higher fasting and postprandial plasma melatonin levels than healthy subjects; (b) plasma ghrelin, both in LC and healthy controls reach the highest values under fasting conditions, but decline postprandially, especially after oral application of melatonin or Trp; and (c) plasma melatonin, gastrin, ghrelin and insulin levels are altered significantly in LC patients with portal hypertension compared with that in healthy controls possibly due to their portal systemic shunting and decreased liver degradation.

To investigate the effects of ADH and ALDH gene polymorphism on the development of alcoholism, alcohol liver cirrhosis and alcohol chronic pancreatitis among Polish individuals.We determined the allele and genotype of ADH2, ADH3 and ALDH2 in 198 subjects: 57 with alcohol cirrhosis, 44 with alcohol chronic pancreatitis and 43 "healthy alcoholics"; 54 healthy non-drinkers served as controls. Genotyping was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method on white cell DNA.In the population examined the ADH2*1 allele frequency was 97.97%. The tests did not show the ADH2*3 allele. The ADH3*1 allele frequency was 57.07%. The ADH2*1 and the ADH3*1 alleles were statistically more common among patients who abuse alcohol in comparison with the controls. The ADH2*2 allele was not detected in any of the patients with chronic alcohol pancreatitis. The ADH2*1/*1 and the ADH3*1/*1 genotypes were statistically significantly more common among the patients who abuse alcohol than in the control group. All patients were ALDH2*1/*1 homozygotic. Patients with the ADH3*1 allele and the ADH3*1/*1 genotype started to abuse alcohol significantly earlier in comparison to the patients with the ADH3*2 allele and the ADH3*2 /*2 genotype.In the Polish population examined, the ADH3*1 allele and the ADH3*1/*1 genotype are conducive to the development of alcoholism, alcohol liver cirrhosis and alcohol chronic pancreatitis. However, the ADH2*2 allele is likely to protect against these conditions. Genetic polymorphism of ALDH2 shows no correlation with alcohol addiction or alcohol cirrhosis and alcohol chronic pancreatitis. The ADH3*1 allele and the ADH3*1/*1 genotype are conducive to alcohol abuse starting at a younger age.

Background: Genetic polymorphism of enzymes involved in alcohol metabolism plays a relevant role in etiopathogenesis of alcohol disease. The aim of the present study was to find in the Polish population the CYP2E1 genotypes that are likely to be responsible for higher susceptibility to alcohol disease of the liver and chronic alcohol pancreatitis. Methods: The CYP2E1 genotype and c1 and c2 alleles frequency were examined in 198 patients. Genotyping of the CYP2E1 was performed using polymerase chain reaction–restriction fragment length polymorphism methods on white cell DNA. Results: In the examined population encompassing 198 subjects, the c2 allele was present only in 1.5% of patients. It was found only in patients abusing alcohol. In the group of patients with alcoholic cirrhosis, it was present in 3.5% of cases, whereas in patients with chronic alcoholic pancreatitis, in 2.3%. The genotype c1/c2 was present in 3% of subjects. The genotype c2/c2 was not found in any patient. Heterozygotes c1/c2 were present only in patients consuming excessive amounts of ethanol; in 7% of patients with alcoholic cirrhosis and in 4.5% of those with chronic alcoholic pancreatitis. The c2 allele occurred only in men. None of the examined women had the genotype c1/c2. Conclusions: Our studies suggest that the frequency of the c2 alleles in Polish population is low. Because of their rare frequency, it is difficult to conclude explicitly that the presence of the c2 allele promotes alcoholic damage to alimentary organs among Poles. It seems, however, that they pose the risk of alcoholic cirrhosis; their role in chronic alcoholic pancreatitis is difficult to assess.

Neurofibromas of the stomach can occur in the course of Recklinghausen’s disease. Sporadic gastric neurofibroma appears rarely. This tumour may look like an ulcer and can be a cause of abdominal pain, nausea, and bleeding from the gastrointestinal tract. We reported a 61-year-old women complaining of stomachache for several months. Gastroscopy revealed a tumour with ulceration in the prepyloric part of the stomach. Helicobacter pylori infection was also present. Helicobacter pylori eradication and prolonged treatment of proton pump inhibitors did not decrease the ailments or the size of the tumour. It was not possible to determine the nature and origin of the tumour by carrying out examinations such as endoscopic ultrasound and computed tomography of the abdomen. Only after surgery and histopathological examination with immunohistochemistry was this tumour identified as a neurofibroma. In order to differentiate the tumour the following immunohistochemical examinations were carried out: CD34 (slightly +), CD117 (–), S-100 (+), desmin (–), NSE (+), GFAP (–), SMA (–), bc12 (–), CD99 (–), ALK1 (–), and MiB (1–1.5%). In such cases excision of the tumour is the preferred treatment.

Aim: To find the ADH3 genotypes in the Polish population likely to be responsible for higher susceptibility to alcohol disease of the liver and chronic alcohol pancreatitis. Method: The ADH3 genotype and ADH3*1 and ADH3*2 alleles frequencies were examined in 198 patients. Genotyping of the ADH3 was performed using PCR-restriction fragment length polymorphism methods on a white cell DNA. Results: The genotype ADH3*1/ADH3*1 was found to be significantly more frequent in alcohol abusers compared with non-drinkers. The examinations of the group of alcohol abusers showed that the genotype ADH3*2/ADH3*2 occurred statistically significantly less frequently in patients with chronic pancreatitis than in those without alimentary lesions (healthy drinkers). The alleles ADH3*1 and genotype ADH3*1/ADH3*1 were significantly more frequent in men than in women, whereas alleles ADH3*2 and genotype ADH3*2/ADH3*2 were more common in women. Conclusions: The genotype ADH3*2/ADH3*2 is likely to be a protective factor for chronic pancreatitis. Variations in ADH3 genotypes may account for some of the differences in prevalence of alcohol dependence between genders in the Polish population.

Heterotopic or ectopic tissue is a congenital anomaly defined as the presence of the tissue outside its normal location. This tissue is usually discovered incidentally and may be asymptomatic or may present with non-specific gastrointestinal (GI) symptoms. Two types of heterotopic tissues, pancreatic and gastric, predominantly occur in the GI tract. The frequency of ectopic pancreas found in autopsy studies is approximately 0.5%-13.7%. Heterotopic pancreatic tissue can be located anywhere along the GI tract; the most common sites are the stomach (27.5%), duodenum (25.5%), colon (15.9%), esophagus, and Meckel`s diverticulum. It has been found in approximately one per 500 surgical procedures involving the upper GI tract. It can also occur in the gallbladder, biliary tract, spleen, liver, omentum, mesentery, lung and pelvis. Likewise, heterotopic gastric mucosa can occur anywhere along the GI tract yet its most common locations are different from those of heterotopic pancreatic tissue. In this paper we present heterotopy characteristics in particular locations. Gastric or pancreatic heterotopy, although rare, should be taken into consideration in differential diagnosis of unexplainable abdominal pain, bleeding from the GI tract or weight loss. Once heterotopy has been detected, appropriate treatment can be implemented which will reduce the risk of complications.

Angiogenesis is believed to be implicated in the pathogenesis of alcoholic liver disease (ALD). We aimed to explore the usefulness and accuracy of plasma angiogenic biomarkers for noninvasive evaluation of the severity of liver failure and ALD outcome. One hundred and forty-seven patients with ALD were prospectively enrolled and assessed based on their (1) gender, (2) age, (3) severity of liver dysfunction according to the Child-Turcotte-Pugh and MELD scores, and (4) the presence of ALD complications. Plasma levels of vascular endothelial growth factor (VEGF-A) and angiopoietins 1 and 2 (Ang1 and Ang2) were investigated using ELISAs. Multivariable logistic regression was applied in order to select independent predictors of advanced liver dysfunction and the disease complications. Significantly higher concentrations of Ang2 and VEGF-A in ALD patients as compared to controls were found. There was no difference in Ang1 levels in both groups. A positive correlation of Ang2 levels with INR (Rho 0.66;P<0.0001) and its inverse correlation with plasma albumin levels (Rho –0.62;P<0.0001) were found. High Ang2 concentrations turned out to be an independent predictor of severe liver dysfunction, as well as hepatic encephalopathy and renal impairment. Ang2 possessed the highest diagnostic and prognostic potential among three studied angiogenesis-related molecules.

Aim. Determination of risk factors relevant to 90-day prognosis in AH. Comparison of the conventional prognostic models such as Maddrey’s modified discriminant function (mDF) and Child-Pugh-Turcotte (CPT) score with newer ones: the Glasgow Alcoholic Hepatitis Score (GAHS); Age, Bilirubin, INR, Creatinine (ABIC) score, Model for End-Stage Liver Disease (MELD), and MELD-Na in the death prediction.Patients and Methods. The clinical and laboratory variables obtained at admission were assessed. The mDF, CPT, GAHS, ABIC, MELD, and MELD-Na scores’ different areas under the curve (AUCs) and the best threshold values were compared. Logistic regression was used to assess predictors of the 90-day outcome.Results. One hundred sixteen pts fulfilled the inclusion criteria. Twenty (17.4%) pts died and one underwent orthotopic liver transplantation (OLT) within 90 days of follow-up. No statistically significant differences in the models‘ performances were found. Multivariate logistic regression identified CPT score, alkaline phosphatase (AP) level higher than 1.5 times the upper limit of normal (ULN), and corticosteroids (CS) nonresponse as independent predictors of mortality.Conclusions. The CPT score, AP > 1.5 ULN, and the CS nonresponse had an independent impact on the 90-day survival in AH. Accuracy of all studied scoring systems was comparable.

Alpha-fetoprotein (AFP) is a tumor marker used in clinical diagnosis and for monitoring the course of treatment. Serum concentration of AFP in excess of several hundred ng/ml is nearly 100 percent positive predictive value for hepatocellular carcinoma. The aim of this study was evaluation of AFP serum concentration in patients with different chronic liver diseases and the relationship between the concentration of AFP and gender in the studied groups of patients.The study includes 359 patients: 72 with autoimmune hepatitis, 27 with cancer metastatic to the liver, 53 with nonalcoholic fatty liver disease, 207 with liver cirrhosis and 40 healthy volunteers as control group. The concentration of AFP was examined in all patients.The highest AFP concentration occurred in the patients with autoimmune hepatitis, with metastatic liver cancer and with liver cirrhosis 16.81 +/- 5.49 ng/ml, 9.67 +/- 1.48 ng/ml i 8.42 +/- 2.73 ng/ml (p0.001 compared to the control group) respectively. Considering the classification of cirrhosis according to Child-Pugh Score the mean concentrations of AFP were: in Class A - 7.03 +/- 2.29 ng/ml, B - 7.59 +/- 2.45 ng/ml i C - 10.02 +/- 2.40 ng/ml. There were no statistically significant differences in the mean AFP concentrations between the patients with nonalcoholic fatty liver disease and the control group. Also showed no differences in the average concentration of AFP in men and women in study groups of patients (p0.05).Elevated serum AFP concentration typically up to several ng/ml is observed in autoimmune hepatitis, metastatic liver cancer and liver cirrhosis. Concentration of AFP correlates with the severity of liver cirrhosis. Simple steatosis of liver as one of the forms of nonalcoholic fatty liver disease is characterized by normal serum concentration of AFP. No relationship between AFP concentration and gender in patients with chronic liver disease is observed.

The presence of ascites is usually associated with portal hypertension, usually due to cirrhosis of the liver, with portal vein thrombosis, congestive cardiac failure, nephrotic syndrome, pancreatitis, tuberculosis. Approximately 10% of all cases of ascites occurs in malignant tumors, mostly of ovarian cancer. The purpose of this publication is to present the case of 63-year-old woman who has a basic and initial sole manifestation of disease--cancer of the ovary--was increasing ascites.

Because of numerous limitations for liver biopsy, a noninvasive marker of liver cirrhosis is sought. Promising indicators seem to be matrix metalloproteinases (MMPs) that are responsible for degradation of extracellular matrix. The aim of the study was to evaluate the gelatinase activities (MMP-2 and MMP-9) in patients with different stages of alcoholic cirrhosis. Sixty-seven outpatients who presented various stages of alcoholic cirrhosis according to Child–Turcotte–Pugh criteria and 26 healthy control subjects were enrolled. Blood samples were collected for MMP-2 and MMP-9 activities. A significant decrease of serum MMP-2 activity was noted in stages B and C of cirrhosis in comparison with control. Serum MMP-9 activity did not depend on the stage of cirrhosis. The MMP-2 levels, but not those of MMP-9, may be of value in understanding the pathogenesis and progression of alcoholic cirrhosis.

Melatonin and its precursor, l-tryptophan, have been shown to exert gastroprotective effects in animals, but their influence on the gastric damage by aspirin (ASA) in humans has been sparingly investigated. In this study, we designed to determine the effects of melatonin and l-tryptophan on ASA-induced gastric mucosal damage, gastric microbleeding, mucosal generation of prostaglandin E(2), and plasma melatonin, and gastrin levels. Three groups of healthy male volunteers (n = 30) with intact gastric mucosa received daily for 11 days either ASA alone or that combined with melatonin or tryptophan. Gastric blood loss and mucosal damage were evaluated at 3rd, 7th, and 11th days of ASA administration by endoscopy using Lanza score. ASA alone caused a marked rise of gastric damage and gastric blood loss, mainly at day 3rd and 7th, but they were significantly reduced at 11th day. Pretreatment with melatonin or tryptophan remarkably reduced ASA induced gastric lesions and microbleeding. Gastric mucosal generation of PGE(2) was suppressed by about 90% in all subjects treated with ASA alone without or with addition of melatonin or tryptophan. Plasma melatonin was markedly increased after treatment with melatonin or tryptophan plus ASA, but it was also raised significantly after application of ASA alone. Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone. We conclude that melatonin and its precursor tryptophan given orally significantly reduce gastric lesions induced by ASA possibly due to (a) direct gastroprotective action of exogenous melatonin or that generated from tryptophan and (b) gastrin released from the gastric mucosa by melatonin or tryptophan.

Alcohol dependence poses a serious medical and sociological problem. It is influenced by multiple environmental and genetic factors, which may determine differences in alcohol metabolism. Genetic polymorphism of the enzymes involved in alcohol metabolism is highly ethnically and race dependent. The purpose of this study was to investigate the differences, if present, in the allele and genotype frequency of alcohol dehydrogenase 1B (ADH1B), ADH1C and the microsomal ethanol-oxidizing system (MEOS/CYP2E1) between alcohol-dependent individuals and controls and also to determine if these genotypes cause a difference in the age at which the patients become alcohol dependent. The allele and genotype frequencies of ADH1B, ADH1C, and CYP2E1 were determined in 204 alcohol dependent men and 172 healthy volunteers who do not drink alcohol (control group). Genotyping was performed by PCR-RFLP methods on white cell DNA. ADH1B*1 (99.3%) and ADH1C*1 (62.5%) alleles and ADH1B*1/*1 (N = 201) and ADH1C*1/*1 (N = 85) genotypes were statistically more frequent among alcohol-dependent subjects than among controls (99.3 and 62.5%, N = 201 and 85 vs 94.5 and 40.7%, N = 153 and 32, respectively). Differences in the CYP2E1 allele and genotype distribution between groups were not significant. The persons with ADH1C*1/*1 and CYP2E1*c1/*c2 genotypes became alcohol dependent at a considerably younger age than the subjects with ADH1C*1/*2, ADH1C*2/*2 and CYP2E1*c1/*c1 genotypes (28.08, 25.67 years vs 36.0, 45.05, 34.45 years, respectively). In the Polish men examined, ADH1C*1 and ADH1B*1 alleles and ADH1C*1/*1 and ADH1B*1/*1 genotypes favor alcohol dependence. The ADH1B*2 allele may protect from alcohol dependence. However, subjects with ADH1C*1/*1 and CYP2E1*c1/*c2 genotypes become alcohol dependent at a considerably younger age than the subjects with ADH1C*1/*2, ADH1C*2/*2 and CYP2E1*c1/*c1 genotypes.

The purpose of this experiment was to investigate the role of PPAR ligands in the course of inflammation and of rosiglitazone, a PPAR-gamma-specific agonist, on the course of experimental acute pancreatitis (EAP).EAP was induced by administration of 5% sodium taurocholate injected into the pancreatic duct. The inflammatory activity was evaluated by biochemical scores (alpha-amylase, lipase, aminotransferases, and bilirubin), morphological changes (determined by light microscopy, H+E stained), and immunohistochemical reactions (ICAM, nitrotyrosine).Rosilgitazone administered in the course of EAP at a dose 50 mg/kg p.o. decreased the intensity of morphological changes (edema, inflammatory infiltrates, necrosis, and erythrocyte extravasations). In the rosiglitazone-treated animals all the biochemical parameters of EAP were statistically significantly decreased. Immunohistochemical reactions against ICAM-1 and nitrotyrosine showed that rosiglitazone decreased the intensity of inflammatory reactions in the groups of treated animals.PPAR-gamma agonists modulate the course of the inflammatory reaction. The administration of rosiglitazone decreased the intensity of the inflammatory process in the course of sodium taurocholate-induced EAP.

The aim of the study was to analyse the prevalence of H. pylori infection in adult inhabitants of Lublin Province. The effects of living conditions and lifestyle on the infection frequency were evaluated. The study included 585 adults randomly chosen for the epidemiological analysis of H. pylori infection in the Lublin region within the project commissioned by the Ministry of Health (PCZ 08-09) and State Committee for Scientific Research (C007/P05/2000). The study was based on a personal questionnaire and determinations of anti/Hp antibodies in IgG class using the ELISA method. High titres of anti/Hp antibodies (24 IU/ml) were demonstrated in 78.5 % of the subjects. In Lublin Province the infected individuals constitute 72 % of inhabitants, in the big towns--74 % and in small towns--95 %. According to the place of birth: among those born in the country 87 % are infected, compared to 78.4 % in the small towns and 64 % in the big towns, respectively. Positive test results were observed in 79 % of farmers, 78 % of manual workers and 75 % of mental workers. The percentage of the affected neglecting basic hygienic rules exceeded 90 %. With increased frequency of hygienic measures the number of the H. pylori infected individuals decreased to 65 %. The prevalence of H. pylori infection among the inhabitants of the Lublin region is lower than that found in town inhabitants. Lublin Province shows the lowest level of H. pylori infection in Poland. The H. pylori infection is strongly affected by the lack of basic rules of personal hygiene and improper diet.

Congenital nonhemolytic hyperbilirubinemias (CNH) are quite rare pathology of liver. They occur most often in children, but are common in adults too. A common feature of congenital nonhemolytic hyperbilirubinemias is an abnormal serum bilirubin level without other abnormalities in routine liver functional tests. Liver histology on light microscopy is normal. Hereditary genetics defect of enzymes taking part in metabolism of bilirubin is the cause of CNH. They are divided into two groups: with unconjugated hyperbilirubinemia (Crigler-Najjar syndrome, Gilbert syndrome) and conjugated hyperbilirubinemia (Dubin-Johnson syndrome and Rotor syndrome). Because CNH in adults are benign disorders and the prognosis is excellent, patients do not require any specific therapy. Is important to take the differential diagnosis. Once the diagnosis of congenital nonhemolytic hyperbilirubinemia is confirmed, patients should be informed of the disease process and its benign nature to prevent needless work-up in the future. In present, CNH are treated as cosmetic defects and no therapy is applied.

In the recent years, the prevalence of adenocarcinomas of the esophagus has substantially increased. At present its prevalence in the USA is comparable to that of squamous carcinoma (5/100,000 a year). In 80-90% of cases esophageal adenocarcinoma is located in 1/3 of the lower esophagus and is mainly derived from Barrett's esophagus (BE). The role of Helicobacter pylori (Hp) infection in the pathogenesis of gastritis and gastric ulcer disease has been well known and documented. However, its role in the pathogenesis of esophageal reflux disease, its complications, particularly regarding the risk of Barrett's esophagus and adenocarcinoma is still being studied. The relation between Hp infection and BE has been discussed for many years. The importance of the problem is warranted by the wide prevalence of both Hp infection and reflux disease in the population. The above mentioned findings confirm the protective effects of Hp infection in BE. Despite numerous studies some doubts concerning the relations between Hp infection and BE are still to be explained.

The Helicobacter pylori infection is considered the most frequent factor of morbidity and mortality in the diseases of the upper alimentary tract. It is responsible for duodenal and gastric ulcers. It may contribute to the development of MALT lymphoma and gastric carcinoma. The H.p. infection is a widespread phenomenon, its intensification is associated with the socioeconomic status and increases with age. The aim of the study is to analyse the epidemiological trends of the H.p. infection, the effects of environmental factors, lifestyle, diet and sanitary habits on the incidence of H.p. infection in the adult population of the Lublin region. The study included 585 adults randomly chosen for epidemiological analysis within the project ordered by the Ministry of Health and State Committee for Scientific Research. The personal questionnaires were completed and serum levels of antibodies against H.p. were determined. The positive results were found in 78.52% of the examined participants. In the youngest group, the positive result was observed in 46% of cases. In the successive age groups a systematic increase in the number of the infected was found--from 46% to 100%. The highest number of the infected individuals live in provincial towns--94.6%, the lowest--in the country--71.9%. The infections are significantly affected by sanitary conditions: poor personal hygiene--the incidence about 90%. The infection incidence is also affected by alcohol consumption--increases with consumption of high-grade alcohols--82.4% (compared to 67.5% among non-drinkers) and decreases in those drinking low-grade alcohols (beer)--75.8% (84.9% in non-drinkers). No effects of the economic status and education on the H.p. infection incidence were observed.

The aim of our study was to check the significance of portal blood velocity /PBV/ in evaluation of the severity of liver disease. Duplex doppler sonography evaluation of PBV was performed in 20 patients (pts) with liver cirrhosis (7 women, 13 men, aged 34-75) and 10 pts with normal liver function (controls). We checked it during fasting and 30 minutes after a meal. The diagnosis of liver cirrhosis was based on clinical, laboratory and sonographic criteria. The severity of liver cirrhosis was classified according the Child-Pugh score as class A--6 pts.; class B--10 pts. and class C--4 pts. The lowest values of the mean baseline PBV (during fasting) were observed in cirrhotic pts class C (15.9+/-4.2 cm/s vs class B 18,1+/-7.8 cm/s vs class A 20.4+/-8.6 cm/s vs controls 21.6+/-3.8 cm/s). A similar situation appeared after our evaluation of PBV values in the postprandial state (class C 16.5+/-4.8 cm/s vs class B 19.8+/-9.1cm/s vs class A 22.4+/-6.4 cm/s vs controls 29.6+/-10.6 cm/s). The increment of PBV after a meal in pts with the Child-Pugh class C was significantly diminished compared to control group (0.6+/-4.1cm/s vs 8.0+/-5.2 cm/s; p0.05). We concluded that the postprandial portal blood velocity assessment is useful for evaluation of the severity of liver disease.

The aim of our study was assessment of the long-term influence of interferon-alpha (IFN-alpha) treatment on the serum marker of the hepatocarcinogenesis level-alpha-fetoprotein (AFP)-in patients (pts) with chronic viral hepatitis (cvh) B and C. Thirty seven pts (21 with HCV and 16 with HBV infection (20 women, 17 men, aged 24-62) were included in the study. Pts were administered IFN-alpha in the dose of 9-15 MU per week, thrice a week, for 16 weeks (HBV group) or 24-52 weeks (HCV group). Effectiveness of IFN-alpha treatment was evaluated on the basis of the HBV DNA and HCV RNA level in blood. The serum AFP values were determined before and 4-7 years after IFN-alpha treatment. The baseline serum AFP level was increased in 26 out of 37 pts (70%) (14/21 from HCV group; 12/16 from HBV group). After the 4-7 years' follow-up it remained increased only in 2 out of 37 pts (5%). AFP values significantly decreased after IFN-alpha treatment (17.58+/-19.09 IU/ml vs 7.95+/-21.78 IU/ml; p0.05; normal range 0-5 IU/ml) in both HBV and HCV, responder and non- responder groups. These results support the hypothesis that IFN-alpha therapy could diminish the risk of liver carcinogenesis in pts with cvh B and C. It significantly decreases the serum AFP level. Its beneficial effect was observed both in responders and in non-responders.

Due to their complex and not fully known etiopathogenesis as well as difficulties in treatment, chronic hepatitis and cirrhosis still remain one of the main problems of hepatologists. Nowadays, the use of IFN alpha is considered the most effective method of treatment in chronic hepatitis. Recently, a new property of IFN, i.e. its effects on the reduction of fibrosis, has been discovered. The aim of the paper was to examine the effects of IFN alpha on biochemical parameters (AlAt and AspAt activities), on the metabolic function of the liver and its morphologic picture observed under the light and electron microscope after the 3- and 6-week CCl4-induced damage. The experiments were carried out in Wistar male rats. To evaluate the liver function, the test of aminophenazone elimination in the isolated perfused rat livers was used according to Miller modified by Hafte. Additionally, AspAt and AlAt activities were determined. The liver specimens were analysed under the light and electron microscope and using immunohistochemical methods. The findings show that after the 3-week CCl4-induced liver damage, IFN alpha does not significantly affect AlAt and AspAt activities, irrespective of the dose used. IFN alpha administered after the 6-week damage significantly changes those activities when the doses used are high. It was found that carbon tetrachloride does not result in evident cirrhotic changes, however it activates Ito cells, causes focal retraction of the stroma and fibrosis. The increased number of Ito cells in Disse's space observed in immunohistochemical and ultrastructural examinations is indicative of the activation of liver fibrotic processes following CCl4 administration in both variants used. IFN alpha substantially weakens fibrogenesis of the CCl4-damaged liver which is visible in the decreased number of Ito cells and weaker expression of the stroma retraction. Moreover, IFN alpha administered to the experimental animals after the CCl4-induced injury of the liver increases aminophenazone clearance, especially when used in higher doses. Positive effects of IFN confirmed in the studies suggest that the drug may be used in patients with chronic hepatitis and early cirrhosis since it is likely not only to eliminate the virus but also to improve the liver function and reduce fibrosis.

Acute pancreatitis leads to hypoxia caused by vasoconstriction and to activation of lysosomal and digestive enzymes resulting in pancreas autodigestion and damage. This causes activation of leucocytes and increased expression of adhesive molecules enabling margination and adhesion of activated leucocytes to the endothelium. Activated leucocytes are the source of proinflammatory cytokins and oxygen-free radicals which intensify the inflammatory response. The reports indicating that adenosine may prevent activation of the above-mentioned processes in ischaemia prompted us to undertake this study. The study was performed in two stages. The first stage was to evaluate the effects of agonists and antagonists of adenosine receptors on normal pancreas while the second one was to determine the influence of these substances on the development of caerulein-induced acute pancreatitis. During the first stage, the animals were injected intraperitoneally with the substances examined: the A1 receptor antagonist--DPCPX, the A2 receptor agonist--CGS 21680, the A2 receptor antagonist--ZM 241385 and the A3 receptor agonist--IB-MECA and then received intravenous saline. The control animals were subjected only to the 12 h intravenous infusion of 0.15 M NaCl. During the second stage, after the intraperitoneal administration of adenosine receptor agonists and antagonists (as in the first stage), acute pancreatitis was induced with the 12 h intravenous infusion of 5 micrograms/kg/h caerulein. Identical acute pancreatitis was induced in the control animals, however no other substances were administered. The pancreatic tissue samples were collected directly after intravenous infusion. The severity of inflammatory processes in the pancreas was evaluated on the basis of the plasma amylase activity, pancreatic weight and enhancement of histopathological changes observed in this organ. In the animals infused with saline alone, no effects of the substances examined on the pancreatic weight, plasma amylase activity and histopathological features were observed. The intravenous caerulein infusion induced acute pancreatitis expressed as bigger pancreatic weight, increased plasma amylase activity and tissue damage (oedema, cell vacuolization, leucocyte infiltration). The A2 receptor agonist administration preceding the induction of acute pancreatitis decreased the pancreas damage caused by caerulein. Lower weight of the pancreas and decreased plasma amylase activities were observed; on histopathological examination--oedema, leucocyte infiltration and intensity of alveolar cell vacuolization were lower. On the other hand, intraperitoneal pretreatment with the A2 receptor antagonist intensified the pancreas injury. The A1 receptor blockade and A3 receptor stimulation in the animals injected with caerulein did not affect the pancreatic weight, plasma amylase activity or histopathological picture of the organ. The administration of A2 receptor agonists decreases the organ injury in caerulein-induced acute pancreatitis in rats. This action may result from modulating effects of these substances on different stages of the cascade of inflammatory reactions. However, the present study did not reveal any effect of the A1 receptor agonist or A3 receptor antagonist on inflammatory processes in the experimental model described.

Chronic pancreatitis is a disease whose pathomechanism has not yet been fully explained. Some progress has been made in recent years, however, mainly due to the identification and description of pancreatic stellate cells (PSCs). In 1998 Bachem observed that the vitamin A-storing cells present in the pancreas, when subjected to activation, transformed into myofibroblasts capable of producing collagens I and II and fibronectin, which contributes to fibrosis in chronic pancreatitis. The development of chronic pancreatitis also seems likely to be affected by the cytokines, among other things, as a result of repeated PSC activation. The current literature provides more and more data suggesting that cytokines play an important role in the regulation of inflammation and fibrosis in CP. A major role in the pathogenesis of chronic pancreatitis is attributed to interleukin 1, 6, 10, tumour necrosis factor a (TNF-a) and transforming growth factor b1 (TGF-b1). All these factors have pro- and anti-inflammatory effects, and act simultaneously. Their effects on PSCs can be synergistic, antagonistic or complementary. Further comprehensive studies are needed to determine precisely the role of the individual cytokines and PSCs, as well as their relationships. However, the present state of our knowledge suggests that repeated episodes of AP and thus exposure to increased cytokine secretion may contribute to persistent chronic activation of PSCs, resulting in pancreatic fibrosis and chronic pancreatitis.

Background. The aim of this study was to determine the possible relationship between the activity of three different antioxidant enzymes — peroxidase superoxide dismutase, catalase, and glutathione peroxidase — and carbon tetrachloride-induced injury. Methods. Male Wistar rats weighing 200–250 g were used in the experiments. Rats of the experimental groups were given carbon tetrachloride 0.5 ml/kg i.p. in olive oil (5 mmol/kg body mass) for 1 or 3 days. Control group rats were injected with olive oil only for the same period. Brain, liver, kidney, and heart supernatants were used for measurement of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) activities. Results. No statistically significant changes in SOD and GPX activities were observed in the liver after CCl4 administration, but catalase activity was significantly increased after 24 h and remained at that level during the course of the study. In the brain, SOD and catalase activities decreased after 24 h of experiment, but GPX activity statistically significantly increased at all time points studied. Increased activities of SOD, catalase, and GPX were found in heart after CCl4 intoxication. The CCl4 injection in our experiment caused a reduction of SOD and catalase activities and increased GPX activity in the kidney. Conclusions. The results suggest that change in antioxidant enzyme activities may be relevant to the ability of the liver and other investigated organs to cope with oxidative stress during CCl4 poisoning.

Melatonin (MT) and its precursor L-tryptophan (TRP) are implicated in the protection of gastric mucosa against aspirininduced lesions and in the acceleration of healing of idiopathic gastro-duodenal ulcers, but no information is available whether these agents are also effective in healing of gastroduodenal ulcers accompanied by Helicobacter pylori (H. pylori) infection. In this study three groups A, B and C, each including 7 H. pylori-positive patients with gastric ulcers and 7 H. pylori-positive patients with duodenal ulcers, aging 28-50 years, were randomly assigned for the treatment with omeprazole 20 mg twice daily combined with placebo (group A), MT administered in a dose of 5 mg twice daily (group B) or TRP applied in a dose of 250 mg twice daily (group C). All patients underwent routine endoscopy at day 0 during which the gastric mucosa was evaluated and gastric biopsies were taken for the presence of H. pylori and histopathological evaluation. The rate of ulcer healing was determined by gastroduodenoscopy at day 0, 7, 14 and 21 after the initiation of the therapy. Plasma MT, gastrin, ghrelin and leptin were measured by specific RIA. At day 21, all ulcers were healed in patients of groups B and C but only 3 out of 7 in group A of gastric ulcers and 3 out of 7 in duodenal ulcers. Initial plasma MT showed similar low levels in all three groups but it increased several folds above initial values in ulcer patients at day 7, 14 and 21. Plasma gastrin and leptin levels showed a significant rise over initial values in patients treated with omeprazole and placebo, MT or TRP while plasma ghrelin levels were not significantly affected by these treatments. We conclude that MT or TRP added to omeprazole treatment, significantly accelerates healing rate of H. pylori infected chronic gastroduodenal ulcers over that obtained with omeprazole alone and this likely depends upon the significant rise in plasma MT and possibly also in leptin levels, both hormones involved in the mechanism of gastroprotection and ulcer healing.

Background and Aims: Fatigue is a common symptom of chronic liver diseases (CLD), including non-alcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CH-C). The mechanisms or correlates of fatigue in these patients have not been well studied. We aimed to determine if there is a correlation between self-reports of physical activity associated fatigue (peripheral fatigue) or more global lack of energy and motivation (central fatigue); with serum markers of inflammation, or with abnormalities of glucose and lipid metabolism. Methods: 31 untreated patients (age 52.5 ±6.8 years, 66.7% male, BMI 32.4 ± 5.5, 26.7% DM, 0% cirrhosis) with CLD (biopsy proven NAFLD or CH-C with viremia) participated in the study. Fasting blood samples were obtained and were assessed for levels of cytokines (IL-6, IL-8, and TNF-α), serotonin, C-peptide insulin, liver enzymes (AST, ALT), glucose, and lipids (triglycerides, total cholesterol, HDL, LDL, and the non-HDL fraction). Cytokines, serotonin, and C-peptide insulin were measured by ELISA following the manufacturer's protocols. The remaining parameters were measured by the Cholestech LDX system. Selfreports included standardized and valid measures of depression (short form of CES-D), vitality/energy (vitality subscale of the SF36) and level of activity (Human Activity Profile). Patients were then divided into tertiles by MET value. The middle third was omitted from further analysis; the remaining top third (those with MET >8.8, representing strenuous activity) and bottom third (those with MET 7 and a transformed vitality index score