[Double-blind clinical experiences with a new anti-rheumatic drug: ibuprofen. Gastroscopic and gastrobioptic study of cases of drug intolerance].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Pallone.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Helicobacter pylori-induced gastric inflammation is thought to be largely regulated by cytokines. PATIENTS AND METHODS: The expression of interferon-gamma, interleukin-12, interleukin-4, interleukin-10, interleukin-8, and interleukin-17 mRNA was examined on gastric mucosal samples from 24 children by semiquantitative reverse transcription polymerase chain reaction and southern blotting. Biopsy-based tests, serology, and urea 13C breath test were used to assess Helicobacter pylori status. Gastric biopsies were also evaluated for bacterial density, chronic inflammation, and acute inflammatory activity. RESULTS: Interferon-gamma, interleukin-12, interleukin-8 and interleukin-17 expression was higher in Helicobacter pylori-infected (n=13) than uninfected (n=11) children. Conversely, interleukin-4 and interleukin-10 expression did not differ between Helicobacter pylori-infected and uninfected children. In Helicobacter pylori-infected children, interferon-gamma, interleukin-12, interleukin-8 and interleukin-17 expression correlated with bacterial density, and Interferon-gamma and interleukin-12 expression with chronic inflammation score. CONCLUSIONS: The findings of this study indicate that, in children, Helicobacter pylori-induced inflammatory response would favour production of proinflammatory cytokines and development of cell-mediated immunity, namely Th1 response.
The aetiology of Crohn's disease is unknown and, therefore, no curative treatments are currently available. Crohn's disease treatment requires knowledge of several variables affecting patient's responsiveness including: characteristics of the disease and of the host, as well as the specific purposes of treatment and the characteristics of the effective drugs. Currently available drugs for active Crohn's disease include: a) old drugs (oral/topical salicylates, conventional steroids); b) old drugs with a new face (immunosuppressives, antibacterial drugs); c) new drugs (budesonide, anti-cytokines/cytokines, probiotics). Among the old drugs, corticosteroids (1 mg/kg) are the most effective, with a 65-85% induction of remission, when compared to high dose sulphasalazine (3-5 g/day) (12%) and 5-aminosalicylic acid (4 g/day) (25%). The following drugs represent current treatment modalities in steroid/refractory active Crohn's disease. Immunosuppressives, including azathioprine (2-2.5 mg/kg) and 6-mercaptopurine (1-1.5 mg/kg) are less effective than steroids (30-40% vs 65-85%), but in chronic active Crohn's disease they show a 76% "steroid-sparing" effect and 63% fistula closure. The reported efficacy of methotrexate (25 mg/kg) and cyclosporine A in fistulous Crohn's disease needs to be confirmed. Antibiotics, such as metronidazole and ciprofloxacin (1 g/day) are effective in perianal or colonic active Crohn's disease. Budesonide, a steroid with low systemic absorption, shows an efficacy comparable to prednisone in active small bowel Crohn's disease. Bowel rest and enteral feeding are effective in active Crohn's disease. To summarize, conventional steroids still represent the most effective drugs in active Crohn's disease. However, refractory disease, steroid-dependence, drug-side effects and/or complications may require two main alternative management strategies: a) surgical resection in localized or primary Crohn's disease; b) alternative drugs in extensive or recurrent Crohn's disease.
The evidence of a beneficial role of antibacterial drugs in Crohn's disease is largely empirical. Data accumulate to show that these drugs may well be used as an adjunctive therapy to oral anti-inflammatory drugs. Circumstantial evidence has also been provided that antibacterial drugs are effective in relieving symptoms related to bacterial overgrowth and when used for specific indications such as perianal lesions.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.