Results of screening in Lublin Province, Poland, for colorectal cancer and neoplastic polyps - the role of environmental factors.

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.

Quality of life of patients with irritable bowel syndrome before and after education.

OBJECTIVES: 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). 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.

The genetic predisposition and its impact on the diabetes mellitus development in patients with alcoholic chronic pancreatitis.

The most common cause of chronic pancreatitis (CP) is alcohol abuse. The aim of the present study was to identify patients with genetic predisposition to CP abusing alcohol. The question posed was whether CP manifests at a younger age and diabetes mellitus develops earlier in individuals with genetic predisposition. The study encompassed 79 patients with alcoholic chronic pancreatitis (ACP) and control group (100 persons). The following mutations were determined: R122H and N29I of PRSS1 and N34S of SPINK1 as well as E366K and E288V of SERPINA 1. No R122H and N291 mutations were observed in the group of ACP patients and in controls. Moreover, there was no E288V mutation. In 79 ACP patients, six SPINK 1 (N34S/wt) mutations were observed. In the control group, one heterozygous SPINK 1N34S gene mutation was found (P = 0.0238). Two PiZ mutations were identified in patients with ACP and one analogical mutation in controls. Amongst patients with ACP as well as SPINK1 and PiZ mutations, the onset of disease was observed earlier and developed earlier. The prevalence of SPINK1 mutation is higher in patients with ACP than in healthy populations. This mutation together with the effects of alcohol accelerates the development of ACP and of diabetes mellitus.

Role of MMP-2 and MMP-9 and their natural inhibitors in liver fibrosis, chronic pancreatitis and non-specific inflammatory bowel diseases.

BACKGROUND: There is a growing evidence that matrix metalloproteinase (MMP)-2 and MMP-9 (gelatinases) play an important role in the pathogenesis of numerous disorders, especially with inflammatory etiology and extracellular matrix (ECM) remodeling. Despite the fact that gelatinases involve in liver cirrhosis is provided in the literature, their role in the pathogenesis of chronic pancreatitis and non-specific inflammatory bowel diseases is still under investigation. DATA SOURCES: We carried out a PubMed search of English-language articles relevant to the involvement of gelatinases in the pathogenesis of liver fibrosis, pancreatitis, and non-specific inflammatory bowel diseases. RESULTS: The decreased activity of gelatinases, especially MMP-2, is related to the development of liver fibrosis, probably due to the decrease of capability for ECM remodeling. Similar situation can be found in chronic pancreatitis; however, reports on this matter are rare. The presence of non-specific inflammatory bowel diseases results in MMP-9 activity elevation. CONCLUSION: The fluctuation of gelatinases activity during liver fibrosis, chronic pancreatitis and non-specific inflammatory bowel diseases is observed, but the exact role of these enzymes demands further studies.

Neurofibroma of the stomach without Recklinghausen's disease: a case report.

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.

Pancreatic and gastric heterotopy in the gastrointestinal tract.

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-related biomarkers in patients with alcoholic liver disease: their association with liver disease complications and outcome.

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.

Hepatomegaly, weight loss and general malaise - the first manifestations of primary systemic amyloidosis.

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.

MicroRNAs-role in lung cancer.

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.

Association of serum adiponectin, leptin, and resistin concentrations with the severity of liver dysfunction and the disease complications in alcoholic liver disease.

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.

Alkaline phosphatase: the next independent predictor of the poor 90-day outcome in alcoholic hepatitis.

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.

[Serum iron parameters in chronic liver diseses]. / Parametry gospodarki zelazem w przewleklych chorobach watroby.

UNLABELLED: Iron is an essential micronutrient of almost all organisms, which is involved in many metabolic processes. Disorders of serum iron balance that relate mainly to its deficiency are frequently observed in patients with liver diseases. The aim of the study was the evaluation of serum iron parameters in patients with different chronic liver diseases and analysis of the relationships between serum level of iron, ferritin and transferrin in women and men in groups examined. MATERIAL AND METHODS: The study includes 424 patients: 151 with alcoholic liver cirrhosis (ALC), 53 with nonalcoholic fatty liver disease (NAFLD), 54 with autoimmune hepatitis (AIH), 19 patients with hepatocellulare cancer (HOC), 34 with primary biliaris cirrhosis (PBC), 39 with chronic HCV hepatitis, 48 with chronic HBV hepatitis, 15 with primary sclerosans cholangitis (PSC) and 11 patients with hemochromatosis. Forty two healthy volunteers were the control group. RESULTS: The highest mean serum level of iron was observed in patients with hemochromatosis and was 278.56 +/- 25.04 mg/dl. The mean level of iron was statistically significant different in patients with HCC in comparison to the patients with ALC (p = 0.0000), with AIH (p = 0.0108) and NAFLD (p = 0.00768). The mean level of ferritin was statistically significantly higher among patients with hemochromatosis (p = 0.0000), with ALC (p = 0.0037) and NAFLD (p = 0.0442) than in the controls. Patients with AIH, HCC, HCV infection, PSC and hemochromatosis showed higher serum level of transferin than the controls (p = 0.0000). The mean level of iron and ferritin was lowerin women than in men in the patients with ALC (p = 0.0088, p = 0.0018 respectively). The mean level of ferritin was significantly lower in men than in women among patients with NAFLD. (p = 0.0065). There were no statistically significant differences in the mean level of examined parameters between the sexes. CONCLUSION: Reduced serum level of iron is observed in chronic liver diseases. Elevated ferritin level is typical for patients with ALC and NAFLD. Differences in the level of iron, ferritin and transferin between men and women concemrn the patients with ALC while among patients with NAFLD only ferritin level differences are found.

The effects of the adenosine A3 receptor agonist IB-MECA on sodium taurocholate-induced experimental acute pancreatitis.

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 [corrected] 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.

The BARD score and the NAFLD fibrosis score in the assessment of advanced liver fibrosis in nonalcoholic fatty liver disease.

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.

[Evaluation of alpha-fetoprotein concentration in patients with chronic liver diseases]. / Ocena stezenia alfa-fetoproteiny u pacjentów z przewleklymi schorzeniami watroby.

UNLABELLED: 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. MATERIAL AND METHODS: 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. RESULTS: 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 (p < 0.001 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 (p > 0.05). CONCLUSIONS: 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 N34S mutation of the SPINK1 gene and alcoholic chronic pancreatitis.

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.

The decrease of serum MMP-2 activity corresponds to alcoholic cirrhosis stage.

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.

[Ascites as the first manifestation of ovarian cancer in the disseminated stage--case report]. / Wodobrzusze jako pierwszy objaw raka jajnika w stadium rozsianym--opis przypadku.

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.

Activated and inactivated PPARs-γ modulate experimentally induced colitis in rats.

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.

Melatonin or L-tryptophan accelerates healing of gastroduodenal ulcers in patients treated with omeprazole.

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.