Biomedical subjects

Leokadia Bak-Romaniszyn

Publications and source records attributed to Leokadia Bak-Romaniszyn.

8 recordsLinked to original sources

PubMed2006

Potential role of LPS in the outcome of Helicobacter pylori related diseases.

In this study we asked a question whether H. pylori LPS with or without LewisXY (Le) determinants as well as LBP (lipopolysaccharide binding protein) and sCD 14 molecules recognizing bacterial LPS may be involved in atherogenesis. Sera from 57 patients with coronary heart disease (CHD), 27 H. pylori infected dyspeptic patients-H.p.(+) and 49 healthy controls (HC) were tested for IgM and IgG to H. pylori LPS expressing LeX (LPS LeX) or LeXY (LPS LeXY) determinants and to a glycine acid extract (GE). Immune complexes (ICs) of Lewis antigens and specific IgM or IgG were also determined. The prevalence of anti-GE IgG and IgA was significantly higher in CHD as compared to HC and the same as in the H.p.(+) group. The highest levels of anti-GE IgG were detected only for CHD group. CHD patients showed upregulation of IgG to LPS LeX and LeXY. In contrast, an upregulation of IgM to such LPSs was found for healthy subjects. The levels ofLeY-anti-LeY IgG ICs were higher in CHD patients than in healthy controls similarly to the levels of LBP. There was no difference in sCD14 concentration between CHD and HC groups. The results obtained in this study indicate that H. pylori infections may be the risk factors of atherosclerosis due to: 1) an enhanced humoral response to H. pylori surface antigens, 2) a host predisposition to respond to Lewis determinants present in H. pylori LPS by IgG, 3) increased levels of serum LBP.

Acute-Phase Proteins↗

PubMed2004

[Irritable bowel syndrome--pathogenesis, management].

Irritable bowel syndrome creates many diagnostic and treatment difficulties in a general practitioner practice as well as in a specialist practice. Etiopathogenesis of this illness still elicit some controversy. In a diagnostic process, apart from an organic basis excluding, the most important is a medical history of a patient because of the fact that a right symptoms interpretation usually allows a correct diagnosis establishment. A treatment is in its premise a symptomatic treatment, is long-lasting and based on a mutual trust between a doctor and a patient. Basic information concerning this illness is presented in this article.

Antidepressive Agents↗

PubMed2004

[Peptic ulcer disease etiology, diagnosis and treatment].

Authors in this article present etiology, clinical manifestations, diagnostic procedures and treatment of peptic ulcer disease in children and adults. Increased gastric acid output, Helicobacter pylori, NSAIDs and stress are the basic risk factors in peptic ulcer disease. H. pylori infection is a widely known risk factor in peptic ulcer disease and influences diagnostic and treatment procedures. Primary ulcer disease concerns mainly duodenum and is accompanied by H. pylori infection. Gastroscopy and Helicobacter tests are the only reliable procedures to diagnose peptic ulcer disease. Nowadays the most important aim in peptic ulcer treatment is the H. pylori eradication. Therapy with two antibiotics and a protein pomp inhibitor eradicates the bacteria, treats the ulceration and lowers the number of ulcer recurrence. In non-infected H. pylori ulcers or in a long-term treatment protein pomp inhibitors and H2-inhibitors are effective as well in gastroprotective therapy.

Adult↗

PubMed2003

Helicobacter pylori lipopolysaccharide in the IL-2 milieu activates lymphocytes from dyspeptic children.

In this study, we assessed the proliferative response of peripheral blood mononuclear leukocytes (PBML) from 33 children/young adolescents with chronic dyspepsia, to H. pylori LPS in the presence and absence of IL-2 as a T cell growth factor. A rapid urease test (RUT) and a presence of Helicobacter-like organisms (HLO) in the biopsy specimens allowed us to distinguish RUT/HLO-positive (17/33) and -negative (16/33) patients. H. pylori LPS alone induced a proliferation of PBML from 4 out of 33 dyspeptic patients. IL-2 increased the prevalence of the response to LPS to 59% and 74% of RUT/HLO-positive and -negative patients, respectively. PBML from RUT/HLO-positive patients responded significantly less intensively to H. pylori LPS in the presence of IL-2, to IL-2 alone and to H. pylori LPS+IL-2. However, there was no difference in PHA-driven proliferation of PBML from the patients of those two groups. A negative correlation between the responsiveness to H. pylori LPS of PBML and occurrence of type B inflammation in gastric mucosa was demonstrated. The results suggest a contribution of H. pylori LPS to an outcome of H. pylori infection. It is speculated that H. pylori LPS by an activation of immunocompetent cells may reduce gastric inflammation, decrease bacterial load and prolong H. pylori infection.

Adolescent↗

PubMed2003

Serological differentiation of Helicobacter pylori CagA(+) and CagA(-) infections.

Many Helicobacterpylori strains causing gastroduodenal diseases have a cagA gene encoding CagA protein, a virulence factor of these bacteria. Anti-CagA antibodies produced by the majority of people infected with CagA(+) strains can indicate such an infection. In this study, the efficacy of three immunoenzymatic tests for detecting CagA(+) and CagA(-) infections were compared: immunoblot (Milenia ID Blot H. pylori IgG; MB) and ELISA conducted either with a recombinant immunodominant fragment of CagA (rCagA) or the full-length CagA molecule (flCagA). The 13C-urea breath test (13C-UBT) was used for establishing H. pylori status. The serum samples from 157 individuals were used for serodiagnosis. H. pylori CagA(+) infection was detected in H. pylori-infected individuals with similar frequencies by MB (64%) and flCagA-ELISA (60%) and a little less frequently by rCagA-ELISA (53%). There was a high coincidence between the negative results of these three tests for H. pylori-uninfected individuals with no anti-CagA IgG in the serum (96-100%). The results show that rCagA-ELISA and, especially, flCagA-ELISA are easy, inexpensive and useful noninvasive assays for the discrimination of CagA(+) and CagA(-) H. pylori infections in subjects examined by urea breath test.

Adolescent↗

PubMed2002

Detection of specific Helicobacter pylori DNA and antigens in stool samples in dyspeptic patients and healthy subjects.

In this study stool samples from dyspeptic patients and healthy subjects were used for detection of specific Helicobacter pylori antigens and DNA by immunoenzymatic test (PPHpSA) and semi-nested PCR (ureA-PCR), respectively. The H. pylori status was estimated by invasive endoscopy-based rapid urease test and histology or noninvasive urea breath test (UBT), and by serology (ELISA, Western blot). The coincidence of H. pylori-negative invasive tests or UBT and negative antigen or DNA stool tests was very high (mean 95%). The PPHpSA results were found positive for 56% and ureA-PCR for 26% of individuals with H. pylori infection confirmed by invasive tests or UBT. The detection of specific H. pylori antigens and especially DNA in feces is not sufficient as a one-step diagnosis of H. pylori infection.

Adolescent↗

PubMedDate not supplied

[Assessment of the response of peripheral blood mononuclear leukocytes on Helicobacter pylori infection in children].

In the study the proliferative response of peripheral blood mononuclear leukocytes (PBML) from children with chronic dyspepsia (chr. d) to H.p. antigens was investigated. From 38 children aged 7-18, with chr. d., blood was collected just before upper GI endoscopy. Twenty one patients were found to be H.p. (+). PBML were used for the cultures and were stimulated with heat-killed H.p. G27 bacteria, heated and unheated glycine extract (GE) of H.p. G27 or with H.p. LPS containing Lewis X and Lewis Y determinants, in the presence or absence IL-2. The cell proliferation was estimated on the basis of [3H] - thymidine incorporation. In the cultures, the phenotype of responding cells was determined by an EIA with monoclonal antibody to human CD3, CD4 and CD8. PBML from patients H.p. (-), responded to killed H.p. bacteria and to heated GE more frequently and more intensively than PBML from the H.p.(+). IL-2 enhanced PBML response to these antigens. Unheated GE did not induce PBML proliferation even in the cultures with IL-2. LPS alone induced proliferation of PBML from 3 patients (2 H.p. - and 1 H.p.+). However, in the presence of IL-2, LPS induced proliferation of PBML from 15 patients. In the cultures of PBML stimulated with whole bacteria or heated EG, T cells dominated. In the cultures of PBML from H.p. (+) we found a higher percentage of CD8 cells in comparison with the cultures of PBML from H.p. (-). Data demonstrate a significant variation in the response of PBML from dyspeptic children to H.p. antigens.

Adolescent↗

PubMedDate not supplied

[Drug sensitivity of Helicobacter pylori strains in children and young people from the region of Łódź].

Combined therapy with a proton pump inhibitor and two antibiotics (metronidazole, clarithromycin and amoxicillin or tetracycline) is applied in the treatment of H. pylori infection. The effects of the treatment depend on drug sensitivity of H. pylori. Growing resistance to some of the applied antibiotics has been observed. The aim of the study was to assess drug sensitivity of Helicobacter pylori strains which were isolated from the gastric mucosa of children and young people living in the macroregion of Łódź. The study comprised 45 children aged between 5 and 18 years. Biopsy specimens were put on transport medium, incubated in microaerophilic environment, then identified. Drug sensitivity to metronidazole, clarithromycin, amoxicillin and tetracycline was assessed. We found resistance to metronidazole in 18% (8/45) children, resistance to clarithromycin in 16% (7/45) children and resistance to both antibiotics in 4% (2/45) children. No resistance to amoxicillin or tetracycline was noted.

Adolescent↗