Drugs online research references









Am J Gastroenterol. 1998 May;93(5):732-6.
Treatment of gastric MALT lymphoma by Helicobacter pylori eradication: a study controlled by endoscopic ultrasonography.

Nobre-Leitao C, Lage P, Cravo M, Cabecadas J, Chaves P, Alberto-Santos A, Correia J, Soares J, Costa-Mira F.

Servico de Gastrenterologia, Centro de Investigacao em Patobiologia Molecular, Departamento de Patologia Morfologica, Instituto Portugues de Oncologia Francisco Gentil, Lisboa.

OBJECTIVE: Previous studies have demonstrated a link between Helicobacter pylori infection and low grade B-cell gastric MALT lymphoma. The aim of this study was to evaluate the effect of Helicobacter pylori eradication in 17 patients with low grade B-cell gastric MALT lymphoma stage EI. METHODS: For disease staging EUS and CT scan were systematically performed. Eight patients were excluded from the present series because stage EII disease was diagnosed. To demonstrate B-cell monoclonality, immunohistochemistry and polymerase chain reaction were used. H. pylori eradication was performed with triple therapy. RESULTS: H. pylori was eradicated in all patients after first (n = 15) or second line (n = 2) treatment. Histologic regression of lymphoma was observed in all patients after a median period of 2 mo. Disappearance of monoclonality according to polymerase chain reaction took significantly longer (7 mo). At the end of the study, four of 16 patients still exhibited persistent monoclonal bands. Relapse of lymphoma occurred in two patients associated with H. pylori reinfection/recrudescence. CONCLUSION: Eradication of H. pylori seems to be an effective therapy in patients with stage EI gastric MALT lymphoma, although long-term results are still uncertain. Endoscopic ultrasonography is useful for a more accurate staging of the disease. The clinical significance of detecting monoclonality by polymerase chain reaction remains to be determined.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9625118&dopt=Abstract

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Farmaco. 1996 Aug-Sep;51(8-9):569-77.
Quinoxaline chemistry. Part 6--Synthesis and evaluation of antiulcer and gastroprotective activity of 2-[arylmethylmercapto-, arylmethylsulfinyl-, piperazinyl-3-R-substituted]quinoxalines.

Piras S, Loriga M, Paglietti G, Demontis MP, Varoni MV, Fattaccio MC, Anania V.

Istituto di Chimica Farmaceutica e Tossicologica dell'Universita di Sassari, Muroni.

Thirty compounds possessing quinoxaline structure bearing either substituted arylmethylmercapto-, arylmethylsulfinyl group or a piperazinyl moiety in position 2 were prepared in order to evaluate an antiulcer and gastroprotective activity in rat pylorus ligature, in comparison with omeprazole and ranitidine at the dose of 100 mg/kg after oral administration. Among the compounds of the first group one third showed a moderate activity being about half potent as omeprazole whereas in the second group compound 5b exibited an activity superior to that of ranitidine accompanied with the lowest incidence of lesions and mortality and another compound (5i) was equiactive as ranitidine.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8930110&dopt=Abstract

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Nippon Rinsho. 1992 Jan;50(1):122-30.
[H2-receptor antagonist-refractory ulcer--its pathophysiology and role of proton-pump inhibitors]

[Article in Japanese]

Arakawa T.

Third Department of Internal Medicine, Osaka City University Medical School.

Among H2-receptor antagonist (H2RA)-refractory ulcers, non-responders that did not heal after 5 months therapy had high intraluminal pH in the basal condition and high sensitivity to inhibition of acid secretion by H2RA but possessed gastric mucosa to generate less prostaglandins. Combination therapy of PGE1-analogue with H2RA healed these ulcers by 60%. Proton-pump inhibitor (PPI) exerted a complete inhibition of acid secretion in these patients and the rate of healing was 88%. Helicobacter pylori was present in the mucosa of all 4 ulcer patients refractory to treatment with PPI. The ulcers healed in 3 out of 4 patients after eradication of H. pylori. It is suggested that PG supplement or complete inhibition of acid secretion is effective for ulcers in H2RA-non-responders. PPI-refractory ulcers may relate to H. pylori infection.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1347325&dopt=Abstract

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