PubMed Health⌕ Search

Biomedical subjects

Gianni Testino

Publications and source records attributed to Gianni Testino.

12 recordsLinked to original sources
PubMed2005

[Steatosis and hepatitis C].

Steatosis and hepatitis C are two common liver diseases. Epidemiological and experimental data indicate that hepatitis C predisposes to non alcoholic fatty liver disease and the prevalence of coexistent hepatitis C and steatosis is two-three times higher than it would be expected if these were completely independent processes. Two conditions have been defined in course of hepatitis C: the "metabolic fat", characterized by a correlation between steatosis and metabolic alterations and the "viral fat", characterized by a direct action of HCV. Actually, "mixed forms" are often present. Up to today, most of the authors believe that the presence of steatosis accelerates the progression of fibrosis, and therefore the progression to cirrhosis, increases the risk of developing hepatocellular carcinoma, and decreases the antiviral therapy response percentage. The treatment must associate the common antiviral therapy with all the measures fit for facing the metabolic problems, with particular reference to the antioxidant therapy.

Antiviral Agents↗
PubMed2004

[Gastric preneoplastic changes].

Gastric cancer (GC) is the second most common cause of cancer related death worldwide. The 5-year relative survival rate ranges from 10 to 20% of cases. Therefore, it is necessary to diagnose gastric non invasive neoplasia (formerly dysplasia). Correa suggested more than 20 years ago that there was a histological cascade leading to GC: chronic active gastritis --> atrophy (AG) --> achlorydria with nitrocompounds increase --> intestinal metaplasia (IM) type I --> IM type III --> low grade dysplasia (LGD) --> high grade dysplasia (HGD) --> GC. The discovery of Helicobacter pylori infection has imposed a revision of the various pathogenetic stages: 1) GC may arise in the same context as IM and dysplasia, but without any documentable precursor. GC can develop in a context of normochloridria; 2) there are not sufficient data to support endoscopic surveillance for patients with AG; 3) there are doubts about the real necessity to operate histologically a subdivision of IM in subtypes: probably it is more important the extent of IM; 4) dysplasia is the only true histological marker of CG. In fact, LGD is associate or progressed to GC in the 9% of cases, HGD is associated or progressed to GC in the 74% of cases. It emerges the real oncologic risk of dysplasia. Such data are confirmed by immunohistochemical study of the dysplastic lesions. Therefore, an appropriate follow-up of non invasive neoplasia increases the likelihood of CG being detected in its potentially curable stage.

Cell Division↗
PubMed2002

[Hepatocarcinoma in HCV compensated correlated liver cirrhosis: role of treatment with interferon].

The hepatocarcinoma (HCC) represents one of the major causes of morbidity and mortality in course of chronic HCV correlated hepatopathy. Up to today there are no reliable therapies which can delay or avoid the arising of HCC, nonetheless various Authors have noticed a decrease of such incidence in the subjects treated with interferon (IFN). Such encouraging results have not yet found univocal confirmation in course of compensated cirrhosis (Child-Pugh A). In our experience a cohort of 122 patients prospectively followed was analysed retrospectively to asses the effect of IFN therapy (mean follow-up 96 +/- 18.3 months). We conducted a randomized study in compensated cirrhosis with abnormal ALT and HCV-RNA positive serum (post-transfusional infection). Fifty-nine patients (mean age 55.3 +/- 7) received IFN (3 MU three times a week for 12 months) (8 stopped therapy for side effects), 71 did not receive IFN (mean age: 56.8 +/- 8). Baseline characteristics were similar. IFN therapy does not reduce the risk of HCC in compensated cirrhosis. In IFN treated patients it has been noted an improvement in relation with worsening and death/OLT. Moreover, in the non responder group, the number of negative events has been higher than in the sustained responder group and in subjects with relapse. On the contrary, no particular differences have been noticed in relation with the arising of HCC. It can be hypotized that the therapy with IFN does not reduce the risk of HCC in compensated cirrhosis. Such condition represents by itself a risk factor. It can be concluded that the therapy with IFN can be effective in reducing the possibility of clinical-laboratoristic worsening. However, even in case of substained response, the follow-up for the arising of HCC must always be done.

Carcinoma, Hepatocellular↗
PubMed2002

[Clinical postoperative surveillance of gastric carcinoma].

Up to today no agreement has been reached in relation with gastric remnant surveillance. In the cases of partial gastrectomy for benign pathology, most of the Authors agree in believing that in the asymptomatic subject a follow-up is necessary after 15-20 years only from the surgical intervention. Differently, for the cases of partial gastrectomy for malignant neoplasia, it has not been well defined yet the clinical surveillance. Certainly, a surgical intervention in case of relapse presents remarkable difficulties. The relapses are often located in lymphnodes site or metastasis are present and, therefore, the relapses are local in a low percentages. Besides, sometimes the local relapses cannot be re-operated. In spite of such considerations, the personal opinion is that to act in asymptomatic subjects a regular follow-up, in patients operated for early cancer above all. That is justified by the possibility to notice, by means of endoscopy with multiple biopsies, of pre-neoplastic (epithelial dysplasia) or precocious neoplasia lesions, with the aim of obtaining a satisfactory radical surgical intervention.

Follow-Up Studies↗
PubMedDate not supplied

Is it possible with an immunophenotypic study to foresee the oncologic risk of epithelial gastric dysplasia?

BACKGROUND/AIMS: Epithelial gastric dysplasia is considered the only true marker of gastric cancer. High-grade dysplasia is a surgical therapy needing lesion and low-grade dysplasia is considered a lesion with a low oncologic risk. The aim of this experience was to verify whether there are any immunohistochemical evaluations which may enable one to foresee more precisely the evolution of epithelial gastric dysplasia. METHODOLOGY: Immunophenotypic evaluation was effected in 70 cases of low-grade dysplasia (41 males, average age: 57.4) and in 50 cases of high-grade dysplasia (31 males, average age: 58). These cases were retrospectively selected and the studied samples are represented by gastric biopsies obtained in the course of endoscopy performed for dyspepsia. Epithelial gastric dysplasia diagnosis was done according to Goldstein and Lewin and the clinical subdivision was effected using the criteria of Rugge et al. Four antigens were studied using Abs against pepsinogen C, gastric foveolar M1, intestinal CAR-5 and pancreatic DU-PAN-2 Ags. RESULTS: Epithelial gastric dysplasia is characterized by a progressive reduction of gastric markers with a progressive expression of enteropancreatic antigens. Low-grade dysplasia is characterized by a frequent gastro-enteropancreatic coexpression, and high-grade dysplasia by a frequent enteropancreatic coexpression or by no markers expression. Low-grade dysplasia with greater enteropancreatic markers progresses frequently towards gastric cancer; high-grade dysplasia with enteropancreatic markers only is associated/progresses to gastric cancer, while high-grade dysplasia with gastric markers or gastric-enteropancreatic markers is included in the group with persistent or regressed cases. CONCLUSIONS: If confirmed in further studies, such results could modify the evaluation of epithelial gastric dysplasia, not only in terms of histochemical techniques, but also of immunohistochemical techniques.

Disease Progression↗
PubMedDate not supplied

Interferon therapy does not prevent hepatocellular carcinoma in HCV compensated cirrhosis.

BACKGROUND/AIMS: Recent experiences suggest that interferon may significantly decrease the incidence of hepatocellular carcinoma. We conducted a randomized study with interferon versus no therapy in hepatitis C virus Child A cirrhosis with abnormal alanine aminotransferase and HCV-RNA positive serum with the aim to investigate the incidence of hepatocellular carcinoma, worsening of cirrhosis's stage and death or orthotopic liver transplantation. METHODOLOGY: A cohort of 122 patients prospectively followed was analyzed retrospectively to assess the effect of interferon therapy (mean follow-up: 96 +/- 18.3 months). We only chose patients with hepatitis C virus infection who had undergone blood transfusion before 1980. Hepatitis C virus serotype was determined by hepatitis C virus serotyping 1-6 assay (Murex Biothec Limited Temple Hill, Dartford, Kent, UK). HCV-RNA level was determined by bDNA, Chiron Corporation Emeryville, CA. Diagnosis of hepatocellular carcinoma was made on the basis of the appearance of local lesions at periodic ultrasound examination of the liver and confirmed with spiral computed tomography. Fine needle biopsy under sonographic guidance was effected. Fifty-nine patients (mean age: 55.3 +/- 7) received interferon (3MU three times a week for 12 months), 8 stopped therapy for side effects, 71 did not receive interferon (mean age: 56.8 +/- 8). Baseline characteristics were similar. RESULTS: It emerges how interferon does not reduce the risk of hepatocellular carcinoma in compensated cirrhosis. In interferon treated patients an improvement in relation with worsening and death/orthotopic liver transplantation has been noted. CONCLUSIONS: The use of the interferon seems to be scarcely useful when structural alterations of the cirrhotic kind show up, as cirrhosis represents by itself a risk factor for hepatocellular carcinoma. Nevertheless, in relation to the worsening of cirrhosis's stage the interferon therapy can be useful in compensated cirrhosis.

Alanine Transaminase↗
PubMedDate not supplied

Type-2 hepatorenal syndrome and refractory ascites: role of transjugular intrahepatic portosystemic stent-shunt in eighteen patients with advanced cirrhosis awaiting orthotopic liver transplantation.

BACKGROUND/AIMS: TIPS (transjugular intrahepatic portosystemic stent-shunt) has been used increasingly in the management of refractory variceal bleeding. Its role in the management of refractory ascites and hepatorenal syndrome still awaits further prospective studies. Type-2 hepatorenal syndrome is a moderate steady renal impairment. It arises spontaneously and it is the main mechanism of refractory ascites. Precipitating factors may lead to type-1 hepatorenal syndrome. Hepatorenal syndrome is a common complication of advanced cirrhosis with a 3-month mortality of more than 90% unless treated by orthotopic liver transplantation. However, because of the short survival of patients with hepatorenal syndrome and the limited availability of organs, only a small percentage of patients with hepatorenal syndrome can actually reach orthotopic liver transplantation. That is why awaiting orthotopic liver transplantation we have submitted some suitable patients to a TIPS setting. METHODOLOGY: We have considered eighteen consecutive patients affected by advanced cirrhosis (Child-Pugh 10-12) awaiting orthotopic liver transplantation and suitable for TIPS treatment for the presence of type-2 hepatorenal syndrome (10 males, average age 44.5). The criteria for the diagnosis of hepatorenal syndrome and refractory ascites have been effected according to a consensus recommendation. Organic kidney disease was excluded. After mild intravenous sedation and analgesia a puncture needle was advanced transjugular in a catheter through the inferior cava into one of the three hepatic veins. Subsequently, an intrahepatic branch of the portal vein was punctured and the shunt was established by the implantation of Wallstent (diameter 10 mm; Boston, Scientific, Natick, MA). In all patients, we compared serum creatinine, creatinine-clearance, sodium excretion and urine volume before the intervention and 12 weeks after TIPS. The differences among groups were analyzed using paired Student's t-test. RESULTS: The stent shunt was successfully established in all eighteen patients. Complications occurred in 4 patients (temperature above 38 degrees C or vomiting). No patients have developed hepatic encephalopathy resistant to medical treatment. As for the ascites a complete response with total remission of ascites was obtained in eight patients, while a partial response with the presence of sonographically detectable ascites--without the need of paracentesis--was obtained in ten patients. As regards renal functional parameters we have evidenced a significant improvement after TIPS. CONCLUSIONS: We can notice how the setting of TIPS, at least in the presented case, has allowed the treatment of ascites and, furthermore, has lead to improvement of the renal functional parameters. It all implies the enormous advantage of a better management of the patient waiting for orthotopic liver transplantation and, most of all, the advantage of preparing the patient for the surgical intervention with normal renal functional parameters: in fact, it is well known that the increase of serum creatinine influences the pre- and post-orthotopic liver transplantation course, and in particular can modify the mortality rate of the patient list. The lack of effective alternative treatment modalities and the almost universally fatal outcome of hepatorenal syndrome make TIPS an attractive option in the treatment of hepatorenal syndrome as a bridge to orthotopic liver transplantation.

Adult↗
PubMedDate not supplied

[High and low grade gastric epithelial dysplasia: clinical management, endoscopic assessment of p53].

Epithelial dysplasia is considered the only one true histological marker of gastric cancer. In the present study we have evaluated the real clinical importance of epithelial dysplasia divided into low-grade (70 patients, mean age 59.2 years) and high-grade (50 patients, mean age 58 years) dysplasia. Furthermore, it has been made a comparison with the corresponding endoscopic picture and an evaluation of the real meaning of p53 positivity. The clinical outcome subdivision of epithelial dysplasia was effected according to the criteria of Rugge: association with or progression to gastric cancer, persistence or regression. The endoscopic patterns have been divided into ulcerous lesions and non-ulcerous lesions. The immunohistochemical study has been carried out with the utilization of a p53 antibody (Dako, Glostrup, Denmark). From the analysis of the data it comes out that low-grade dysplasia is associated with or progressed to gastric cancer in a low percentage of cases (about 8.5%), while high-grade dysplasia is associated with or progressed to gastric cancer in a high percentage of cases (about 74%), by this proving itself to be a real histological marker of gastric cancer. The cases of epithelial dysplasia associated with or progressed to gastric cancer are significantly associated with an endoscopic picture of gastric ulcer (ulcer-cancer). Nonetheless, the cases of epithelial dysplasia in correspondence of non-ulcerous lesions have been noticed to be associated with or progressed to advanced gastric cancer. The evaluation of p53 did not positively correlate with the clinical progression of the epithelial dysplasia and with TNM classification in case of gastric cancer. Therefore, the evaluation of p53 does not represent a useful marker in the clinical practice.

Adult↗