The incidence rate of surgical interventions in patients with Crohn's disease treated with anti-tumour necrosis factor biologics.

BACKGROUND: Anti-tumour necrosis factor alpha drugs (anti-TNF-α) effectively reduce the risk of surgery in Crohn's disease (CD). Unsatisfactory response to anti-TNF-α agents leads to the development of disease complications in a great percentage of patients. Simultaneously, possible predictive factors for ares during biological treatment remain uncertain. AIMS: To investigate the incidence rate of intestinal resection during biological treatment and search for predicting factors for ares demanding a surgical intervention. METHODS: A retrospective study of 68 patients qualified for anti-TNF-alpha therapy. The data consisting of demographic details, disease duration and laboratory results before the first drug administration and at the post induction period were collected. The association between these parameters and loss of response (LOR) demanding a surgical intervention was evaluated. RESULTS: LOR to the anti-TNF-alpha therapy was observed in 10/68 patients (14.7%). Mean disease duration at initiation of therapy was statistically longer in operated patients (8.8 ± 2.04 y vs. 4.93 ± 4.29 y; p < 0.02). That group revealed higher CRP values in post induction period compared to group with sustained response (48.24 ± 61.99 mg/l vs. 7.29 ± 13.43 mg/l; p < 0.05), contrary to hematocrit levels, which were lower in this group at each point of the study (30.58 ± 6.19% vs. 36.69 ± 16.0%; p = 0.04) (18.62 ± 18.19% vs. 40.27 ± 4.72%; p < 0.05) (4.01 ± 0.9 x106/µl; p = 0.009) (40.27 ± 4.72 g/dl vs. 18.62 ± 18.19 g/dl; p < 0.05). CDAI was significantly higher at post induction evaluation in the group with LOR (260.75 ± 98.1 vs. 118.12 ± 4.59; p < 0.05). CONCLUSION: CRP and CDAI, expressing in ammation severity, RBC, Hgb, Hct and the disease duration may serve as predictive factors for LOR to biological therapy.

Serum Cyclophilin A Correlates with Increased Tissue MMP-9 in Patients with Ulcerative Colitis, but Not with Crohn's Disease.

BACKGROUND: Cyclophilin A (CyPA) is an immunomodulatory protein, high expression of which correlates with poor outcome of patients with inflammatory diseases. However, its role in inflammatory bowel disease (IBD) has not been studied. AIM: This study analyzes the correlation between cyclophilin A, matrix metalloproteinase (MMP)-9, and tissue inhibitor of MMP (TIMP)/MMP-9 complexes in the inflamed and non-inflamed colon mucosa of UC and CD patients. METHODS: Serum and biopsy specimens from inflamed and non-inflamed colonic mucosa of 38 patients with IBD (19 with UC and 19 with CD) and 16 controls were included in our study. We measured serum and tissue level of CyPA, and tissue level of TNF-α, MMP-9, TIMP-1/MMP-9, and TIMP-2/MMP-9 using ELISA method. RESULTS: Our results indicated that serum, but not tissue CyPA is increased in UC, rather than in CD patients, compared to the control. The increase correlated with higher tissue concentration of MMP-9 and TNF-α, especially in the UC group. Moreover, we observed significantly higher level of TIMP-1/MMP-9 in UC and CD group, which overlapped with the change in MMP-9. There was no change in TIMP-2/MMP-9 in the analyzed groups. CONCLUSION: The current study suggests that serum CyPA may be an independent additional marker of IBD, especially of UC. Higher CyPA level may be followed by increased MMP-9 in those patients. However, further studies are necessary to verify the role of CyPA in IBD development.

G protein-coupled receptor 55 (GPR55) expresses differently in patients with Crohn's disease and ulcerative colitis.

AIM: To investigate the levels of G protein-coupled receptor 55 (GPR55) expression in colonic tissue of inflammatory bowel disease (IBD) patients and healthy controls, and its potential implication in IBD treatment. METHODS: Fifty patients were enrolled in our prospective study: n = 21 with Crohn's disease (CD) and n = 16 with ulcerative colitis (UC); 19 women and 18 men. Control consisted of 13 non-IBD patients. In each subject, two biopsies were taken from different colonic locations. In IBD patients, biopsies both from endoscopically inflamed and non-inflamed areas were drawn and the development of inflammation confirmed in histopathological examination. GPR55 mRNA and protein expression were measured using real-time PCR and Western blot, respectively. RESULTS: GPR55 expression at mRNA and protein level was detected in all samples tested. The level of GPR55 mRNA expression in non-inflamed colonic areas was comparable in all analyzed groups (p = .2438). However, in the inflamed tissues GPR55 mRNA expression was statistically significantly (p < .0001) higher (6.9 fold) in CD patients compared to UC. Moreover, CD patients manifested higher (12.5 fold) GPR55 mRNA expression in inflamed compared with non-inflamed colonic tissues (p < .0001). Although no significant differences were stated, GPR55 protein level tends to decrease in IBD as compared to control. CONCLUSIONS: Different patterns of GPR55 expression at mRNA level were observed in IBD patients. We speculate that GPR55 is crucial for the mucosal inflammatory processes in IBD, particularly in CD and its expression may affect disease severity, and response to treatment. The GPR55 receptors may become an attractive target for novel therapeutic strategies in IBD.

G Protein-Coupled Receptor 30 (GPR30) Expression Pattern in Inflammatory Bowel Disease Patients Suggests its Key Role in the Inflammatory Process. A Preliminary Study.

BACKGROUND AND AIMS: G protein-coupled receptor 30 (GPR30) is a recently de-orphanized estrogen receptor that mediates the effects of estrogens on different cells. It has been postulated that in inflammatory bowel diseases (IBD) activation of GPR30 blocks the pathways dependent on pro-inflammatory cytokines. The aim of our study was to investigate GPR30 expression in patients with IBD and its potential implication in future therapies. METHODS: Fifty-seven patients were enrolled in our study: 20 subjects with Crohn's disease (CD), 22 with ulcerative colitis (UC) and 15 controls. In each subject, biopsies were taken from various left-colonic locations. Gene and protein expression of GPR30 was quantified using real time RT-PCR or Western blot. RESULTS: GPR30 mRNA and protein expression were detected in all tested colonic tissues. No significant differences in GPR30 gene expression were observed. In non-inflamed areas, GPR30 protein was strongly increased in CD patients, but moderately in UC patients (p= 0.014 and p=0.143, respectively, vs. controls). In CD patients, a significantly lower GPR30 protein content in inflamed than in non-inflamed tissue was observed (p=0.039). The change was independent of patient gender. CONCLUSION: Our observations indicate that GPR30 may play a role in the development and progression of inflammatory lesions in IBD, thus affecting disease severity, and consequently IBD treatment. Therefore, GPR30 may become an attractive target for novel anti-IBD drugs, particularly in CD.

[Effect of treatment with diet on reducing levels of sex hormones in perimenopausal women with overweight and obesity]. / Wplyw leczenia dieta redukcyjna na stezenie hormonów plciowych u kobiet w okresie okolomenopauzalnym z nadwaga i otyloscia.

UNLABELLED: Nowadays, fight against obesity is a big challenge for the developed countries. Perimenopausal women are especially prone to becoming overweight and obese. This is due to changes in hormone levels and alterations in the sex hormones synthesis pathway. AIM: The aim of this study was to evaluate the levels of sex hormones in overweight and obese women during menopause following the three month period of reducing diet. MATERIALS AND METHODS: The study involved women aged 55±4,75 years. Group I - 33 overweight women (BMI 28,06±1,00 kg/m(2)). Group II - 32 obese women (BMI 34,22±3,79 kg/m(2)). Anthropometric measurements, body composition tested with Bodystat QuadScan 4000 analyzer and levels of sex hormones in the blood was determined before and after the three-months of reducing diet in both groups. Statistical data analysis was performed. RESULTS: After three-months of reducing diet it was noticed that levels of BMI, body fat, FSH, DHEA-S and androstenedione were decreased in a statistically significant manner. A significant increase in estradiol levels after reduction of visceral adipose tissue in both groups, overweight and obese women, was observed. However, only in the group of obese women, a decrease in BMI correlated with a significant increase in estradiol levels. CONCLUSIONS: Application of appropriate reducing diet in perimenopausal overweight and obese women has positive impact on visceral adipose tissue distribution and causes an increase in sex hormones levels. Perimenopausal overweight and obese women should pursue weight reduction to improve their chances of contracting cardiovascular diseases.

Circadian rhythm abnormalities - Association with the course of inflammatory bowel disease.

Crohn's disease (CD) and ulcerative colitis (UC) are the main representatives of inflammatory bowel diseases (IBD), a group of chronic, immune system-mediated inflammatory diseases of the gastrointestinal (GI) tract. The pathogenesis of the intestinal lesions in IBD is not entirely identified and understood: excessive activation of the immune system may come as a result of the interaction of various environmental and infectious factors, genetic predisposition, and the mediation of abnormal intestinal flora. The main objective of the current study is to further identify the risk factors for the development of IBD. Currently, there is very little knowledge about circadian rhythm and IBD and there are only a few studies on the relationship between sleep disturbances and the course of the disease, as well as pro- and anti-inflammatory cytokine profile and general immune system functioning. Furthermore, the relationship between the expression of circadian rhythm genes and severe course of IBD is still unknown. The aim of this review is to show the current state of knowledge about the relationship between circadian rhythm disorders, sleep disturbance and inflammation in the GI tract and to analyze the possibility of employing this knowledge in diagnosis and treatment of IBD.

The influence of family pattern abnormalities in the early stages of life on the course of inflammatory bowel diseases.

Crohn's disease (CD) and ulcerative colitis (UC) belong to the group of inflammatory bowel diseases (IBD), chronic immune mediated diseases of the gastrointestinal (GI) tract with significant negative impact on patients' quality of life. CD and UC are related with the development of chronic inflammatory lesions in the GI tract, causing digestive and absorption disorders. Typical symptoms of IBD are: abdominal pain, vomiting, diarrhea, rectal bleeding, and weight loss. In addition, IBD are often associated with the extraintestinal manifestations, including arthritis and dermatoses. While the cause of IBD is still not fully understood, the psychological aspects are regarded as possible trigger factors. Moreover, most recent studies suggest that family pattern abnormalities associated with stress at the early stages of life may strongly affect health balance. In this paper, the most relevant studies focusing on the association between early life stress and IBD, found in MEDLINE, Cochrane Library and EMBASE are discussed. Possible effects of the early life stress on IBD progression and response to undertaken therapies are analyzed.

Mean Platelet Volume in Crohn's Disease Patients Predicts Sustained Response to a 52-Week Infliximab Therapy: A Pilot Study.

BACKGROUND: The loss of response to infliximab in Crohn's disease (CD) patients is currently a major clinical problem. Recently, mean platelet volume (MPV) has been proposed as a new biomarker of CD activity. Here, we hypothesized that MPV may be used as cheap and efficient biomarker of subclinical inflammation during 52-week therapy in CD patients responding to infliximab induction treatment. AIMS: The aim of study was to establish whether MPV at baseline and pre-infusion at week 14 are good predictors of sustained response after week 14 in CD patients undergoing 52-week infliximab therapy. METHODS: A retrospective study of 30 adult CD patients who underwent a 52-week course of treatment with infliximab and achieved response at week 14 to induction treatment was performed. The association between MPV, baseline disease parameters and maintained clinical response or remission during infliximab therapy was assessed. RESULTS: Higher MPV at week 14 was observed in CD patients with sustained response to infliximab after week 14 than in patients with loss of response (p = 0.0019). In patients with loss of response to maintenance infliximab treatment, lower ΔMPV between baseline and week 14 was calculated (p = 0.0003). MPV > 10.3 fl at week 14 predicts sustained response with 67 % sensitivity and 80 % specificity. ΔMPV between baseline and week 14 >0.4 fl predicts sustained response with 87 % sensitivity and 93 % specificity. CONCLUSION: MPV at week 14 and ΔMPV between baseline and week 14 are good predictors of sustained response to infliximab maintenance treatment in CD patients.

The influence of Helicobacter pylori eradication on the expression and methylation status of the FHIT gene in non-cancerous gastric mucosa of dyspeptic patients.

OBJECTIVE: To investigate the effect of Helicobacter pylori (H. pylori) eradication on the expression level of the FHIT gene and its methylation status in the gastric mucosa of dyspeptic patients with or without a family history of gastric cancer (FHGC). METHODS: In all, 31 patients with H. pylori infection including 13 with FHGC were enrolled in the study. The effectiveness of H. pylori eradication were confirmed by UBT, RUT and multiplex PCR (the presence of selected H. pylori strains) for biopsy samples from the antrum and corpus. Histopathological assessment was also performed. The expression of FHIT mRNA was determined by quantitative reverse transcription-polymerase chain reaction and the methylation status of the FHIT promoter was assessed by methylation-specific polymerase chain reaction. RESULTS: After H. pylori eradication, the improvement of inflammation from superficial gastritis to normal mucosa (G → N) was observed in 39% of the patients without FHGC and in 54% of those with FHGC. FHIT mRNA expression was increased in patients without FHGC after H. pylori eradication (P < 0.05), while there was no statistically significant change in gene methylation status after H. pylori eradication (P > 0.05). For the samples from those with FHGC, the FHIT mRNA expression was not significantly changed and the methylation status fluctuated evenly. CONCLUSIONS: H. pylori eradication results in the improvement of gastric mucosal inflammation and histopathological non-atrophic changes. The FHIT gene expression is increased in patients without FHGC, which may contribute to the prevention of GC development.

The Diagnosis of Sigmoid Liposarcoma in a Young Male with Metabolic Syndrome.

The clinical picture and risk factors are decisive in differential diagnosis. It was proved that patients with metabolic syndrome have increased incidence of malignant tumours. The visceral adipose tissue releases active proteins that promote oncogenesis. We are presenting a case of 34-year-old male with metabolic syndrome suffering from pain in left iliac fossa with accompanying variable stool pattern. At first, the sigmoid diverticulosis was suspected. Patient's condition after the treatment has improved. The ambulatory, partial colonoscopy revealed a cauliflower-like, balloting, wide-base growth in the sigmoid that narrowed its lumen. The biopsy did not reveal atypical growth characteristics. Because of tumour type and enlarged regional lymph nodes seen in abdomen CT scan, the segmental colon resection and end-to-end anastomosis was performed in the area of sigmoid-rectal junction. Macroscopically, there were no visible metastases in the operation field. The surgery and postoperative period ran without any complications. On histopathological examination, the removed tumour was a well differentiated liposarcoma (WDL) stemming unusually from adipose tissue of colonic submucosa in an obese male. WDL is a hard to diagnose tumour, especially in early stages of its growth. In the presented case, the tumour was completely resected.

[The clinical significance of GastroPanel in diagnostics of Helicobacter pylori eradication efficiency in patients with dyspepsia with correlation of family history of gastric cancer]. / Kliniczne znaczenie GastroPanelu w diagnostyce skutecznej eradykacji Helicobacter pylori u chorych z dyspepsja w zaleznosci od rodzinnego wystepowania raka zoladka.

UNLABELLED: Gastric cancer remains a significant medical and social problem. Familial, hereditary, social, and demographic factors increase the susceptibility of subjects to cancer development, especially those infected with Helicobacter pylori (H. pylori). Apart from genetic studies, there are ongoing biochemical studies of possible practical value in assessment of the risk of gastric cancer development. The GastroPanelBiohit test, that include determination of the levels of gastrin (G-17), pepsinogen I (PGI), pepsinogen II (PGII) and antibodies IgG/IgA against H. pylori in serum, allowed us to determine whether there are any abnormal changes in the gastric mucosa. The aim of the study was to determine whether GastroPanel parameters, identified in patients with dyspeptic symptoms (with or without history of gastric cancer in first degree relatives) before and after successful eradication of H. pylori, have any clinical value, especially in gastric cancer development. MATERIAL AND METHODS: The study comprised 61 patients aged 18-56 years with symptoms of dyspepsia. In all patients, the preliminary urea breath test (UBT) for the presence of H. pylori was performed and the positive result qualified for further study. For final analysis, 42 patients were approved, who were divided into two groups: group I (a control group) - 22 patients with negative family history of gastric cancer among the relatives of first degree, group II - 20 patients with positive history of gastric cancer among the relatives of first degree. All the patients had the gastroscopy with the biopsy of gastric mucosa for the histopathological evaluation. Additionally, the GastroPanel test was performed. RESULTS: In the blood serum of the patients with H. pylori infection, the concentrations of gastrin (G-17), pepsinogen I (PGI) and pepsinogen II (PGII) did not depend on family history of gastric cancer (p > 0.05). Successful eradication of H. pylori decreases the levels of G-17, PGI and PGII (statistical significance p < 0.05), and this correlates with the histopathological changes of gastric mucosa. The patients with positive family history of gastric cancer had more intense H. pylori colonization of gastric mucosa (IV degree of insensitivity of infection in UBT; group I - 22% vs group II - 69%) as compared to the control group. After effective eradication of H. pylori, statistically significant decreases of IgG H. pylori antibodies and of the level of gastrin (p < 0.05) in blood serum were seen (in a 3 months follow up) only in the control group. CONCLUSIONS: Independently of the history of familial gastric cancer, the GastroPanelBiohit test provides important clinical data useful for diagnosis, for assessment of effectiveness of H. pylori eradication therapy and in evaluation of the degree of the inflammatory changes in gastric mucosa.

[Effect of Helicobacter pylori eradication on the expression level of SATB1 and c-Myc genes in gastric mucosa of patients with family history of gastric cancer]. / Wplyw eradykacji Helicobacter pylori na poziom ekspresji genów SATB1 i c-Myc w blonie sluzowej zoladka u pacjentów z dyspepsja w zaleznosci od rodzinnego obciazenia wystepowaniem raka zoladka.

UNLABELLED: Helicobacter pylori (H. pylori) is a class 1 gastric carcinogen with the proved influence on gastric cancer development. The products of SATB1 and c-Myc genes play important role in cancer development and their levels are elevated in gastric cancer tissues. The aim of the study was to analyze an effect of H. pylori eradication on the expression of the SATB1 and c-Myc genes in the gastric mucosa of dyspeptic patients with family history of gastric cancer. MATERIAL AND METHODS: Twenty patients enrolled to the studies were divided into two groups: nine patients (group I) without the family history of gastric cancer, and eleven patients with the family history of gastric cancer (group II). Endoscopic biopsies of gastric mucosa were taken from the antrum and corpus of H. pylori-infected subjects before and after bacteria eradication. The corresponding levels of expression were determined by analysis of the respective mRNA levels with the use of the real-time RT-PCR method. The level of each mRNA was normalized to the levels of mRNA of two reference genes, RPL29 and GAPDH. RESULTS: Independently of stomach topography, the antrum versus corpus, in the group I patients the levels of mRNA of SATB1 and c-Myc after eradication were higher in the following cases: SATB1/ GAPDH p = 0.017914 (antrum); SATB1/RPL29 p = 0.046400 (corpus); SATB1/GAPDH p = 0.027709 (corpus). For group II patients no statistically significant increase of the level of the c-Myc and SATB1 genes was observed. CONCLUSIONS: Patients with the family history of gastric cancer and H. pylori infection, with reversible histopathological changes of the gastric mucosa, have significantly higher levels of SATB1 and c-Myc genes expression as compared to the patients without family history of gastric cancer, regardless of the topography of the stomach. After successful eradication, the SATB1 mRNA level in samples of patients with the family history of gastric cancer did not increase, in contrast to the control group of patients. Presumably, the observed effect is associated with hypermethylation of the promoter of that gene. However, the level of c-Myc gene expression was not significantly different before and after removal of the bacteria, for both groups of patients.

Family history of gastric cancer correlates with decreased expression of HINT1 tumor suppressor gene in gastric mucosa of dyspeptic patients.

Gastric cancer (GC) is the fourth most common cancer and the second most common cause of cancer-associated mortality worldwide. Approximately 10% of gastric cancers are hereditary and a small percentage of these cases (1-3%) have been classified as a single hereditary syndrome (hereditary diffuse gastric cancer). We previously demonstrated that a family history of gastric cancer (FHGC) contributes to a predisposition towards the development of gastric cancer. Our data revealed that for dyspeptic patients whose first-degree relative(s) succumbed to GC, the levels of the fragile histidine triad pro-apoptotic protein in gastric mucosa were decreased. Another member of the histidine triad protein superfamily is histidine triad nucleotide-binding protein 1 (HINT1), a novel tumor suppressor that plays an inhibitory role in the control of gene transcription. The study comprised 38 ethnically homogeneous patients with dyspeptic symptoms without concomitant chronic diseases (18 controls/20 patients with FHGC). The results showed that the samples from the control patients predominantly exhibited non-atrophic changes (approximately 90%), whereas atrophic changes occurred more frequently in patients with FHGC. Notably, the expression levels of the HINT1 gene were markedly higher in the samples with atrophy taken from the antrum of FHGC patients compared to the non-atrophic samples. Moreover, the levels of HINT1 mRNA in samples obtained from the antrum of patients with FHGC were lower compared to analogous samples from the control individuals. The decreased levels of HINT1 mRNA in the antrum samples of patients with the FHGC indicate that it is a factor predisposing those patients to the development of gastric cancer.

Gastric ghrelin in relation to gender, stomach topography and Helicobacter pylori in dyspeptic patients.

AIM: To investigate the level of gastric ghrelin in stomach mucosa of dyspeptic patients in relation to Helicobacter pylori (H pylori) infection, bacterial cytotoxicity, topography and gender. METHODS: The study comprised 40 premenopausal women (19 H pylori positive) and 48 men (17 H pylori positive) with functional dyspepsia. All gastric biopsy specimens revealed normal mucosa or non-atrophic gastritis. Gastric ghrelin concentration was determined by Enzyme linked immunosorbent assay. The cagA and vacA strains of bacterial DNA were identified by multiplex polymerase chain reaction. RESULTS: In general, infection with H pylori caused an increase in gastric ghrelin level regardless of gender and stomach topography. Significantly more hormone was present in both, non-infected and H pylori positive female samples, as compared to males. The distribution of bacterial strains showed cagA(+) vacA s1m1 and cagA(-) vacA s2m2 genotypes as the most common infections in the studied population. A tendency to higher ghrelin levels was observed in less cytotoxic (cagA negative) strain-containing specimens from the antrum and corpus of both gender groups (without statistical significance). CONCLUSION: An increase in gastric ghrelin levels at the stage of non-atrophic gastritis in H pylori positive patients, especially in those infected with cagA(-) strains, can exert a gastroprotective effect.

Helicobacter pylori infection and family history of gastric cancer decrease expression of FHIT tumor suppressor gene in gastric mucosa of dyspeptic patients.

BACKGROUND: The expression of a fragile histidine triad (FHIT) protein is lost in stomach tumors. The study aimed at determining whether FHIT expression is affected by Helicobacter pylori infection, strain virulence (vacA and cagA genes) and histopathological changes in the gastric mucosa of patients with functional dyspepsia having first-degree relatives with gastric cancer. MATERIALS AND METHODS: Eighty-eight never-smoking patients with functional dyspepsia were selected for the study, and 48 of them had first-degree relatives with gastric cancer. Bacterial DNA amplification was used to identify H. pylori colonization. The level of FHIT gene expression was determined by qRT-PCR (mRNA) and Western blot (FHIT protein) analyses. RESULTS: For patients having first-degree relatives with gastric cancer FHIT expression was lower (mRNA by ca. 40-45% and protein by 30%) compared with the control patients (p < .05). H. pylori infection decreased the FHIT mRNA level by 10-35% and the protein level by 10-20%. Bacterial strain vacA(+)cagA(+) lowered FHIT mRNA by ca. 30-35% in the antrum samples of both groups and in corpus samples of patients with first-degree relatives with gastric cancer (p < .05). The FHIT mRNA level was twice as high in control H. pylori-negative patients with intestinal metaplasia, compared with those with non-atrophic gastritis. CONCLUSIONS: The decreased FHIT gene expression associated with hereditary factors and with H. pylori infection, especially with vacA(+)cagA(+)-positive strains, may be related to gastric carcinoma development.

[Gastrin secretion in patients with functional dyspepsia]. / Wydzielanie gastryny u osób z dyspepsja czynnosciowa.

UNLABELLED: The pathogenesis of functional dyspepsia is very complicated and its etiology is still not clear. One of the supposed pathophysiological mechanisms are disturbences of gastric acid secretion and gastric motility. Recently, it has been recognized, that in the pathogenesis of above disturbances may play a role enterohormones, like gastrin. AIM: To establish if in patients with functional dyspepsia the level of gastrin concentration changes and wheather it correlates with type and grade of symptom's intensity. MATERIAL AND METHODS: The study included 50 subjects between of 20 to 54 years with diagnosed functional dyspepsia (according to the Rome III Criteria). The study group was divided into two subgroups: group I--25 subjects with Epigastric Pain Syndrome--EPS and group II--25 subjects with Postprandial Distress Syndrome--PDS. Control group comprised 20 healthy subjects (without any clinical or morphological symptoms of digestive tract disease). In each patient due to gastrointestinal tract organic disease exclusion the gastroscopy, histological examination of gastric mucosa, ultrasonography of abdomen and laboratory tests were performed. H. pylori infection was detected using fast urea test (CLO-test), confirmed by histopathological examination (stained Giemsa method) and non-invasive urea breath test (UBT-13C) using mass spectrophotometer FANci 2 (Fisher Analyser Instrumente GmbH). In each patient the level of gastrin concentration in blood serum, in fasting state, was determined, based on ELISA method considering the length of the weave lamda=430 nm. The study group was also divided into 3 subgroups, using 10-points scale of symptom's intensity: --grade 1--mild (1-3 points); --grade 2--moderate (4-6 points); --grade 3--severe (7-10 points). RESULTS: The concentration of gastrin in blood serum in healthy subjects was 2.4 +/- 1.23 pmol/L. In patients with functional dyspepsia was significantly higher; in patients with Epigastric Pain Syndrome--7.51 +/- 2.46 pmol/L (p < 0.05), in patients with Postprandial Distress Syndrome - 6,92 +/- 2.18 pmol/L (p < 0.05). There were no significant differences in dependence on pain's intensity in EPS--the concentrations in subgroups 1, 2 and 3 were: 7.36 +/- 1.4 pmol/L, 7.53 +/- 2.43 pmol/L and 7.64 +/- 2.55 pmol/L. The gastrin concentration in PDS in dependence on symptom's intensity in subgroup 1 was 6.34 +/- 1.2 pmol/L, in subgroups 2 and 3 were higher: 6.99 +/- 2.31 pmol/L and 7.42 +/- 2.2 pmol/L, but the differences were not statistically significant. In patients with functional dyspepsia, infected with H. pylori the gastrin concentration was significantly higher and was 15.28 +/- 5.3 pmol/L (p < 0.05). There were no significant differences in dependence on type of dyspepsia. CONCLUSIONS: The gastrin concentration in blood serum in fasting state in patients with functional dyspepsia is higher than in control subjects, both in patients with Epigastric Pain Syndrome--EPS as well as with Postprandial Distress Syndrome--PDS. The grade of symptom's intensity does not correlate with increase of gastrin concentration.

[24-hour urinary 5-hydroxyindole acetic acid excretion in patients with ulcerative colitis]. / Wydalanie kwasu 5-hydroksyindolooctowego z moczem u osób z wrzodziejacym zapaleniem jelita grubego.

UNLABELLED: The experimental data show that in mucosal injury of the alimentary system serotonin metabolism and secretion is disturbed. Such suggestions are also drawn in discussions concerning pathogenesis of ulcerative colitis. THE AIM OF THE STUDY: To perform a quantitative evaluation of 24-hour urine excretion of a major serotonin metabolite-5-hydroxyindole acetic acid (5-HIAA) in patients with ulcerative colitis (UC). MATERIAL AND METHODS: The studied group comprised 50 patients with exacerbated UC, aged 21-56 years. Among them 25 had mild and 25 severe exacerbation according to Trulove's and Witts criteria. The control group comprised 25 healthy persons. On the study day the patients remained on standard liquid diet--Nutrdrink 3 x 400 ml with the caloric value of 1800 kcal. 5-HIAA concentration was measured by ELISA method applying IBL antibodies (RE 59131), and the results were presented in mg/dl and then the value of 24-hour urine excretion was calculated. Results. In the group o patients with severely exacerbated UC 5-HIAA excretion was significantly lower that in healthy volunteers--1.66 +/- 0.98 mg/24 hi 5.77 +/- 0.46 mg/24 respectively (p < 0.05). The results of 5-HIAA excretion showed positive correlation with serum albumin concentration. In the group of patients with mild colitis such significant changes and correlations were not observed. CONCLUSIONS: (1) In severe exacerbations of UC serotonin metabolism is largely changed. (2) 24-hour serotonin excretion can have a predictive value in UC.

[The role of RAD 51 gene polymorphism in patients with colorectal cancer in the Polish subpopulation]. / Rola polimorfizmu genu RAD51 u chorych z rakiem jelita grubego w subpopulacji polskiej.

UNLABELLED: DNA repair processes assure genomic integrity and play the crucial role in protecting against carcinogenic factors. Mutations in DNA repair genes, which code proteins engaged in repair processes, may lead to carcinogenesis and among others also to colorectal cancer development. RAD51 gene encodes a protein of DNA homologues recombination repair. AIM OF THE STUDY: To evaluate the role of RAD51 gene polymorphism in patients with colorectal cancer in Polish subpopulation Materials and methods. The studied group comprised 100 colorectal cancer patients (aged 57-75) and 236 age, sex-, age- and ethnicity-matched cancer-free controls. Genotypes were determined in DNA from peripheral blood lymphocytes by PCR-RFLP. RESULTS: An association between colorectal cancer occurrence and the G/C variant of the 135 G/C RAD51 polymorphism was found (OR 2.45; 95% CI 1,45-4,14) (p > 0.05). CONCLUSIONS: The G/C variant of the 135 G/C RAD51 polymorphism may be associated with the increased risk of colorectal cancer development.

Expression of somatostatin receptor subtype 3 in the gastric mucosa of dyspeptic patients in relation to Helicobacter pylori infection and a family history of gastric cancer.

BACKGROUND AND AIM: The cytotoxic activity of Helicobacter pylori contributes significantly to the pathogenesis of gastric carcinoma. A preliminary study suggested that somatostatin receptor subtype 3 (SSTR3) might play a role in cell apoptosis and the growth of gastric cancer. The aim of the present study was to determine the influence of H. pylori infection and a family history of gastric cancer on the expression of SSTR3 in the gastric mucosa of non-cancer patients with dyspepsia. METHODS: The expression of the SSTR3 gene in the gastric mucosa of the stomach antrum and corpus of 53 patients was determined by the use of quantitative reverse transcription-polymerase chain reaction. RESULTS: The SSTR3 mRNA level was lower in the H. pylori-infected patients, as compared to the non-infected patients, independently of a family history of gastric cancer and stomach topography. The greatest decrease of approximately 40% and 35% (P < 0.05) was observed for the antrum of the H. pylori-positive patients without and with a family history of gastric cancer, respectively. In the corpus, these differences were much smaller, regardless of a family history of gastric cancer. Interestingly, for H. pylori-negative patients, the density (at the mRNA level) of the SSTR3 receptor in the antrum was higher than in the corpus mucosa. CONCLUSIONS: A decrease in the density of SSTR3 (especially in the antrum) in individuals with H. pylori infection and particularly with a family history of gastric cancer may point to an environmental and inherited predisposition in the development of distal gastric cancer.