[The role of intraepithelial lymphocytes in pathogenesis of small intestinal bacterial overgrowth syndrome]. / Rola limfocytów sródnablonkowych w patogenezie zespolu przerostu bakteryjnego jelita cienkiego.

Small intestinal bacterial overgrowth (SIBO) is a frequent cause of chronic abdominal complaints. So far, a lot information has been gathered on its pathogenesis but are still doubts that raise question why its causes chronic diarrhea in some and constipation in other patients. AIM: The aim of the study was to assess the number of endothelial lymphocytes (IELs) in the duodenal and ileum mucosa in patients with SIBO with dominant diarrhea (SIBO-D) and dominant constipation (SIBO-C). MATERIALS AND METHODS: The study was performed in 30 healthy patients (group I) and 40 patients with SIBO and diarrhoea (group II), and in 4o patients with constipation (group III). To diagnose SIBO the lactulose hydrogen breath test (LHBT) was performed. To determine the number of intraepithelial lymphocytes in duodenal and jejunal mucosa the histological assessment was performed using haematoxylin-eosin staining. Moreover, immunochistochemical method was used to assess the number of enterochromatoffin cells (EC, chromogranin A - LK-2H10) in these some parts of the gut. RESULTS: The results of LHBT were similar in group II and III - 75,6±18,1 ppm and 66,9±16,2 ppm(p>0,05). The number of IELs in duodenal mucosa in controls was 14,6±4,1/100 EN, in group II - 28,3±6,8/100 EN (p<0.01), and in group III - 23,0±9,9/100 EN (p<0,05), and similar differences were in jejunal mucosa. The number of EC in both parts of the gut was higher in SIBO compared to controls. Furthermore, in patients with SIBO-D the number of IELs in duodenum, as well as in jejunum, was positively correlated with the number of EC cells ( p<0,05, p=0,056, respectively). CONCLUSIONS: In patients with SIBO, particularly with SIBO-D, increased number of IELs I EC cells may be a cause of diverse abdominal symptoms.

The analysis of ALK gene rearrangement by fluorescence in situ hybridization in non-small cell lung cancer patients.

INTRODUCTION: ALK gene rearrangement is observed in a small subset (3-7%) of non-small cell lung cancer (NSCLC) patients. The efficacy of crizotinib was shown in lung cancer patients harbouring ALK rearrangement. Nowadays, the analysis of ALK gene rearrangement is added to molecular examination of predictive factors. AIM OF THE STUDY: The frequency of ALK gene rearrangement as well as the type of its irregularity was analysed by fluorescence in situ hybridisation (FISH) in tissue samples from NSCLC patients. MATERIAL AND METHODS: The ALK gene rearrangement was analysed in 71 samples including 53 histological and 18 cytological samples. The analysis could be performed in 56 cases (78.87%), significantly more frequently in histological than in cytological materials. The encountered problem with ALK rearrangement diagnosis resulted from the scarcity of tumour cells in cytological samples, high background fluorescence noises and fragmentation of cell nuclei. RESULTS: The normal ALK copy number without gene rearrangement was observed in 26 (36.62%) patients ALK gene polysomy without gene rearrangement was observed in 25 (35.21%) samples while in 3 (4.23%) samples ALK gene amplification was found. ALK gene rearrangement was observed in 2 (2.82%) samples from males, while in the first case the rearrangement coexisted with ALK amplification. In the second case, signet-ring tumour cells were found during histopathological examination and this patient was successfully treated with crizotinib with partial remission lasting 16 months. CONCLUSIONS: FISH is a useful technique for ALK gene rearrangement analysis which allows us to specify the type of gene irregularities. ALK gene examination could be performed in histological as well as cytological (cellblocks) samples, but obtaining a reliable result in cytological samples depends on the cellularity of examined materials.

Hepatitis and the polyglandular autoimmune syndrome, type 1.

Autoimmune polyglandular syndrome, type 1 (APS-1) is a rare syndrome. Here we present a case report of a 24-year-old female patient who complained of progressive weakness. While autoimmune hepatitis was diagnosed, no improvement of biochemical parameters was obtained after immunosuppressive treatment. Hypoparathyroidism and adrenocortical failure were identified. Her health status clearly improved once proper control of the calcium-phosphate metabolism was obtained and after the administration of substitution hydrocortisone doses, leading to full normalization of biochemical liver tests. The reported case illustrates a rare form of APS-1 failure, in which the diagnosed autoimmune hepatitis was only the first symptom.

[The assessment of nitric oxide metabolites in gastric juice in Helicobacter pylori infected subjects in compliance with grade of inflammatory lesions in gastric mucosa]. / Ocena stezenia metabolitów tlenku azotu w soku zoladkowym u zakazonych Helicobacter pylori z uwzglednieniem stopnia zmian zapalnych w blonie sluzowej zoladka.

UNLABELLED: The infection of H. pylori causes inflammatory lesions in gastric mucosa--until atrophic gastritis, intestinal metaplasia, dysplasia (precancerous states) and finally to gastric cancer or lymphoma. The mechanism of mentioned disturbances is complicated, no doubt that nitric oxide plays here very important role. It is proved, that H. pylori causes essential oxygen metabolism disturbances by activation of inflammatory infiltration's cells to oxide reactive forms as nitric oxide formation. Nitric oxide as oxide radical could react with other free radicals and contribute to oxidative lesions of gastric mucosa and alterations of its structure. The aim of the study was try to answer the question: 1. Is this the relationship between NO metabolites concentrations in gastric juice and morphological state of gastric mucosa? 2. Does H. pylori eradication influence on NO metabolites concentrations in gastric juice? 3. Does H. pylori eradication influence on grade of inflammatory lesions in gastric mucosa? MATERIAL AND METHODS: The study included 75 subjects between of 21 to 60 years, infected with H. pylori with diagnosed (according to the Sydney system) different stages of chronic gastritis progression. The type of inflammation, activity, the presence of atrophy, intestinal metaplasia and H. pylori infection were assessed. The study group was divided into 3 subgroups: group I--25 subjects with chronic active gastritis, group II--25 subjects with chronic atrophic gastritis without intestinal metaplasia, group III--25 subjects with chronic atrophic gastritis with intestinal metaplasia. Control group comprised 20 healthy subjects, without H. pylori infection. In each patient during gastroscopy 5 biopsy specimens for histopathologic examination and for urea test and 3 ml gastric juice were collected. The concentration of nitric oxide metabolites in gastric juice was determined with spectrophotometric method, based on Griess reaction. 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). In H. pylori--infected patients the above mentioned investigations were performed three times -before, in 8 weeks and in 12 months after antibacterial treatment's finish. In antibacterial therapy we use 7-days three-drugs therapy (omeprasole, amoksycillin and clarythromycin). RESULTS: The concentration of nitric oxide metabolites in gastric juice in healthy subjects was 6.81 +/- 2.23 micromol. In patients with chronic gastritis, H. pylori infected was significantly higher--in patients with chronic active gastritis was 9.29 +/- 2.19 micromol/l, in patients with chronic atrophic gastritis--10.25 +/- 2.31 micromol/l (p < 0.01), in patients with intestinal metaplasia--11.89 +/- 2.46 micromol/l (p < 0.01). 8 weeks after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 8.18 +/- 1.63 micromol/l, in patients with chronic atrophic gastritis--10.02 +/- 2.28 micromol/l, in patients with intestinal metaplasia--10.83 +/- 2.32 micromol/l. The differences were not statistically significant. 12 months after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 6.90 +/- 1.43 micromol/l, in patients with chronic atrophic gastritis--7.22 +/- 2.01 micromol/l, in patients with intestinal metaplasia--7.56 +/- 1.98 micromol/l. The differences were statistically significant--p < 0.05, p < 0.01. 8 weeks after antibacterial treatment's finish in each patient also the gastroscopy was performed and another biopsy specimen for histopathologic examination were collected. Only in group I in microscopic image the decreased of inflammation intensity was find (both in antrum and in corpus)--however the differences were not statistically significant. In the other groups the alterations in gastric mucosa do not improve significantly. The gastroscopy was performed again in 12 months after antibacterial treatment's finish. In group I the significant decrease or regression of inflammatory infiltration (in corpus and in antrum) was found. Also in group II the significant decrease of the grade of atrophy and similarly in III group the improvement of histopathological state were observed. CONCLUSIONS: 1. The increase of NO metabolites concentration demonstrates positive correlation with grade of inflammatory lesions in gastric mucosa. 2. The effective antibacterial therapy causes the decrease of NO metabolites concentration in gastric juice, especially in patients with chronic active gastritis. 3. Eradication influence on decrease of grade of lesions' progression in gastric mucosa just in 12 months after effective antibacterial therapy.

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.

[Somatostatin receptor subtype 3 (SSTR3) mRNA level in gastric mucosa of patients with dyspepsia]. / Poziom mRNA receptora somatostatyny typu 3 (SSTR3) w blonie sluzowej zoladka u osób z dyspepsja.

UNLABELLED: Somatostatin (SST) inhibits cellular processes related to secretion, motor activity and cell proliferation. It operates through SSTR1-5 receptors. Density of the SSTR3 receptor is decreased in gastric adenocarcinoma. AIM: Determination of the SSTR3 mRNA level in gastric mucosa of patients with dyspepsia, in respect to stomach topography, H. pylori infection, patient gender and the type of histopathological changes was aimed in these studies. MATERIALS AND METHODS: A real time RT-PCR method was used to determine the SSTR3 mRNA level in samples collected from the stomach antrum and corpus of 27 patients with dyspepsia (18-59 years old) without family history of cancer. RESULTS: Among Hp(-) patients, the level of the SSTR3 mRNA in samples taken from the antrum was by ca. 65% higher (p < 0.05) than from the stomach corpus. Infection with H. pylori significantly decreased the SSTR3 level in antrum (ca. 50%, p < 0.05), especially in females. Among the Hp(+) patients, the development of histopathological changes in that part of stomach was accompanied by decrease of the expression of SSTR3 receptor (p > 0.05). CONCLUSIONS: H. pylori infection related reduction of the SSTR3 density in the antrum mucosa speaks for the need of eradication of these bacteria in the prevention of distal gastric cancer.

[Estimation of gastric mucosa morphological changes in subjects with asymptomatic Helicobacter pylori infection and family history of gastric cancer]. / Ocena zmian morfologicznych blony sluzowej zoladka u osób z bezobjawowym zakazeniem Helicobacter pylori obciazonych rodzinnym wystepowaniem raka zoladka.

Helicobacter pylori is a known carcinogen but the natural history of gastric carcinoma development has not been recognized thoroughly and early diagnostics is difficult particularly in asymptomatic infection. The aim of own study was gastric mucosa morphological estimation in subjects with asymptomatic H. pylori infection. Investigations were performed in 60 subjects, aged 24-55 years with family history of gastric cancer and with asymptomatic (group I; n=30) and symptomatic infection (group II; n=30). The infection and its severity were confirmed with breath test with the use of 75 mg of 13C labelled urea and Olympus FANci-2 analyzer. Gastric mucosa macro- and microscopic state was evaluated according to 4-degree Sydney scale. In group II macroscopic changes were more pronounced than in group I (p=0.032); no such differences were seen in microscopic picture (p=0.625). The extent of macro- and microscopic changes demonstrated positive correlation with the results of breath test (group I: r=0.8169; group II: r=0.8393). In subjects with family history of gastric cancer H. pylori infection both, symptomatic and asymptomatic causes similar gastric mucosa histopathological changes including intestinal metaplasia. The degree of morphological changes demonstrates positive dependence with the severity of infection.