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Diet and nutritional status affect intestinal inflammation in patients with inflammatory bowel disease (IBD). The aim of this study was to use a cluster analysis to assess structural similarity between different groups of parameters including short-chain fatty acid (SCFA) levels in stool as well as hematological and inflammatory parameters (such as serum C-reactive protein (CRP) and proinflammatory and anti-inflammatory cytokines). We also assessed similarity between IBD patients in terms of various biochemical features of disease activity and nutritional status. A total of 48 participants were enrolled, including 36 patients with IBD and 12 controls. We identified four main meaningful clusters of parameters. The first cluster included all SCFAs with strong mutual correlations. The second cluster contained red blood cell parameters and albumin levels. The third cluster included proinflammatory parameters such as tumor necrosis factor-α, CRP, platelets, and phosphoric, succinic, and lactic acids. The final cluster revealed an association between zonulin and interleukins IL-10, IL-17, and IL-22. Moreover, we observed an inverse correlation between IL-6 and body mass index. Our findings suggest a link between nutritional status, diet, and inflammatory parameters in patients with IBD, which contribute to a better adjustment of the nutritional treatment.

Inflammatory bowel disease (IBD) represents a group of chronic inflammatory disorders characterized by dysbiosis and altered short-chain fatty acid (SCFA) level. The association between individual SCFA levels and cytokine levels is unknown.We aimed to determine the fecal SCFA levels in patients with IBD in relation to disease severity and the serum levels of pro- and anti-inflammatory cytokines.The study included 61 patients with IBD (inactive, 22; active, 39) and 16 controls. Fecal levels of organic acids (acetic, lactic, propionic, butyric, isovaleric, isobutyric, and valeric), serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), IL-17, and IL-22, complete blood count and C-reactive protein (CRP) were measured.Patients with active IBD had reduced butyric, acetic, valeric, and isovaleric acid levels and elevated lactic acid levels in stool. Hemoglobin levels were positively correlated with the levels of acetic and butyric acids (R = 0.266 and R = 0.346, respectively; P0.05). In addition, CRP levels were inversely correlated with butyric acid levels (R = -0.573; P0.05). Higher serum TNF-α levels were observed in patients with active IBD compared with controls (6.64 pg/ml vs 2.05 pg/ml, P0.05). No relationship was noted between the SCFA profile and cytokine levels.The study showed that determination of SCFA levels can be used to evaluate the activity of IBD. The relationship between individual SCFA and cytokine levels seems to be complex and requires further studies.

Intestinal inflammation in inflammatory bowel disease (IBD) is closely linked to nutrition. This study aimed to evaluate associations between nutritional, inflammatory, and intestinal barrier parameters in patients with IBD. We assessed nutritional status, fecal short-chain fatty acid profile, serum cytokine levels, and mRNA expression of enzymes and tight junction proteins in intestinal biopsies obtained from 35 patients, including 11 patients with inactive IBD, 18 patients with active IBD, and six controls. Patients with active IBD were characterized by hypoalbuminemia, fluctuations in body weight, and restriction of fiber-containing foods. In addition, they had significantly reduced levels of isovaleric acid and tended to have lower levels of butyric, acetic, and propionic acids. Patients with active IBD had higher mRNA expression of peroxisome proliferator-activated receptor γ and inducible nitric oxide synthase, and lower mRNA expression of claudin-2 and zonula occludens-1, compared with patients with inactive IBD. Moreover, patients with a body mass index (BMI) of ≥25 kg/m2 had higher median tumor necrosis factor-α levels that those with a lower BMI. We comprehensively evaluated inflammatory parameters in relation to IBD activity and nutritional status. The discrepancies between proinflammatory and anti-inflammatory parameters depending on IBD activity may be related to nutritional factors, including diet and abnormal body weight.

Proton pump inhibitors (PPIs) are the first-choice drugs used to prevent and treat acid-related diseases. However, a lack of satisfactory response to the standard PPI dose (“PPI failure”) is often reported, especially in patients with gastroesophageal reflux disease. Poor compliance seems to be one of the main causes of PPI failure; hence, it is crucial to gain knowledge on how to properly administer PPIs. In this review, we aimed to evaluate the effect of food, beverages, and dosing regimen on pharmacokinetics and pharmacodynamics of PPIs and to frame recommendations for healthcare professionals to improve both patient’s counseling and compliance to treatment with PPIs. A total of 201 papers were identified following a literature search. After full-text evaluation, 64 studies were included in the review. Co-administration of PPIs with a meal may affect both their bioavailability and effectiveness; however, the influence of food depends on the type of drug and its formulation. Except for pantoprazole, PPIs can be administered in the morning or evening; however, morning intake generally provides better daytime control of gastric acidity. In most cases, the choice of the proper schedule of administration should be based on the patient’s symptoms and individual dosing preferences.

Introduction Micronutrient deficiency can occur in patients with inflammatory bowel disease (IBD) regardless of the disease activity and extent. Objectives We aimed to evaluate the serum concentrations of selected trace elements in adult patients with IBD in clinical remission, with involvement limited to the colon, and receiving immunosuppressive treatment. Patients and methods We enrolled 32 patients with IBD (mean [SD] age, 41.0 [15.2] years) and 30 healthy controls (mean [SD] age, 39.1 [11.8] years). Serum selenium (Se), iron (Fe), copper (Cu), and zinc (Zn) levels as well as complete blood count were measured in both groups. Results Patients with IBD had lower Zn concentrations than controls (mean [SD], 0.76 [0.13] mg/l vs 0.83 [0.13] mg/l, P = 0.047). No significant differences were observed for Se (mean [SD], 0.90 [0.24] μmol/l vs 0.93 [0.19] μmol/l) and Cu levels (mean [SD], 1.03 [0.27] mg/l vs 0.97 [0.22] mg/l). Compared with controls, patients with IBD had lower red blood cell count (mean [SD], 4.4 [0.6] 106/ml vs 4.7 [0.4] 106/ml, P = 0.03), hemoglobin (mean [SD], 12.7 [2.2] g/dl vs 14.3 [0.8] g/dl, P = 0.001), and Fe levels (mean [SD], 14.2 [9.4] μmol/l vs 23.4 [2.7] μmol/l, P=0.0001). Patients with IBD showed a positive correlation between Se and Fe (R = 0.499; P = 0.004) as well as Se and hemoglobin levels (R = 0.579; P = 0.001). Conclusions Patients with IBD, despite maintaining clinical remission, should undergo systematic laboratory test for anemia or micronutrient deficiencies.

Irritable bowel syndrome (IBS) is a chronic functional gastrointestinal disorder diagnosed on the basis of Rome IV criteria. Stress is an important contributor to the development of IBS symptoms, while personality, perceived self-efficacy, resilience, and coping strategies may be indirectly involved in the modulation of the body's response to various stressors. The aim of this study was to assess the effect of selected personality traits and stress with IBS symptoms. We enrolled 129 participants (59 men and 70 women) aged from 18 to 61 years. The study group included 94 patients with IBS, while the control group comprised 35 participants without a diagnosed psychosomatic disorder and chronic comorbidities. Participants were assessed using a self-designed questionnaire as well as the Coping Inventory for Stressful Situations, NEO-Five Factor Inventory, 25-item Resilience Coping Scale (Skala Pomiaru Prężności - SPP-25), and General Self-Efficacy Scale. We observed a significant effect of personality, perceived self-efficacy, resilience, and coping strategies in patients with IBS. Moreover, stress was shown to be associated with disease severity, while the type of a coping strategy was related to the frequency of symptoms. The groups differed in terms of personality traits such as resilience, self-efficacy, extraversion, and neuroticism. Our study confirms the significant effect of personality traits and coping strategies in patients with IBS.

Growing number of studies suggests link between circadian rhythms and inflammatory bowel diseases (IBD) manifestation. We hypothesize that: 1) IBD are associated with increased eveningness and sleep disturbances; 2) eveningness and sleep disturbances are related to more severe IBD symptoms. In total, 129 participants were enrolled to this study, divided into three groups: 34 Crohn's disease (CD) patients, 38 ulcerative colitis (UC) patients and 57 healthy controls (HC) group. They all fulfilled a questionnaire, consisting of the Composite Scale of Morningness (CSM), Seasonal Pattern Assessment Questionnaire (SPAQ), Pittsburgh Sleep Quality Index, Inflammatory Bowel Disease Questionnaire (IBDQ) and Multidimensional Fatigue Inventory (MFI). Multiple regression models controlled for age and sex revealed that in CD group higher eveningness measured with CSM was associated with higher general fatigue, physical fatigue, mental fatigue and reduced motivation measured by MFI. Lower CSM morning affect is associated with greater general fatigue, physical fatigue and more reduced activity. Greater seasonality scores are associated with increased physical fatigue and more reduced activity and motivation. Lower sleep quality measured with PSQI is associated with higher physical fatigue and more reduced activity. Correlational analysis revealed that higher seasonality and lower sleep quality are associated with increased systemic and bowel symptoms and decreased emotional and social functions measured with IBDQ. In UC group, eveningness is associated with greater general fatigue, physical fatigue and more reduced activity. Higher CSM morning affect is associated with decreased general fatigue, physical fatigue and less reduced activity. Higher CSM circadian preference scores are associated with decreased general and physical fatigue, and less reduced activity. Increased seasonality is associated with more physical fatigue. Lower sleep quality is associated with greater general and physical fatigue. To our best knowledge this is the first study evaluating associations between chronotype and sleep disturbances with IBD symptoms. We have found that chronotype preferences, whose role in IBD has been until now overlooked, may be one of the important factors contributing to fatigue in this clinical group.

Introduction: Proton pump inhibitors (PPIs) are widely prescribed for several gastrointestinal conditions, often as long-term therapy. The effects of long-term PPI use have not been fully elucidated. Objectives: We aimed to determine the association between long-term PPI use and complete blood count parameters, particularly red blood cell (RBC) count, white blood cell (WBC) count, and hemoglobin concentrations, as well as serum levels of selected micronutrients such as selenium (Se), iron (Fe), copper (Cu), and zinc (Zn). Patients and methods: We enrolled 37 patients on long-term PPI therapy (mean [SD] age, 57.1 [15.4] years) and 30 healthy controls (mean [SD] age, 39.3 [11.8] years). In each group, complete blood count, and serum Fe levels were performed, and serum Cu, Zn, and Se levels were measured using atomic absorption spectrometry. Results: Red blood cell and WBC counts were lower in the PPI group compared with controls (mean [SD], 4.24 [0.55]×106/μl vs 4.7 [0.4]×106/μl; P

Oxidative stress with an excessive free radical production and a reduction in the activity of protective antioxidants is considered as one of the mechanisms responsible for gluten toxicity. However, its role in celiac disease (CD) is unclear.Evaluation of plasma nonenzymatic antioxidant capacity in patients with CD (both untreated patients and those receiving gluten-free diet [GFD]) by measuring the ferric reducing ability of plasma (FRAP) as well as assessing selected plasma antioxidants.The study included 169 adult patients: 48 patients with untreated active CD, 72 patients with CD on a GFD, and 49 healthy controls. In each group, we measured the serum levels of selected antioxidants (uric acid, bilirubin, albumin, and vitamin E) and used the FRAP assay to assess the total antioxidant capacity (TAC) of plasma. In each patient, serological and histopathological activity of CD was also evaluated.There were no significant differences in the TAC of plasma measured with the FRAP assay between the study groups. Patients with CD had higher uric acid levels compared with controls (p0.001), while bilirubin levels were lower in patients with active disease than in controls (p0.05). Serum vitamin E levels were lower in all patients with CD compared with controls (p0.01).The FRAP assay is not the method of choice for assessing the TAC of plasma in patients with CD. Owing to high serum uric acid levels, the FRAP assay results in these patients may be overestimated despite the reduced levels of other plasma antioxidants.

The aim of the study was to analyze the effect of celiac disease(CED) on the upper-gut motility and release of enteral hormones (ghrelin and pancreatic peptide (PP)).the study included 25 patients diagnosed with CED and 30 healthy controls. Gastric myoelectric activities (EGG) in a fasted and fed state were recorded. The plasma concentrations of ghrelin and PP were determined. R e s u l t s: CED patients presented in a fasted state a decreased percentage of normogastria 54.8 ± 24.5 vs. 86 ± 12.3%, p = 0.02 and slow wave coupling (SWC) 52.7 ± 13.4 vs. 77.4 ± 11.9%; p = 0.00001 with increased dominant power (DP) 11.6 ± 1.5 vs. 11.1 ± 1.1. Contrary to the controls, they did not show an improvement in the percentage of normogastria, DP and SWC when examined in a fed state (p 〈0.05). Furthermore, CED patients presented with significantly lower fasting plasma concentrations of ghrelin 156.8 ± 86.7 vs. 260.2 ± 87.6 pg/ml, p = 0.0002 and significantly higher fasting PP levels than did the controls 265.2 ± 306.3 vs. 54.1 ± 54.6 pg/ml, p = 0.0005. C o n c l u s i o n: CED affects gastric myoelectric activity (decreasing normogastria and coupling) and causes changes in fasting concentrations of enteral hormones (decrease in ghrelin and an increase in PP). Gastric myoelectric response to food is abolished in CED patients, probably due to the neurohormonal changes induced by primary inflammation associated with this disease.

INTRODUCTION Celiac disease (CD) is an immune-mediated enteropathy related to permanent gluten intolerance, characterized by gastrointestinal symptoms as well as nongastrointestinal symptoms, including neurologic ones. The presence of neuron-specific enolase (NSE), interleukin 10 (IL-10), and antiganglioside M1 (anti-GM1) antibodies has been demonstrated for neurologic conditions as well as immune disorders with neurologic manifestations. OBJECTIVES The aim of the study was to determine the concentrations of IL-10, NSE, and anti-GM1 antibodies in the course of CD and their correlation with changes in electrogastrography (EGG) and with heart rate variability (HRV). PATIENTS AND METHODS The study included 68 participants: 34 patients with CD and 34 healthy individuals. We assessed the concentrations of IL-10 and NSE as well as the presence of anti-GM1 antibodies in serum. We investigated correlations between the concentrations of IL-10, NSE, and anti-GM1 antibodies and the results of EGG and HRV. RESULTS Patients with CD had a higher level of anti-GM1 antibodies than controls (1.38 ng/ml [0.98-2.03 ng/ml] vs 0.81 ng/ml [0.35-1.15 ng/ml]). Median IL-10 concentrations in patients with CD differed significantly from those in controls (7 pg/ml [4.33-11.48 pg/ml] vs 4.27 pg/ml [2.44-7 pg/ml]; P = 0.010). In HRV analysis, a positive correlation between IL-10 concentrations and very low frequency spectrum was observed (r = 0.63; P = 0.003). There was no correlation between the concentrations of IL-10, NSE, or anti-GM1 antibodies and EGG parameters. CONCLUSIONS Chronic inflammation in the course of CD may lead to autonomic nervous system impairment and development of neurologic disorders. Therefore, anti-GM1 antibodies and IL-10 may be considered as markers of nervous system impairment in the course of CD.

INTRODUCTION Celiac disease (CD) is an immune-mediated enteropathy related to permanent gluten intolerance, characterized by gastrointestinal symptoms as well as nongastrointestinal symptoms, including neurologic ones. The presence of neuron-specific enolase (NSE), interleukin 10 (IL-10), and antiganglioside M1 (anti-GM1) antibodies has been demonstrated for neurologic conditions as well as immune disorders with neurologic manifestations. OBJECTIVES The aim of the study was to determine the concentrations of IL-10, NSE, and anti-GM1 antibodies in the course of CD and their correlation with changes in electrogastrography (EGG) and with heart rate variability (HRV). PATIENTS AND METHODS The study included 68 participants: 34 patients with CD and 34 healthy individuals. We assessed the concentrations of IL-10 and NSE as well as the presence of anti-GM1 antibodies in serum. We investigated correlations between the concentrations of IL-10, NSE, and anti-GM1 antibodies and the results of EGG and HRV. RESULTS Patients with CD had a higher level of anti-GM1 antibodies than controls (1.38 ng/ml [0.98-2.03 ng/ml] vs 0.81 ng/ml [0.35-1.15 ng/ml]). Median IL-10 concentrations in patients with CD differed significantly from those in controls (7 pg/ml [4.33-11.48 pg/ml] vs 4.27 pg/ml [2.44-7 pg/ml]; P = 0.010). In HRV analysis, a positive correlation between IL-10 concentrations and very low frequency spectrum was observed (r = 0.63; P = 0.003). There was no correlation between the concentrations of IL-10, NSE, or anti-GM1 antibodies and EGG parameters. CONCLUSIONS Chronic inflammation in the course of CD may lead to autonomic nervous system impairment and development of neurologic disorders. Therefore, anti-GM1 antibodies and IL-10 may be considered as markers of nervous system impairment in the course of CD.

Both ulcerative colitis (UC) and primary sclerosing cholangitis (PSC) are chronic and progressive diseases of uncertain etiology, that may affect one patient. Approximately 70% of PSC cases are also diagnosed with UC, whereas in the group of UC the prevalence of PSC is about 2-5%. The aim of the study was to compare clinical courses of PSC and UC in patients diagnosed with both diseases to those with the confirmed diagnosis of either PSC or UC. Three groups were distinguished and evaluated: patients with PSC and UC (n = 17) and two control groups: patients with PSC (n = 4) and with UC (n = 13). Clinical data, symptoms, laboratory tests, results of the magnetic resonance cholangiopancreatography and colonoscopy were analyzed to compare clinical courses of these diseases between the groups.there is no correlation between clinical course of simultaneous PSC and UC. However, it may differ depending on co-occurrence of the other disease.

Introduction: Coeliac disease is a chronic inflammatory disorder of the gastrointestinal tract, of autoimmune etiology, in genetically predisposed persons. The role of the gastric lesions and their influence on the clinical course of that disease have not been explained. Aim: To evaluate the frequency of morphological lesions in the gastric mucosa in adults with coeliac disease and their effect on the clinical picture of gluten enteropathy. Material and methods: Ninety patients, including 35 patients with coeliac disease and 55 with dyspeptic symptoms (control group) were examined. Clinical studies comprised history of disease, physical examination, blood tests and gastroscopies. Biopsies from the gastric and distal part of the duodenal mucosa were stained with haematoxylin-eosin, for estimation of the intensity of mucosal changes and a count of the intraepithelial lymphocytes (IEL). Immunohistochemical studies with anti-CD3 antibodies were performed for the identification of CD3+ lymphocytes. Results: An increased number of IEL was observed in coeliac patients treated as well as not treated with gluten, compared with the control group. Lymphocytic gastritis (LG) was observed in 8.6% of coeliac patients. Patients with coeliac disease and LG presented intense dyspeptic symptoms. Presence of CD3+ T lymphocytes was revealed in the gastric and duodenal mucosa with immunohistochemical staining. Conclusions: Morphological lesions in the gastric mucosa belong to gastroenteropathy in the course of coeliac disease and may induce dyspeptic symptoms. Taking biopsies from the distal part of the duodenum in patients with dyspeptic symptoms should be considered. Streszczenie Wstep: Celiakia jest przewleklą chorobą zapalną przewodu pokarmowego o podlozu autoimmunologicznym, wystepującą u osob predysponowanych genetycznie. Znaczenie zmian pa tologicznych w blonie śluzowej zolądka u chorych na celiakie i ich wplyw na przebieg kliniczny tej choroby nie zostaly dotąd w pelni poznane. Cel: Ocena czestości wystepowania zmian histopatologicznych w blonie śluzowej zolądka u doroslych osob z celiakią oraz wplywu tych zmian na obraz kliniczny choroby. Material i metody: Do badan wlączono 90 pacjentow, w tym 35 chorych na celiakie i 55 osob z objawami dyspeptycznymi (grupa kontrolna). Obejmowaly one wywiad chorobowy, badanie przedmiotowe, badania krwi oraz panendoskopie. Wy cinki z blony śluzowej zolądka i cześci pozaopuszkowej dwunastnicy barwiono hematoksyliną i eozyną. Oceniano nasilenie zmian zapalnych oraz liczbe limfocytow środnablonkowych (intraepithelial lymphocytes – IEL). Za pomocą badania immunohistochemicznego z zastosowaniem przeciwcial monoklonalnych anty-CD3+ identyfikowano limfocyty CD3+. Ocene bioptatow z dwunastnicy w kierunku celiakii wykonano zgodnie z klasyfikacją Marsha. Wyniki: U chorych na celiakie, zarowno nieleczonych, jak i leczonych dietą bezglutenową, obserwowano wzrost IEL, jednak ich liczba byla znamiennie wieksza u chorych niestosujących diety bezglutenowej. Limfocytarne zapalenie zolądka rozpoznano u 8,6% chorych na celiakie. Osoby te podawaly nasilone dolegliwości dyspeptyczne. W badaniu immunohistochemicznym wykazano obecnośc naciekow limfocytow T CD3+ zarowno w bioptatach blony śluzowej zolądka, jak i cześci pozaopuszkowej dwunastnicy.

Short-chain fatty acids play an important role in the physiology and metabolism of the colon. Disturbed balance of such compounds in human gut can significantly contribute to etiological factors of various gastrointestinal disorders and it may also increase the risk of developing cancer or cardiovascular diseases. The aim of the study was to select the optimal parameters for acetic, propionic and butyric acids extraction from stool samples. The experimental conditions were optimized with respect to the solvent sample shacking time, sample ultrasounds (Ultrasound-Assisted Extraction, UAE) exposure time and the number of extractions from the particulate stool samples. The screening of experimental parameters was conducted with fractional factorial design of experiments, namely 3(3-1). The optimal conditions for UAE were found, namely ultrasound digestion time of 40 min (at 35°C), shaking time of 4 min, and the three subsequent extractions.

Candida albicans frequently inhabits the gastrointestinal tract of humans leading to gastrointestinal candidiasis, especially following suppression of gastric acidity, but studies on the relation between this fungal infection and gastric pathology are limited due to lack of convenient animal models resembling Candida infection in humans. MATERIAL AND METHODS. We compared the effects of C. albicans and vehicle inoculation on gastric secretion and healing of gastric ulcers induced by acetic acid in rats treated with 1) ranitidine (30 mg kg(-1) day(-1) s.c.) and 2) aspirin (ASA) (60 mg kg(-1) day(-1) i.g.) with or without probiotic bacteria Lactobacillus acidophillus. At day 0 and at 4, 15 and 25 days after ulcer induction, the ulcer area, the gastric blood flow (GBF), the quantitative gastric cultures of Candida and the expression of mRNAs for pro-inflammatory cytokines IL-1beta and TNF-alpha and growth factors EGF and TGFalpha were assessed in the gastric mucosa.Gastric acid output was reduced by over 40% soon after Candida inoculation and this effect persisted during all time intervals tested. The area of ulcers in control rats significantly decreased at day 15 and the ulcers disappeared almost completely after 25 days of their induction. In contrast, the ulcers were present until day 25 in Candida-inoculated rats followed by a fall in GBF and a rise in plasma gastrin levels, these effects being significantly attenuated by the co-treatment with Lactobacillus. Candidiasis was accompanied by up-regulation of mRNA for IL-1beta, TNF-alpha, EGF and TGFalpha and a significant increment in plasma IL-1beta and TNF-alpha levels.1) Persistent colonization with Candida could be achieved in rats treated with antisecretory agents or non-steroidal anti-inflammatory drugs (NSAIDs) such as ASA; 2) candidiasis reduces gastric acid secretion, while delaying ulcer healing possibly due to the impairment in GBF in the ulcer area and enhanced expression and release of IL-1beta and TNFalpha and 3) probiotic therapy could be useful in the treatment against the deleterious action of fungal infection on the healing of pre-existing gastric ulcers.

An increasing resistance of Helicobacter pylori (H. pylori) to antimicrobial agents leads to the need of regional monitoring of the prevalence resistant strains (according to the Maastricht/Florence consensus report, 2012). The aim of the study was to assess the resistance to levofloxacin of H. pylori strains isolated from adult patients of Małopolska region in Poland. Bioptates taken from gastric mucosa during gastroscopy constituted the material for the study. Two hundred ten H. pylori strains were isolated from 811 patients. A majority of strains (171) came from patients before the treatment of H. pylori infections while the remaining 39 strains were isolated from patients after the failed therapy. Susceptibility of H. pylori to levofloxacin was determined by strips impregnated with antibiotic gradient (E-test, bioMerieux). The obtained minimum inhibitory concentration (MIC) values ranged from 0.002 mg/L to 32 mg/L. The percentage of strains resistant to levofloxacin amounted to 8.10% (17/210). Among the group of strains isolated from patients before the treatment, 5.85% (10/171) of H. pylori strains were resistant to levofloxacin. In the group of strains isolated from patients after the treatment 17.95% (7/39) of strains were resistant. The difference in the frequency of H. pylori strains resistant to levofloxacin in patients before and after the treatment of the infection due to H. pylori was statistically significant (p = 0.0297). The low percentage of H. pylori strains resistant to levofloxacin justify that the introduction of a triple therapy with levofloxacin is a good alternative in the treatment of H. pylori infections, especially in regions with high prevalence of H. pylori strains resistant to clarithromycin (20%).

Endoscopic examination of the upper gastrointestinal tract (upper GI) with macroscopic and histopathological evaluation provides essential tool to differentiate the organic and functional causes of dyspepsia. The distinction, however, is often smooth and not fully defined. The aim of this study was to assess the frequency and type of the macroscopic and histopathological changes in the upper GI endoscopy in patients with symptoms of dyspepsia.A retrospective study was performed on 212 patients with dyspepsia, at the age of 18-84 years, including 60 patients to 45 years of age (group I) and 152 patients older than 45 (group II) who underwent gastroscopy. The severity of esophagitis was classified according to the Los Angeles Classification and gastritis according the updated Sydney system. Biopsy specimens were taken from the gastric and duodenum for histopathological examination. The presence of H. pylori infection has been established on the basis of histopathological examination and positive rapid urease test.Reflux esophagitis was found in 18 patients (8.5%), slightly more common in people over 45 years of age (group I--5%, group II--9.2%). The mild forms of esophagitis occurred most frequently. A more advanced form of inflammation and Barrett's esophagus was found only in patients over 45 years of age. Normal gastric and duodenal mucosa was revealed in 30% of patients in group I and 9.2% in group II. The most common endoscopic lesion was gastritis, mostly erythematous-exudative and less often atrophic. The presence of H. pylori infection was varied in the different types of inflammation. H. pylori infection occurred most frequently in the case of erosive and follicular gastropathy. The most common location of H. pylori infec- frequent in older patients. Peptic ulcer was found in 4.7% of patients (group I--5%, group II--4.6%). In one patient (61 years old) stomach cancer was diagnosed and in one patient (45 years old) Crohn's disease of the upper GI was diagnosed. The majority of patients had normal duodenal mucosa. In 3.3% of patients (group I--8.3%, group II--1.3%), who had not previously diagnosed celiac disease, histopathological changes typical of celiac disease has been shown. In all patients, in whom biopsy specimens were taken from normal duodenal mucosa (14% of patients), histopathological examination revealed the presence of non-specific inflammation, regardless of the coexistence of H. pylori infection.Regardless of the severity of lesions of the upper GI endoscopy in patients with dyspepsia, it is advisable to take biopsy from the gastric and duodenal mucosa, which allows for an individualized management of these patients. Celiac disease should be considered in the diagnosis of the causes of dyspepsia. Further studies of microscopic duodenitis in patients with dyspepsia are needed.

We present the case of 51 year old man with 10 year history of ulcerative colitis. Results of laboratory test revealed increased serum levels of iron, ferritin as well as moderate hiperbilirubinemia. Transferrin saturation index was high, 98,7% (N50%). Long lasting remission of inflammatory bowel disease, including lack of bleeding from gastrointestinal tract disclosed hereditary hemochromatosis presence in that patient.

Background This study investigated a possible role of Escherichia coli in propagation and perpetuation of the chronic inflammation in ulcerative colitis (UC). The lesions of UC are located superficially on the rectal and/or colonic mucosa. It is suggested that the commensal bacteria of the digestive tract may play a role in the pathogenesis of UC. Several studies have demonstrated proliferation of E. coli in the gut of UC patients. An increase in the number of E. coli in the inflamed tissue is most probably related to the abundance of iron ions produced by the bacteria. Methods Colon mucosal biopsies were collected from 30 patients with acute-phase UC, both from tissues with inflammatory changes (n = 30) and unchanged tissue with no inflammatory changes (n = 30) from the same patient. Biopsies were also taken from 16 patients with irritable bowel syndrome diarrhea who comprised the control group. Quantitative and qualitative analysis of the biopsy specimens was performed using culture methods and real-time polymerase chain reaction (PCR). Genotyping of the E. coli isolates was done using pulsed-field gel electrophoresis. Multiplex PCR was used to compare the E. coli strains for the presence of genes responsible for synthesis of iron acquisition proteins: iroN, iutA, iha, ireA, chuA, and hlyA. Results We demonstrated that there was a significant increase in the number of E. coli at the sites of inflammation in patients with UC compared to the control group (P = 0.031). Comparative analysis of the restriction patterns of E. coli isolated from inflammatory and unchanged tissues showed that the local inflammatory changes did not promote specific E. coli strains. There was a significant difference in the frequency of the iroN gene in E. coli isolated from patients with UC as compared to the control group. Conclusions The increase in the numbers of E. coli in the inflammatory tissues is related to the presence of chuA and iutA genes, which facilitate iron acquisition during chronic intestinal inflammatory processes.

About 35% of patients with Crohn's disease develop fistulae. Treatment of those changes is a complicated clinical problem. Anti-TNF alpha antibodies are currently the most effective therapy of fistulizing Crohn's disease. Aim of the study is to evaluate results of anti-TNF alpha treatment in patients with fistulizing Crohn's disease.We evaluated results of anti-TNF alpha treatment (both with adalimumab n=10 and infliximab n=19) in 29 patients with fistulizing Crohn's disease treated in years 2008 - 2011 in Gastroenterology and Hepatology Clinic of University Hospital in Krakow.Closure of over 50% of fistulas was achieved by 78,94% patients after induction therapy with infliximab and 50% with adalimumab. Long term remission, evaluated after 52 weeks of treatment, was observed in 46,15% patients treated with infliximab. Best results were observed in perianal fistulas treatment - remission was achieved in 88.2% of patients. Effectiveness of enterocutaneus fistalas therapy was lower, and their healing was observed in 28.57% of patients. We observed no correlation between duration of Crohn's disease, duration of fistulas history or previously used treatment and results of anti-TNF alpha treatment.Anti-TNF alpha treatment has high effectiveness both short and long term in fistulizing Crohn's disease. Tolerance of treatment is very good. We lack clinical data about treatment other fistulas than perianal, but we suspect that effectiveness of anti-TNF alpha in this cases is lower. It is indicated to treat patients with fistulizing Crohn's disease with anti-TNF alpha, because it gives them chance for long remission and improvement of quality of life.

Inflammatory bowel diseases (IBD) constitute a group of incurable, inflammatory GI diseases of unknown etiology and the chronic course, with periods of spontaneous disease remissions and aggravations (Muszynski, 2001). This group of diseases includes Crohn`s disease and ulcerative colitis. They are characterized by inflammatory reactions and changes in the structure of intestinal mucosa (Rzeszutko, 2006). IBD etiopathogenesis is not clearly defined. The most essential etiological issues include environmental factors, genetic conditioning, abnormalities of intestinal immunological mechanisms and the bacterial flora (Konturek, 2001). The inflammation which develops in the intestine is mostly due to improper, low-fiber diet which is based on highly processed products and on the poor physical activity. Familial diseases confirmed in 10% of cases speak for the genetic source. Immunological mechanisms which develop in response to food and bacterial antigens are extremely significant (Muszynski, 2001; Polinska et al., 2009). A markedly increased interest has been observed in the intestinal microflora which is believed to be essential in inducing IBD development and in relapses of its clinical symptoms. Bacteria which are normally resident in the GI tract determine the proper work of intestines and protect from excessive proliferation of undesired microorganisms. The contribution of the intestinal flora to the development of the biofilm, which prevents the colonization of pathogens including fungi of the genus Candida in the GI tract, is extremely significant. The area of interest in fungi which are a part of microflora and constitute a potential source of systemic dissemination by colonizing the GI tract has greatly increased lately (Berhardt & Knoke, 1997). In the normal environment fungi are in balance with the bacterial flora and as commensals do not induce the inflammation. The main cause of its development, however, is the immune system impairment and a decrease of immunity. It affects patients with neoplasms and transplant recipients (Pfaller & Diekema, 2007; Warnock & Campbell, 1996). Other diseases causing inflammations are: diabetes and other endocrinopathies, infections due to HIV virus and also surgical procedures, damaged tissues and inflammations of the

Celiac disease, called gluten enteropathy, is a chronic disorder, characterized by the immunologic answer to the gluten contained in the wheat, barley and oat in genetically predisposed patients. The frequency of celiac disease is estimated on 0.5-1% in the adult population and proportion of diagnosed to non-diagnosed cases is 1 to 7. The clinical picture of that disease in adults presents wide spectrum of gastrointestinal and extraintestinal symptoms. There is 5-10 fold increased risk of its coexistence with other autoimmune diseases, such as diabetes mellitus type I, juvenile arthritis or autoimmune thyroiditis. Abnormal liver function or vascular thrombosis are also observed. Acute abdominal pain as the leading symptom is present in 16.3% of celiac cases. Moreover the increased frequency of the microscopic colitis and gastritis may influence on the persistence of clinical symptoms.

Coeliac disease (gluten enteropathy) is a chronic inflammatory disease of the gastrointestinal (GI) tract of autoimmune etiology in genetically predisposed individuals. It is the most frequent enteropathy with frequency of 1/100 and 1/300 in the adult population in America and Europe respectively. Typical form of celiac disease including abdominal pain, weight loss, nausea is quite rare in adults. In some coeliac patients, symptoms persist in spite of strict gluten free diet. One of the reasons of this is interference of the autoimmune diseases. Results of our studies revealed in the group of 110 patients with diagnosed gluten enteropathy, coexistence of autoimmune disease, such as diabetes mellitus type 1 in 7.2% cases, hyperthyreosis on 1.8% of cases, vitiligo in 0.9% of cases, primary biliary cirrhosis in 2% of cases and rheumatoidal arthritis in 0,9 of cases. In the group of 80 ulcerative colitis patients, coexistence of celiac disease basing on serological histopatological investigation was found in 4 patients (5%).Coexistence of coeliac disease with other autoimmune diseases is quite frequent. Gluten enteropathy symptoms may be interpreted as originating from other autoimmune disease. It can delay the diagnosis of celiac disease and introduction of gluten free diet, which improves the quality of life and protects from dangerous GI complications.

Celiac disease (gluten enteropathy) is chronic immunomediated disorder of gastrointestinal tract in genetically predisposed patients. We present the case of 46 years old man, with already diagnosed several autoimmune disorders, such as: diabetes mellitus LADA type, Graves-Basedow disease and vitiligo. Despite treatment of the above diseases, diarrhea and persistent abdominal pain was observed. Diagnosis of gluten enteropathy based on serology and histological evaluation of biopsies from distal part of duodenum enabled us to introduce gluten free diet, which contributed to attenuation of symptoms and better control of glucose serum levels. We think, that celiac disease should be taken into the consideration in differential diagnosis of chronic diarrhea and persistent abdominal pain, especially in patients with coexisting autoimmune diseases.

Publisher Summary This chapter focuses on the colonization of gastrointestinal (GI) tract by probiotics and fungal. The human GI tract constitutes the second body surface area (250–450 m2). It includes rich microflora of more than 500 species, which makes around 10 microorganisms living in the whole GI tract from the oral cavity area to the colon. These proximal and distal parts of the GI tract are the most densely colonized areas. GI microflora establishes during human life through time-dependent phases. Fungi are a small part of the intestinal microbiota. Many factors such as stress of modern life, reduced physical activity, processed foods, antibiotic therapies, as well as prolonged adaptation of human genes to dynamic changes in the lifestyle seem to derange the host–microflora interplay and contribute to the development of inflammatory and infectious diseases. This process could be attenuated by probiotics. The mechanism that enables probiotics to maintain the balance within the intestine includes production of bacteriocin-like substances, inhibition of pathogens and toxin adherence to the intestinal epithelium, and reduction of the fungal overgrowth.

The aim of the study was the evaluation ofchromogenic agars as a screening media in the routine microbiological diagnostics. 627 clinical samples were cultured on the chromogenic media: chromID S. aureus, chromID MRSA, chromID CPS3 and chromID ESBL from bioMerieux. The results of presumptive identification and detection of selected resistance mechanisms by chromogenic media were compared with results obtained with the conventional methods. Our studies revealed the highest sensitivities of chromID MRSA and chromID CPS3 (90%). The sensivities for chromID ESBL and chromID S. aureus were70%. All media were also highly specific (97%). This specificity for chromID S.aureus and chromID CPS3 was 100%. We conclude, that all tested media showed good performance in presumptive identification and detection of resistance mechanisms.

Celiac disease is the status of the autoimmune answer provoked by gluten ingestion in genetically predisposed people. Recently gluten entheropathy was considered as a rare clinical problem in adults. Celiac disease is an autoimmune disorder that can coexist with other diseases, such as diabetes mellitus type 1 (DMID), thyroid gland diseases. The aim of our study was evaluation of the frequency of coexistence of celiac disease with DMID using the level of anti tissue transglutaminase antibodies (IgA- tTG) and mucosal biopsy from the distal part of the duodenum. An attempt was made to estimate the influence of celiac disease on the intensity of clinical symptoms and metabolic balance in patients with DMID. Our study included 109 patients with DMID, aged 18-52 years. The frequency of the incidence of celiac disease in DMID patients was 9.71%. Gastric symptoms, such as diarrhea, abdominal pain were more frequent in patients with villous atrophy in the intestine. Hyperglycemia and problems with glucose balance in the serum were observed. Introduction of the gluten free diet led to improvement quality of life, less frequent hypoglycemic episodes and disappearance of diarrhea, increase of serum iron and decrease of IgA-tTG level in the serum. It is necessary to measure the level of IgA- tTG in patients with DMID. Diagnosis of celiac disease in patients with DMID and its treatment with gluten free diet causes the clinical, histological and biochemical improvement in these patients.

Celiac disease is increasingly recognized autoimmune enteropathy caused by a permanent gluten intolerance. Gluten is the main storage protein of wheat, in genetically predisposed individuals. Celiac disease risk in first degree relatives is about 10%. Diarrhea and changes of bowel movement, observed as well in celiac disease as in IBS, may lead to misdiagnosis of IBS basing on the Rome criteria or may be associated with coexistence of both diseases. The aim of the study was to assess the celiac disease prevalence in patients with irritable bowel syndrome. The study group comprised 200 patients (120 women and 80 men) aged 18-78 years (mean: 46.7 years) with diarrhoeal form of irritable bowel syndrome (IBS), according to the Rome criteria II. At the beginning and after a three month period anti tissue transglutaminase antibodies (IgA tTG) were estimated. Gastroscopy with biopsy where performed in those with IgA tTG titre above 1/200. 40 patients were immunologically positive and 14 of them have histopathologically proven celiac disease. In the group of patients with detected celiac disease, gluten free diet was applied besides the treatment with trimebutin or mebewerin, recommended for IBS. After 6 months the decrease of IgA tTG titre in the serum was observed. In 5 of these patients IgA tTG level was negative. It was associated with the significant decrease of clinical symptoms, such as diarrhea and flatulence. The remaining symptoms, such as abdominal pain, feeling of incomplete defecation demanded continuation of IBS treatment. With regard to often atypical celiac disease symptoms--adult active searching should be performed to differentiate from irritable bowel syndrome.

Functional dyspepsia belongs to functional disorders of the gastrointestinal tract. Its prevalence is estimated up to 25% of adult population of Western countries. On the contrary to irritable bowel syndrome, functional dyspepsia is slightly more frequent in men. The recent classification of functional dyspepsia includes its two subcategories: postprandial distress syndrome (DS, B1a) and epigastric pain syndrome (EPS, B1b). In the management of functional dyspepsia three strategies are taken into the consideration: 1. early gastroscopy performed in people over 45 years of age and independent of age in case of alarm symptoms. 2. Therapy based on noninvasive H. pylori testing: in young adults with dyspeptic symptoms, without alarm symptoms and not treated with nonsteroid antiphlogistic medications. 3. Empiric treatment: considered as an initial therapy in patients not diagnosed with dyspepsia, without alarm symptoms and in dyspeptic patients despite H. pylori eradication. In the treatment of functional dyspepsia the following treatments are applied: dietary treatment, farmacotherapy with antisecretory drugs, prokinetics, H. pylori eradication, antidepressants and psychotherapy. Directions of the further investigation in functional dyspepsia include: improvement of endoscopic methods, and searching for new groups of medications according to the new Rome III classification of functional dyspepsia, based on its pathophysiology.

In the present study on animal model of ulcerative colitis the influence of fungal colonization on the severity of inflammatory lesions in the colon and the course of their healing was evaluated. The results of our studies revealed, that significant fungal colonization (over 10(4) CFU/ml) delayed ulcer healing in the colon. It corresponded with the decrease of colonic blood flow (CBF) in the region of lesions and increase of interleukin (IL)-1beta, tumor necrosis factor(TNF)-alpha level in the serum. Introduction of antifungal therapy (fluconazole) or probiotic in rats inoculated with Candida accelerated the process of ulcer healing in the colon, expressed through the reduction of macro- and microscopic lesions in the colon and decrease of MPO, IL-beta TNF-alpha serum level.

Present-day methods of successful treatment of inflammatory bowel diseases (IBD) result from a better understanding of their pathophysiology due to advances in preclinical studies in this area of knowledge. Until recently microbiological studies have been focused on the bacterial aspects in pathogenesis of GI disorders, however in the last years an interest in the presence of fungi in the gastrointestinal tract has also increased. In this study using an animal model of ulcerative colitis, the impact of fungal colonization of the colon on the intensity of inflammatory changes in the colonic mucosa and the course of their healing was carried out. The macroscopic and microscopic criteria relating to the changes of weight of examined fragments of the colon were evaluated while assessing differences between groups tested. The intensity of intestinal inflammatory changes was determined by assessment of such parameters, as colonic blood flow (CBF), the level of MPO as a marker of colonic neutrophil infiltration intensity and the plasma levels of IL-1beta; and TNF-alpha concentrations. Results at the 3rd day after TNBS rectal administration revealed an increase of weight of isolated segments of inflammed colon, a decrease of CBF and the 4-5 fold increase of plasma MPO activity. Candida colonization of colon mucosa of rats delayed healing of colonic ulcers, induced by TNBS and this was associated with the increased expression of plasma IL-1beta and TNF-alpha levels. Administration of antifungal (fluconazole) or probiotic (Lacidofil) treatment to C. albicans infected rats exerted favorable effect on healing of inflammatory changes in the colon because the area of ulcerations in groups of rats treated with fluconazole or Lacidofil was significantly smaller in comparison with those inoculated with Candida solution only. Administration of fluconazole or Lacidofil significantly decreased the weight of colon segments, the MPO activity and the plasma IL-1beta and TNF-alpha levels, as compared with respective values in the group receiving Candida only. The results of our studies indicate the deteriorating influence of Candida on the healing process of inflamed colon in the animal model of ulcerative colitis. Concomitant therapy with probiotic or antifungal treatment improved healing of colonic lesions, decreased the weight of inflamed colonic tissue and also attenuated the MPO activity and plasma proinflammatory cytokines IL-1beta and TNF-alpha levels.

The influence of microbiological factor is taken into consideration in the pathogenesis of ulcerative colitis (UC). The aim of studies was to: 1.evaluate the presence of significant fungal colonization, over 10(5) CFU/ml in patients with UC and the control group (irritable colon syndrome, IBS); 2. estimate the influence of antifungal treatment in the activity of UC.We evaluated 72 patients aged from 18-72 years, 60 patients with UC, 12 with IBS. Clinical investigation: initially and after 4 weeks interview and colonoscopy with colon biopsies for histology and mycology were taken. Activity of UC was evaluated according to: clinical, endoscopic and histological IACH criteria. 13 patients with significant fungal colonization were given antifungal treatment. Biopsies for histology were stained with hematoxylin-epsin (H-E). Qualitative and quantitative mycolo-gical evaluation was performed according to Muller method.1. Significant fungal colonization was more frequent in patients with UC history over 5 years, in comparison with shorter disease history and IBS, in 33.3%, 13.8% and 1.3% respectively. 2. Candida albicans was most often isolated in 91.7% of cases. 3. Initial analysis of the activity index of UC in patients with significant and non-significant fungal colonization did not revealed differences between these groups, 13.84 and 14.0 respectively. 3. After 4 weeks stronger decrease of the UC activity index was observed in patients with significant fungal colonization treated with antifungal treatment, in comparison with patients not given antifungal therapy: 8.0 and 10.41 respectively, p0.01. Differences were significant according to clinical 2.23 (C) -3.33 (D), p0.05 and endoscopic cryteria: 3.46 (C) -4.84 (D), p0.01.1. Significant fungal colonization of colon may influence the activation of UC. 2. Longer disease history may be the risk factor of significant fungal colonization in colon. 3. Antifungal treatment in patients with significant colonization caused clinical improvement of UC.

To determine the effect of non-selective cyclooxygenase (COX) inhibitors, selective COX-2 inhibitors and nitric oxide (NO)-releasing aspirin in the healing of ulcerative colitis.Rats with 2,4,6 trinitrobenzenesulfon-ic acid (TNBS)-induced colitis received intragastric (ig) treatment with vehicle, aspirin (ASA) (a non-selective COX inhibitor), celecoxib (a selective COX-2 inhibitor) or NO-releasing ASA for a period of ten days. The area of colonic lesions, colonic blood flow (CBF), myeloperoxidase (MPO) activity and expression of proinflammatory markers COX-2, inducible form of nitric oxide synthase (iNOS), IL-1β and tumor necrosis factor (TNF)-α were assessed. The effects of glyceryl trinitrate (GTN), a NO donor, and 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-​tetramethyl-1H-imidazolyl-1-oxy-3-oxide, onopotassium salt (carboxy-PTIO), a NO scavenger, administered without and with ASA or NO-ASA, and the involvement of capsaicin-sensitive afferent nerves in the mechanism of healing the experimental colitis was also determined.Rats with colitis developed macroscopic and microscopic colonic lesions accompanied by a significant decrease in the CBF, a significant rise in colonic weight, MPO activity and plasma IL-1β and TNF-α levels. These effects were aggravated by ASA and 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC-560), but not celecoxib and counteracted by concurrent treatment with a synthetic prostaglandin E₂ (PGE₂) analog. Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1β and TNF-α mRNAs. Treatment with GTN, the NO donor, significantly inhibited the ASA-induced colonic lesions and increased CBF, while carboxy-PTIO or capsaicin-denervation counteracted the NO-ASA-induced improvement of colonic healing and the accompanying increase in the CBF. These effects were restored by co-treatment with calcitonin gene related peptide (CGRP) and NO-ASA in capsaicin-denervated animals.NO-releasing ASA, in contrast to ASA, COX-1 inhibitors, and SC-560, accelerated the healing of colitis via a mechanism involving NO mediated improvement of microcirculation and activation of sensory nerves releasing CGRP.