GastroPanel® test for non-invasive diagnosis of atrophic gastritis in patients with dyspepsia.

AIM: Atrophic gastritis (AG), first step in the cascade leading to gastric adenocarcinoma, is related to Helicobacter pylori (H. pylori) infection. Currently, the gold standard for the diagnosis of AG is esophagogastroduodenoscopy (EGD) with histological examination of the biopsy specimens. However, since the latter are taken in random order and the distribution of AG is often patchy, histology is only representative of mucosal status. Considering this limitation, a test named GastroPanel®, that measures the blood concentrations of pepsinogen I and II, gastrin-17 and H. pylori antibodies, has been developed as a potential non-invasive biopsy. Aim of this study has been to assess the accuracy of GastroPanel® in patients with AG. METHODS: Forty-seven dyspeptic patients (24 males, mean age 52.2±9.3 years), in follow-up for antral or diffuse AG, were enrolled. All underwent at least two EGDs with random biopsies and blood collection for GastroPanel® parameters examination. RESULTS: Of the 47 patients, 16 (34.1%) had histological diagnosis of antral and 31 (65.9%) multifocal AG; 17 (36.2%) patients had mild and 30 (63.8%) had moderate-severe AG. H. pylori was detected in 39 (82.9%) and intestinal metaplasia was found in all patients. GastroPanel® showed 82.9% sensitivity for the diagnosis of AG and 53.8% for the diagnosis of H. pylori infection. The prediction of advanced atrophy was not sufficiently accurate, neither in patients with antral nor in those with multifocal AG. CONCLUSION: GastroPanel® can be useful for detecting patients with AG. However, it does not reflect the severity of atrophy.

Long-term follow-up and serologic assessment after triple therapy with omeprazole or lansoprazole of Helicobacter-associated duodenal ulcer.

We assessed both the effectiveness of two Helicobacter pylori (Hp) eradication triple therapies and the usefulness of serology in the follow-up. Fifty patients with active or scarred duodenal ulcer were randomized to lansoprazole or omeprazole for 1 to 4 weeks, with clarithromycin 250 mg twice a day and tinidazole 500 mg twice a day for the first week. Endoscopies were scheduled before treatment, after 8 weeks, and after I year. H. pylori status was determined before therapy by rapid urease test and histology and during the follow-up by histology and culture. Serology was determined at baseline and at 6 and 12 months. The regimens were equally effective in inducing ulcer healing (95.8% vs. 87.5%) and eradicating Hp with no recurrences at 12 months. Among 44 patients eradicated, a significant reduction of immunoglobulin G (IgG) titer occurred at 6 (p < 0.0001) and 12 months (p < 0.0001). If a titer reduction of more than 30% was taken as an indicator for Hp eradication, the specificity of enzyme-linked immunosorbent assay was 75% at 6 and 95.4% at 12 months with a 100% sensitivity. Either lansoprazole or omeprazole combined with antibiotics are effective in eradicating Hp. Serology is useful for monitoring Hp eradication provided that an appropriate percent reduction in IgG titer is used after more then 6 months after therapy.

Acute echinococcosis: a case report.

We report the case of a 69-year-old man with acute pulmonary echinococcosis. A computed tomographic scan of the thorax revealed the presence of multiple nodules in both lungs, and laboratory tests showed eosinophilia and the presence of antibodies against Echinococcus granulosus. Therapy with albendazole led to resolution of the pulmonary nodules and a normalization of the white cell count. To our knowledge this is the first described case of acute echinococcosis, as the diagnosis of this disease is usually delayed to chronic phases. Therefore, finding unexplained eosinophilia, especially in association with pulmonary nodules, should lead one to suspect acute hydatid disease.

Antibody against EBV in CSF from HIV-1 and HTLV-I infected patients.

We have measured the levels of antibody (ab) against different Epstein-Barr virus (EBV) antigens in 10 AIDS patients, 7 HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients and 20 control subjects. We found comparable serum levels of anti-EBV ab between AIDS patients, HAM/TSP patients and control subjects. By contrast, anti-EBV ab were present in the large majority of CSF from AIDS patients (70%) and HAM/TSP patients (60%) but only in 15% of control group. Our results support a synergistic role of EBV in retroviral infections of the central nervous system.