Drugs online research references









Rev Esp Enferm Dig. 1995 Apr;87(4):281-7.
[Course of histological lesions of the gastric mucosa after eradication of H. pylori in patients with duodenal ulcer. Initial study and 6-month follow-up]

[Article in Spanish]

Gisbert JP, Boixeda D, Alvarez Baleriola I, Redondo C, De Rafael L, Martin de Argila C, Hernandez Ranz F.

Servicio de Gastroenterologia, Hospital Ramon y Cajal, Madrid.

Helicobacter pylori is the major etiologic agent of chronic active gastritis, and it may be isolated from the gastric mucosa in a high proportion of patients with duodenal ulcer. AIM: To study, in duodenal ulcer patients, the histological changes associated with H. pylori infection in gastric antrum and body, and the improvement of such lesions after eradication, at an early stage and after 6 months. METHODS: 76 patients with duodenal ulcer disease were investigated prospectively. Biopsy specimens taken by endoscopy from the duodenal bulb, antrum, body and gastric fundus were analyzed by microbiological and histological methods. A patient was considered to be H. pylori-positive when microbiology or/and histology demonstrated colonization in any of the locations. An endoscopy with biopsy samples from the antrum and gastric body was performed 1 month after therapy and 4 months later. Different therapy regimens were used: amoxicillin/clavulanic plus omeprazole or ranitidine; triple therapy; and omeprazole or ranitidine alone. RESULTS: All patients were positive by microbiology. Eradication was reached as a whole in 47% (N = 36). In those patients, in gastric antrum, rates of chronic gastritis/chronic active gastritis previous to treatment and 2 and 6 months later were 100%/96%; 38%/23% and 16%/5.6% respectively. At gastric body they were: 54%/38%; 12%/12% and 12%/5.6% respectively. A favourable histologic evolution, globally and of the acute inflammatory component, was observed 1 month after therapy (p < 0.001). Six months later, there was further improvement which did not reach a statistically significant difference compared with the results obtained at the first month. No differences were observed when eradication failed. CONCLUSION: An improvement of antral and gastric body gastritis is associated with H. pylori eradication in duodenal ulcer patients. This successful evolution is observed immediately after eradication, and it is confirmed six months after the diagnosis.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7794634&dopt=Abstract

note: kwd match prilosec online literature





Am J Gastroenterol. 1997 Jun;92(6):1005-11.
Relation of lactoferrin levels in gastric mucosa with Helicobacter pylori infection and with the degree of gastric inflammation.

Nakao K, Imoto I, Ikemura N, Shibata T, Takaji S, Taguchi Y, Misaki M, Yamauchi K, Yamazaki N.

Third Department of Internal Medicine, Mie University School of Medicine, the National Tsu Hospital, Japan.

OBJECTIVES: Lactoferrin (Lf) is an iron-binding glycoprotein present in milk, lacrimae, saliva, and gastroduodenal secretions. In vitro studies disclosed contradicting results regarding the relation of Lf with Helicobacter pylori (HP) infection. This study aimed to investigate the relationship between the gastric mucosal concentration of Lf and HP infection of the stomach. The relationship of the gastric mucosal level of Lf with the gastric mucosal concentration of interleukin-8 (IL-8) and with the intragastric ammonia levels was also assessed. In addition, the gastric mucosal Lf levels before and after irradication of HP infection were also evaluated. METHODS: This study was composed of 27 HP-positive and 12 HP-negative patients with chronic gastritis. Gastric mucosal biopsy specimens were obtained from all subjects by endoscopy, and the degree of histological inflammatory changes were assessed according to the Sydney system. The gastric mucosal levels of Lf and IL-8 were measured by immunoassays. Assessment of the effect of therapy on the gastric mucosal level of Lf was performed in 10 patients with HP-associated duodenal ulcer. RESULTS: Lf, IL-8, and ammonia levels were significantly higher in patients with HP-positive gastritis compared with those with HP-negative gastritis in both the antrum and the gastric body. Histologically, the degree of inflammatory changes correlated significantly with the Lf levels in the gastric mucosa. Furthermore, the degree of HP colonization was more significant in biopsy samples from the antrum than in those from the corpus of the stomach. The gastric mucosal levels of Lf and IL-8 correlated significantly in the antrum and the gastric body. The ammonia intragastric level significantly correlated with the mucosal Lf level in the antrum and in the gastric body. Therapy significantly decreased the Lf levels in the gastric mucosa of the antrum (p < 0.005) and the gastric body (p < 0.005). CONCLUSION: The results of the present investigation showed, for the first time in vivo, that Lf concentration is increased in the biopsy specimens of patients with HP-related gastritis, and that the levels of Lf correlate significantly with the degree of inflammation of the gastric mucosa. The gastric mucosal level of Lf may constitute an excellent marker of HP infection.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9177520&dopt=Abstract

note: kwd match prilosec online literature





Biochem Biophys Res Commun. 1995 Apr 17;209(2):474-82.
Evidence for the ligand-independent activation of the AH receptor.

Lesca P, Peryt B, Larrieu G, Alvinerie M, Galtier P, Daujat M, Maurel P, Hoogenboom L.

Laboratoire de Pharmacologie-Toxicologie, INRA, Toulouse, France.

Benzimidazole derivatives are potent inducers of CYP1A1 in rabbit and human hepatocytes, but apparently do not bind the AH receptor. To resolve this paradoxical behaviour, studies have been concerned with the question of whether an alternative ligand-independent mechanism could explain the activation of the AH receptor. From experiments in cultured rabbit hepatocytes we show that benzimidazoles bind early and transiently to an unknown protein. Moreover, they are able to deplete the AHR in a time- and dose-dependent manner. In contrast, benzimidazoles are unable to induce CYP1A1 mRNA in mouse hepa-1 cells and to deplete the high-affinity AHR form from these cells. Taken together these data suggest that a signal transduction pathway, similar to that involved in the ligand-independent activation of steroid receptors, could only activate the low-affinity forms of AHR as those existing in rabbit and human cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7733914&dopt=Abstract

note: kwd match prilosec online literature














Herbs and Pharmaceuticals Online || Hair Million herbal formula for hair loss and hair growth || Antibiotics and prescription medications online literature ||