Neopterin, a pteridine compound produced by macrophages activated by interferon-gamma, is widely used to assess the activation of cellular immunity. An elevation in serum or urinary neopterin reflects immune activation in many different disorders, including viral infections, cancer, autoimmune diseases or acute myocardial infarction, but less attention has been paid to neopterin concentration in other biological fluids. The aim of the present study was to examine neopterin concentration in gastric juice. An association with the presence of Helicobacter pylori, a bacterium linked to the most common disorders of upper digestive tract, was also investigated. Gastric juice was obtained at endoscopy from 61 patients. Neopterin was determined by a radioimmunoassay and the presence of H. pylori was examined by urease test. The macroscopic finding of bile in gastric juice was associated with significantly higher neopterin levels compared to patients where no bile was noted (15.5 +/- 15.6 vs. 2.1 +/- 3.0 nmol/l, P < 0.001). However, similar concentrations were observed in the H. pylori positive and H. pylori negative patients (7.6 +/- 12.0 vs. 11.1 +/- 14.9 nmol/l). Even in the absence of macroscopic bile contamination, no significant difference could be found between the infected and uninfected patients (2.3 +/- 3.2 vs. 1.3 +/- 1.9 nmol/l), and the patients with duodenal ulcer and normal findings (3.8 +/- 4.6 vs 1.6 +/- 1.9 nmol/l). The contamination of gastric juice with bile represents the limitation for the use of neopterin as a marker of immune activation in the gastric mucosa. Rather than an index of immune activation, gastric juice neopterin concentration represents a marker of duodenogastric reflux.

The authors present a review of contemporary findings concerning treatment of gastroduodenal ulcers with a positive finding of Helicobacter pylori. Only combined anti-Helicobacter treatment leads to the eradication of Helicobacter pylori in 80-96% of the patients. Moreover it leads to gradual recovery from gastritis and bulbitis and thus prevents ulcer recurrence.

UNLABELLEDInflammatory bowel disease can be associated with increased platelet count. Aim of our study was focused on assessing thrombocyte count in evaluation of the activity in Crohn's disease (CD). The study included a total of 19 patients [6 men, 13 women (aged 18-57 years, mean 33, median 28]. All patients were malnourished in active stage of the disease on total parenteral and/or enteral nutrition (TP/EN). Thrombocytes were estimated at the beginning and after 3 weeks of TP/EN in venous blood sample using automatic analyser Coulter Counter JT3 (normal range: 130-380.10(9)/l). Serum prealbumin, transferrin, haptoglobin, alpha 1-orosomucoid and C-reactive protein were measured simultaneously. Thrombocytes count below 400.10(9)/l was found only in 1/19 at the beginning and in 7/19 patients in the end of the study. After 3 weeks of TP/EN a significant platelet count fall was found (mean +/- sd: 472 +/- 98 vs. 354 +/- 110, p < 0.01). A correlation was found between thrombocytes and serum prealbumin (r = -0.3871, p < 0.05), haptoglobin (r = 0.5247, p < 0.001), alpha 1-orosomucoid (r = 0.4857, p < 0.01) a C-reactive protein (r = 0.4354, p < 0.01).CONCLUSIONThrombocyte count helped in the assessing of disease activity in CD on 3-week-TP/EN. Improvement of clinical status, increase of nutritional parameters and decrease of positive acute phase reactants were associated with a fall of platelet count in 15/19 patients.

Helicobacter pylori (Hp) is unequivocally the most frequent cause of antral gastritis and most probably participates in the majority of cases in the aetiology of gastritis affecting the body of the stomach. The close relationship between antral gastritis and duodenal ulceration is documented by the high incidence of Hp in these patients (90-100%). The problem of Hp negative cases of duodenal ulceration was not finally resolved yet. The absence of Hp in duodenal ulcer usually implies a different aetiology (NSAID, gastrinoma etc.). Hp is eliminated by a number of drugs (bismuth preparations, some antibiotics, metronidazole), however, eradication (Hp negativity after a month or longer following termination of treatment) is ensured so far only by a combination of several drugs. Less clear are the relations with gastric ulcers. The presence of Hp in the antral mucosa is substantially smaller, however, when the mucosa near the ulcer is examined it is also almost 100%. The relationship of antral gastritis and non-ulcer dyspepsia is not quite clear. Hp is found in about half the patients and its elimination (e.g. by bismuth preparations), has a favourable impact on inflammatory changes as well as on the patient's complaints. The regression of complaints is more permanent than after antacids which have only a favourable effect on complaints but not on Hp and the inflammation.

Increased immunoglobulin G2 [IgG2] in Crohn's disease in contrast with increased IgG1 in ulcerative colitis was reported in literature data. The aim of our study has been focused on serum IgG subclasses in Crohn's disease with resected bowel (11 patients) and without previous surgery for Crohn's disease (12 patients). All patients were in active stage of the disease on total parenteral nutrition. Serum IgG subclasses were estimated by means of radial immunodiffusion. There was no significant differences between in IgG subclasses in Crohn's disease with and without bowel resection. IgG2 over 4.5 g/l was found only in 2/12 with resected bowel and 1/11 without previous surgery for Crohn's disease. Surprisingly, IgG1/IgG2 ratio below 1.5 was found only in 5/23 persons. In 3/23 patients IgG1 was over 10.5 g/l although there was no doubt about the diagnosis of Crohn's disease. IgG subclasses failed to help in confirmation of the diagnosis of Crohn's disease. Serum IgG subclasses alterations probably are not influenced by bowel resection and/or nutritional status.

Colicins are proteinaceous substances produced by Escherichia coli strains and related bacteria of Enterobacteriaceae family. They are considered to be an important factor in preserving the balance of the intestinal microflora. Their antibiotic action on susceptible bacteria is supplemented with cytotoxicity for several pro- and eukaryotic cells. The large bowel is a natural site of their action. Besides of enhancing oxidoreductive activity of leukocytes in vitro, colicins are also believed to influence inflammatory reaction in vivo. For these reasons, the first part of the present work was concerned with studying colicinogeny in nonspecific inflammatory bowel diseases (IBD). No significant difference has been found out in colicinogeny between a total of 93 IBD-related and 160 healthy controls. In testing leukocyte migration inhibition, colicins of autologous E. coli were used as antigens. The migration index out of normal range showed 36% patients with ulcerative colitis (5/14), 80% patients with Crohn's disease (12/15), and only one clinically healthy control subject (1/16; 6%). The obtained results are considered to be proof of cellular hypersensitivity of IBD patients to colicins of their own E. coli strains. In several colicins the antitumorous effect has been reported in both the in vitro and in vivo experimentation. The second part of this work was concerned with colicinogeny in colorectal cancer. Colicinogenic E. coli were evidenced in 42 subjects (40%) from 105 patients with colorectal carcinoma. Controls showed colicinogenic E. coli in 102/160 clinically healthy subjects (64%), and the difference was as significant as p less than 0.05. In colorectal cancer group, the subjects with proved colicinogeny showed lesser amounts of colicinogenic E. coli strains in contrast with non-colicinogenic ones. In colorectal cancer patients with colicinogenic E. coli strains, B and M colicins were of most frequent occurrence in them no antitumorous effect has been experimentally stated. If changes of colicinogeny were only either the manifestation or consequence of tumor disease, so both the presence or absence of colicinogenic E. coli would have been dependent of clinical patients's condition, stage of disease (in accord with Dukes) or correlated with the tumor markers. For these accounts, a total of 28 colorectal cancer patients underwent a colicinogenic study. However, no colicinogeny dependence was evidenced of either clinical condition or Dukes stage, showing no correlation with any of cancer markers investigated (carcinoembryonic antigen, CA 19-9, alfa-1-fetoprotein, alfa-1-orosomucoid, Cancer serum index, sialic acid, lysozyme).(ABSTRACT TRUNCATED AT 400 WORDS)

Crohn's disease is a disease with unknown etiology of which immunological mechanisms participate. As standard treatment is sometimes ineffective, in 15 patients therapeutic plasmapheresis was used. Before plasmapheresis and immediately after it some immunological parameters were assessed. In the serum a significant drop of all immunoglobulins of the basic classes was recorded: (P less than 0.05) and of circulating immunocomplexes (P less than 0.02). Marked clinical improvement was observed in three patients, which as compared with data in the literature, is somewhat less. The cause is in the author's opinion in the selection of patients (plasmapheresis is usually most successful in patients with marked activity of the disease and non-intestinal symptoms) even in case of less active plasma exchange. Despite this plasmapheresis can be recommended in patients with a poor response to common conservative treatment and in some of them we may expect a marked therapeutic effect with a favourable influence on the prognosis of the disease.

In the literature it is maintained that phenol and p-cresol are produced in humans in the gut by bacteria from dietary protein. Both substances are absorbed from the small intestine and excreted in the urine. If the urinary output of phenol and p-cresol depends really on the dietary protein intake it should decline to zero values during fasting and correlate with the protein supply into the gut. The objective of the present work was therefore to investigate the urinary phenol and p-cresol excretion in fasting obese subjects (21 fasting subjects, 7 subjects with modified fasts--Nutramine R-350) and in subjects treated by complete enteral nutrition by a nasojejunal tube (8 patients with Crohn's disease, 8 with another disease of the gastrointestinal tract). Phenol and p-cresol in 24-hour urine specimens were assessed by gas chromatography in all four groups always on the 1st, 7th and 14th day. In fasting obese subjects the phenol and p-cresol values did not decline (the difference of values from the assumed zero value is significant z = 0.000055). There was no difference between patients with a complete and modified fast. The phenol and p-cresol values did not correlate mutually, nor with the protein intake, nitrogen balance and cumulated nitrogen balance. There are great individual differences in the urinary phenol and p-cresol excretion and it does not depend on the oral dietary protein intake, as hitherto assumed. It has most probably more complex causes and the decisive factor seems to be the metabolic activity of the intestinal bacterial microflora.

The authors evaluate clinical experience based on a correlation between the clinical condition and the finding of Campylobacter pylori (CP) in a total of 1027 specimens of the gastric mucosa. They confirmed the high incidence of CP in patients with a fresh duodenal ulcer (g 7%) but also in the inactive stage of duodenal ulcer disease (97.8%) and in patients with a pyloric ulcer (94.4%). An analogous incidence of CP in patients with so-called isolated duodenitis (in the course of the disease no ulcer lesion was ever detected), i.e. in 95.5%, indicates the relationship of this condition with peptic ulcer disease. The authors indicate diagnostic possibilities as regards CP infection by cultivation, rapid urease tests and microscopic examination and they emphasize the practical value of urease tests. Based on their own experience the authors confirm the high eradication effect of bismuth preparations, in particular bismuth subsalicylate and colloid bismuth subcitrate.

The leukocyte migration inhibition test was performed in 39 patients with Helicobacter pylori infection and in 38 patients without such infection. The culture of Helicobacter pylori was used as antigen. A highly significant inhibitory effect on leukocyte migration was found in patients with Helicobacter pylori infection. The results can be taken as proof of a systemic immune response to helicobacters at the cellular level in patients with Helicobacter pylori infection.

There are several indirect arguments for a possible role of colicins in chronic inflammatory bowel disease (IBD). Colicinogeny was therefore investigated in 54 patients with ulcerative colitis, 39 patients with Crohn's disease, and 160 clinically healthy controls. No significant difference was found among the examined groups. The leukocyte migration inhibition test (with colicins as antigens) was performed to estimate cellular hypersensitivity to colicins. Migration indices not exceeding the normal range in controls contrasted with abnormal values found in 36% of ulcerative colitis and 80% of Crohn's disease patients. The results are believed to be proof of cellular hypersensitivity of IBD patients to colicins of their own Escherichia coli strains. The importance of this finding must be further clarified.

Colicins, bacteriocins of Escherichia coli and related bacteria of Enterobacteriaceae family, form a very heterogeneous group of antibiotically active substances of proteinaceous material. Antitumorous effect of colicins have also been demonstrated experimentally. The large bowel has been found to be a site of their native action. Therefore, our work has been aimed at investigating colicinogenicity in patients with colorectal carcinoma. From a total number of 77 patients with colorectal carcinoma, colicinogenic Escherichia coli was found in 32 persons (41.6%), whereas from a total of 160 control clinically healthy persons, colicinogenic Escherichia coli was found in 102 persons (63.8%). The difference is statistically significant (p less than 0.05). The absence of colicinogenic Escherichia coli may be one of the factors contributing to the origin and development of colorectal carcinoma in some of the patients studied. Studies of patients with adenomatous polyps, members of colon cancer families, and large prospective studies of the general population will be necessary to prove this hypothesis.