Biomedical subjects

Mario Rizzetto

Publications and source records attributed to Mario Rizzetto.

75 records · Page 5Linked to original sources

PubMed2002

Efficacy of lamivudine in HBeAg-negative chronic hepatitis B.

Hepatitis B e antigen (HBeAg)-negative chronic hepatitis B results from infection with hepatitis B virus mutants unable to produce HBeAg. It accounts for 7-30% of patients with chronic hepatitis B virus (HBV) worldwide, with the highest rates reported for Mediterranean Europe and Asia. Interferon (IFN) is currently the only approved therapy for these patients, but it has an unfavorable tolerance profile and limited efficacy. Studies show that responses to IFN are lower in HBeAg-negative than in HBeAg-positive patients; joint HBV DNA loss/ALT normalization is obtained in 38-59% of HBeAg-negative patients treated for 4-24 months with a high rate of virological relapse (54-87%), at 6-24 months posttreatment. Lamivudine is a nucleoside analogue with potent antiviral properties against HBV. Studies show that response rates in HBeAg-negative and HBeAg-positive patients are equivalent. After 12 months of treatment, 65-96% of HBeAg-negative patients have joint HBV DNA loss/ALT normalization, although 48-74% of patients relapse within 1 year posttreatment. 60% of patients have histological improvement after 12 months of treatment. Lamivudine is well tolerated with a safety profile equivalent to that of placebo. The incidence of YMDD variants increases with extended lamivudine treatment, present in up to 57-64% of patients after 2 years. Their clinical impact is unclear; some studies show breakthrough infection associated with their emergence, whereas other studies show maintained response to lamivudine. Lamivudine has benefits over IFN in its safety and efficacy profile in this patient group. Extended lamivudine treatment beyond 2 years is an option, but further investigation is required to define stopping criteria and the impact of YMDD variants.

Antiviral Agents↗

PubMedDate not supplied

Association of Helicobacter pylori infection with ischemic stroke of non-cardiac origin: the BAT.MA.N. project study.

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection has been associated with several vascular obstructive disorders. The infection induces the production of proinflammatory cytokines that could increase platelet aggregates in circulation. The aim of this case-controlled study was to evaluate the prevalence of H. pylori infection in patients with acute ischemic stroke not related to cardiac causes. METHODOLOGY: A group of 80 consecutive patients (58 males, age range: 49-65 years) with acute ischemic stroke was studied. All patients received a cranial CT and/or brain magnetic resonance imaging scan, extracranial vessel duplex ultrasonography, and transthoracic echocardiography. H. pylori infection was diagnosed by means of both 13C urea breath test and IgG antibodies to H. pylori. A group of 320 blood donors (232 males and 88 females, age range: 49-65 years) matched for sex and age served as controls. Among the patients, we investigated the presence of hypertension, cholesterol and glucose levels in serum, fibrinogen in plasma and the smoking habit. RESULTS: The presence of H. pylori infection was higher in patients than in controls: 64/80 (80%) versus 190/320 (59.4%) (P < 0.001); when analyzed for sex in 45/58 (77.5%) among male patients and in 139/232 (59.9%) among controls (P < 0.05); of the females 19 out of 22 (86.3%) patients were infected at variance with only 51/88 (57.9%) of the controls (P < 0.05). Classical risk factors for stroke did not differ among patients with and without H. pylori infection. H. pylori infection was not differently associated with current smoking, serum total cholesterol and glucose levels, fibrinogen value in plasma and hypertension when compared to the H. pylori-negative status. CONCLUSIONS: H. pylori infection appears to be significantly more frequent in middle-aged patients with acute ischemic stroke than in controls.

Aged↗

PubMedDate not supplied

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia.

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.

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