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Biomedical subjects

A Tucci

Publications and source records attributed to A Tucci.

At least 37 records · Page 2Linked to original sources
PubMed1998

Weekend therapy for the treatment of Helicobacter pylori infection.

OBJECTIVES: The aim of the present study was to evaluate the efficacy and the safety of a short-term regimen (weekend therapy) in the cure of Helicobacter pylori infection and to analyze the factors that may influence the success of the treatment. METHODS: Seventy-one patients with gastric colonization by a tinidazole sensitive H. pylori strain (34 duodenal ulcer and 37 nonulcer dyspepsia) received omeprazole 40 mg o.m. for 7 days (from Monday to Sunday) and bismuth 240 mg q.i.d. + amoxicillin 1000 mg/q.i.d. + tinidazole 500 mg q.i.d. for only 2 days (Saturday and Sunday). Endoscopy, histology, culture, urease test, and susceptibility studies were done at entry and 30 days after treatment. RESULTS: Successful eradication was obtained in 84% of patients. The percentage of eradication was higher in duodenal ulcer patients (94%) than in those with nonulcer dyspepsia (74%; p < 0.05), and in patients who received the treatment during hot weather (94%) than in those who received the treatment during cold weather (74%; p < 0.05). Side-effects were induced by the treatment in 17% of patients, and these were all not severe, self-limiting, short-lasting, and did not require specific treatment. CONCLUSIONS: These data suggested that weekend therapy with high doses of drugs represents an effective, safe, and inexpensive therapeutic approach for the treatment of H. pylori infection, particularly in patients with duodenal ulcer. Furthermore, they also confirm the relevant role that short-term treatments may play in the therapeutic approach to H. pylori infection, and highlight some important aspects influencing short-term schedules.

Adult↗
PubMed1997

Outbreak of hepatitis C virus infection in patients with hematologic disorders treated with intravenous immunoglobulins: different prognosis according to the immune status.

The influence of immunodeficiency on the course of hepatitis C virus (HCV) infection is still debated, although a worsening effect has been suggested. We compared the characteristics of hepatitis C in two groups of hematologic patients with different levels of immunocompetence who acquired the same virus strain after treatment with contaminated intravenous immunoglobulins (IVIG). Indications for IVIG therapy were idiopathic thrombocytopenic purpura (ITP) in six patients and hypogammaglobulinemia in 7 patients with various hematologic disorders, who were defined immunodeficient (ID). Infection rate was 100%. Five ID patients never developed HCV antibodies despite serum HCV-RNA positivity. The same HCV genotype was shown in 10 patients tested. Moreover, E1-E2 gene partial nucleotide sequencing, performed in four patients, showed identical or closely related amino acid sequences, thus strongly supporting the hypothesis of a common source of infection. Clinical acute infection did not differ significantly between the two groups, but subsequent liver failure developed in five of the seven ID patients and in none of the ITP patients (P = .04). Liver biopsy, performed in three cases, documented HCV as the only cause of liver damage. Six ID patients died, with liver disease being the primary cause of death in four cases and a contributory cause in two cases. Their median survival after IVIG was 12 months, significantly worse than that of ITP patients (P = .0028). We conclude that immunodeficiency markedly worsens the course of IVIG-acquired HCV infection in hematologic patients.

Adult↗
PubMed1997

Detection of serum antibodies to CagA and VacA and of serum neutralizing activity for vacuolating cytotoxin in patients with Helicobacter pylori-induced gastritis.

Thirty patients with dyspepsia, with histological diagnosis of gastritis, and with endoscopic diagnosis of peptic ulcer disease (PUD) (n = 13) or nonulcer dyspepsia (NUD) (n = 17) were admitted to the study. Helicobacter pylori vacuolating cytotoxin-producing strains (Tox+) were isolated from 14 (46.7%) patients, whereas non-cytotoxin-producing (Tox-) H. pylori strains were isolated from the remaining patients. Of 30 patients studied, 20 (66.7%) had serum cytotoxin neutralizing activity in vitro. Fourteen patients with Tox+ H. pylori strains showed serum cytotoxin neutralizing activity and serum immunoglobulin G (IgG) and IgA antibodies reactive with both 87-kDa H. pylori vacuolating cytotoxin (VacA) and 128-kDa cytotoxin-associated gene product (CagA) by immunoblotting using native enriched preparations of VacA and CagA proteins from H. pylori culture supernatants as the antigens. A 94-kDa antigen cross-reacting with the 87-kDa VacA protein could be demonstrated in culture supernatant with immune sera from humans and animals. All patients (n = 10) lacking serum neutralizing activity were also negative for IgG or IgA against VacA antigen, whereas 6 of the 10 patients showed IgG serum antibody responses against CagA antigen. The prevalence of antibodies to VacA and CagA antigens was significantly (P < 0.001) higher in patients with gastritis (20 and 26 patients for VacA and CagA, respectively, of 30 patients) than in H. pylori culture-negative controls (0 of 27 for both VacA and CagA) and in randomly selected blood donors (17 and 21 for VacA and CagA, respectively, of 120 subjects). All patients with PUD had antibodies to CagA, whereas 13 of 17 (76.5%) patients with NUD had anti-CagA antibodies. Serum IgG antibodies to VacA were present in 9 (69.2%) patients with PUD of 13 patients and in 11 (64.7%) patients with NUD of 17 patients. Anti-CagA antibodies seemed to correlate better with PUD than anti-VacA antibodies.

Adult↗
PubMed1996

A case of hypereosinophilic syndrome is associated with the expansion of a CD3-CD4+ T-cell population able to secrete large amounts of interleukin-5.

Interleukin-5 (IL-5) is the major soluble factor able to mediate hypereosinophilia. We report a case of hypereosinophilic syndrome in which the presence of a population of CD3-CD4+ cells able to overproduce IL-5 was shown. The lack of CD3 and TCRAB membrane expression on otherwise phenotypically normal mature T lymphocytes together with the absence of detectable TCRBV mRNA and clonal rearrangement of TCRB gene suggested that the abnormal lymphocyte population was the expression of a peripheral T-cell lymphoma with an indolent clinical course. Peripheral blood lymphocytes enriched in this population were able to secrete high levels of IL-5 but not IL-4, and no IL-2 or interferon-gamma, when stimulated in vitro with phytohemagglutinin and phorbol myristate acetate. The serum contained eosinophil survival factors whose activity was partially neutralized by a specific antihuman IL-5 antibody. This observation further emphasized the relationship between hypereosinophilic syndrome. IL-5, and T-cell lymphoproliferative disorders.

Aged↗
PubMed1996

Value of serology (ELISA) for the diagnosis of Helicobacter pylori infection: evaluation in patients attending endoscopy and in those with fundic atrophic gastritis.

In the present study we assessed the diagnostic accuracy of four commercial IgG enzyme-linked immunosorbent assay (ELISA) kits (Autoplate, H.pylori-EIA-Well, Enzygnost, Helori-test) and evaluated the performance of these tests in patients with fundic atrophic gastritis. Serum antibodies to Helicobacter pylori were measured in 70 out-patients attending endoscopy for dyspepsia and 43 patients with non-autoimmune fundic atrophic gastritis. Using the cut-off values recommended by the manufacturers, and comparing serological findings with gastric biopsy results of dyspeptic out-patients attending endoscopy, the four kits showed a sensitivity and specificity, respectively, of 91% and 96%, for Autoplate, 67% and 100% for H.pylori-EIA-Well, 79% and 100% for Enzygnost, and 81% and 96% for Helori-test. Evaluation in patients with atrophic gastritis revealed a high prevalence of antibodies to Helicobacter pylori (84%) and it demonstrated that patients with and those without gastric colonization by this microorganism had a similar rate of seropositivity (76-84% vs 50-78%). In conclusion, our data demonstrate that: a) this assay is a reliable and valid method to detect gastric colonization by Helicobacter pylori; b) positive serum antibody associated with a negative detection of Helicobacter pylori in the gastric mucosa suggests mucosal atrophy; c) patients with fundic atrophic gastritis should be excluded from studies investigating the value of serology in diagnosing Helicobacter pylori infection.

Adult↗
PubMed1994

Evaluation of two therapeutic regimens for the treatment of Helicobacter pylori infection.

In the present study we evaluated the efficacy and tolerability of two different therapeutic schedules in eradicating Helicobacter pylori. Forty-six consecutive patients (suffering from either peptic ulcer or non-ulcer dyspepsia) with helicobacter pylori infection were randomly allocated to one of the following two groups: group 1 (n = 23) 2 weeks of treatment with bismuth subcitrate tablets (120 mgx4) + amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4); group 2 (n = 23) 2 weeks of treatment with amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4). Endoscopy, histology and bacterial culture were performed at entry, and 30 and 90 days after treatment. Two group 1 patients and one group 2 patient did not complete the treatment. Successful eradication was obtained in 20/21 (95%) patients treated with triple therapy (group 1) and in 17/22 (77%) patients treated with double therapy (group 2) (p = 0.2). Side-effects occurred in 9/21 (43%) patients of group 1 and in 9/22 (41%) patients of group 2 (p = 0.9). These were all self-limiting and required no specific treatment. These data suggest that combined therapy with amoxycillin and metronidazole, with or without bismuth subcitrate, represents a safe and effective therapeutic approach for the treatment of Helicobacter pylori infection. In our series, triple therapy determined a numerically higher eradication rate than double therapy.

Adult↗
PubMed1993

Occurrence of a silencer of the interleukin-2 gene in naive but not in memory resting T helper lymphocytes.

In the immune system the first activation of a naive T cell by antigen is a key step in the shaping of the peripheral T cell specificity repertoire and maintenance of self-tolerance. In the present study, analysis of the interleukin-2 (IL-2) gene activation shows that naive human helper T cells (cord blood CD4+ T cells, adult CD4+CD45RO- T cells) regulate IL-2 transcription by a mechanism involving both a silencer and an activator acting on the purine-rich IL-2 promoter elements (NF-AT binding sites). By contrast, memory cells, either in vitro activated helper T cells reverting to a resting state, or CD4+ T (memory) clones, or CD4+CD45RO+ T cells isolated ex vivo, no longer have a silencer. Their IL-2 transcription seems to be controlled solely by the transition from inactive to active functional state of a positive transcription factor binding to these promoter elements as well as its cytoplasmic or nuclear location: in resting memory T cells the activator is located in the cytoplasm and is inactive, whereas in stimulated cells it is functional in promoting transcription and now resides in the nucleus. Thus, the regulation of the gene coding for the main T cell growth factor changes irreversibly after the first encounter of T cells with antigen. It is most likely that the presence of a silencer contributes to the more stringent activation requirements of naive CD4+ T cells.

Cell Compartmentation↗
PubMed1993

One-day therapy for treatment of Helicobacter pylori infection.

The present study evaluated the effect of a one-day high-dose combined therapy on Helicobacter pylori infection. Thirty-two consecutive patients (suffering from either peptic ulcer or nonulcer dyspepsia) with Helicobacter pylori infection received omeprazole (40 mg) + bismuth subcitrate (240 mg x 4) + amoxicillin suspension (2000 mg x 4) + metronidazole (500 mg x 4), for only one day. Endoscopy, histology, culture, and susceptibility studies were done at entry and 30 and 90 days after the treatment day. Successful eradication was obtained in 23/32 (72%) patients and gastritis had resolved in 95% of these. Side effects were induced by the treatment in 6/32 (19%) patients, but these were all self-limiting, short-lasting, and did not require any specific treatment. Development of bacterial resistance to metronidazole occurred in 6/9 (67%) non-eradicated patients. These data suggest that one-day treatment with high doses of amoxicillin, metronidazole, bismuth, and omeprazole represents an effective, safe, and inexpensive therapeutic approach for the treatment of H. pylori infection.

Adult↗
PubMed1992

Effects of eleven cytokines and of IL-1 and tumor necrosis factor inhibitors in a human B cell assay.

The effects of different recombinant human cytokines and cytokine inhibitors were compared in a culture system in which cell contact with mutant EL-4 thymoma cells of murine origin efficiently stimulates human B cell proliferation and Ig secretion in conjunction with human T cell supernatant. IL-1 alpha, IL-1 beta, TNF-alpha, and IL-2 co-stimulated B cell proliferation and IgM, IgG, and IgA secretion, whereas IL-3, IL-4, IL-5, IL-6, IFN-gamma, or GM-CSF had weak or no activity in this regard. In contrast, TGF-beta 1 was strongly inhibitory. A very strict hierarchy of cytokine interactions was found in that IL-1 was necessary to induce TNF-alpha responsiveness, and TNF-alpha the IL-2 responsiveness, of the B cells. Most likely the small number of starting B cells in the present assay (300 FACS-separated B cells/200 microliters) minimized the effects of autocrine B cell factors. IL-4 together with IL-1 induced IgE secretion, and the IgE secretion was further increased by TNF-alpha. IFN-gamma had no modulatory effect on the IL-4 dependent IgE response in this system. Pretreatment of B cells with IL-1R antagonist (IL-1ra, which binds to IL-1R) or addition of soluble TNF receptor type 1 (sTNF-R55, which binds to TNF) completely inhibited the IL-1 or TNF-alpha effects, respectively. This occurred in a specific manner; the inhibition was reversed by a large excess of cytokine. IL-1ra also inhibited a B cell response induced by PMA-preactivated EL-4 cells alone. Because B cells responding to such preactivated EL-4 cells did not acquire TNF-alpha responsiveness, no IL-1 was apparently involved under this assay condition. It appears, therefore, 1) that IL-1ra can act on B cells and 2) that this antagonist may not only block IL-1R, but may provide a direct or indirect inhibitory signal interfering even with IL-1-independent B cell activation.

B-Lymphocytes↗
PubMed1992

Excimer laser photorefractive keratectomy in high myopia. A multicenter study.

Excimer photorefractive keratectomy was performed at three centers on 16 highly myopic eyes (8 diopters [D] or more) and followed up for 6 months. Ablation depths ranged from 137 to 230 microns. The preoperative spherical equivalent of myopia ranged from -8.62 D to -14.50 D (mean +/- SD, -11.57 +/- 1.62 D). Six months after surgery, the mean refraction (spherical equivalent) was -0.90 +/- 2.13 D. Eleven of 16 eyes achieved refractions within 2 D of that attempted. All eight patients at one site were treated with a maximum-beam diameter of 6.0 mm and were corrected to within 2 D of that attempted, and all were 20/40 or better uncorrected. Three of eight eyes at the other two sites were treated with a 5.5- or 5.6-mm maximum-beam diameter, which achieved corrections within 2 D of that attempted. The epithelium healed within 3 to 4 days, and there were no erosions. Mild subepithelial reticular haze, similar to that seen with excimer photorefractive keratectomy for lower myopia, was seen in all patients, with two patients experiencing more significant corneal haze. This peaked at 3 to 6 weeks and then gradually diminished. All but two patients had a return of their best corrected preoperative visual acuity to within one Snellen line at 6 months. This preliminary study shows excimer photorefractive keratectomy to be a promising surgical treatment for patients with higher myopia.

Adult↗
PubMed1992

Self tolerance to human A and B histo-blood group antigens exists at the B cell level and cannot be broken by potent polyclonal B cell activation in vitro.

It is generally considered that tolerance to self antigens is less complete in B than in T lymphocytes. However, B cell tolerance through either functional inactivation (anergy) or clonal deletion has been demonstrated in transgenic mice. In the present study, we investigated whether B cells specific for self A/B histo-blood group antigens can be detected in normal humans. It is a key feature of the ABO system that all normal individuals make natural antibodies against those A or B carbohydrates which are not present in their organism. To detect B cells by the limiting dilution approach we used a specific enzyme-linked immunosorbent assay for the quantitation of anti-A/B antibodies, and a culture system in which polyclonal B cell activation occurs through cell contact with EL4 thymoma cells. As was reported for other B cell studies, we frequently detected "polyreactive" immunoglobulin (Ig)M (but not IgG) with apparent autoreactivity but of uncertain significance regarding physiologic conditions. However, A- or B-specific B cell responses occurred with selective patterns in agreement with classical blood group serology in 14 individuals with A, B, AB or 0 blood group phenotypes: 1/11,600 B cells made anti-allo A/B IgM and 1/26,500 B cells such as IgG, while only 1/104,000 B cells apparently made anti-self A/B IgM and 1/350,000 B cells such as IgG. This shows self tolerance at the B cell level. Since anergy of B cells can frequently be broken by polyclonal B cell activation in vitro, and EL4 cells are potent B cell stimulators, the present results argue for either a highly resistant anergic state or for clonal deletion of self-A/B histo-blood group-specific human B cells.

ABO Blood-Group System↗
PubMed1992

Helicobacter pylori infection and gastric function in patients with chronic idiopathic dyspepsia.

Helicobacter pylori infection, histological features of the gastric mucosa, and gastric motor and secretory functions were evaluated in 45 consecutive patients with chronic idiopathic dyspepsia. H. pylori infection was found in 60% of dyspeptic patients, compared with 33% of 15 healthy controls (P = 0.1). No difference was detected in basal or stimulated gastric acid secretion between dyspeptic patients and healthy controls. Gastric emptying was significantly (P less than 0.01) delayed in dyspeptic patients compared with healthy controls when standardized for age and sex. Delayed gastric emptying was associated with a low frequency of H. pylori infection, female gender, and young age. Epigastric pain or burning and postprandial fullness were, respectively, more severe in patients with H. pylori infection (P less than 0.02) and in those with delayed gastric emptying (P less than 0.01). These findings support the existence of separate subsets of patients with chronic idiopathic dyspepsia. Despite the presence of overlaps, there appear to be partially different functional derangements and clinical features in different subgroups of dyspeptic patients.

Adult↗