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Biomedical subjects

G Verme

Publications and source records attributed to G Verme.

At least 19 recordsLinked to original sources
PubMed1992

Fistulosphincterotomy in the endoscopic approach to biliary tract diseases.

We report our experience with 49 patients who underwent fistulosphincterotomy (FS) after cannulation of the common bile duct (CBD) by standard approaches had failed, due to suspected CBD obstruction. Only 4% of our cases turned out to have no biliary obstruction at all. The morbidity rate was 16%, and the mortality rate was 2%. In our series, FS raised the success rate of CBD cannulation from 90% to 96%. Ninety-five percent of successful cannulations were followed by endoscopic treatment. There were no cases of perforation or hemorrhage, and no difference in the success rate between FS in flat papillas and FS in bulging papillas, thanks, perhaps, to the technique we used. Our findings would indicate that FS is a useful procedure involving additional but not prohibitive risks. Nonetheless, it should be used only when CBD obstruction is strongly suspected and standard methods are not successful.

Adult↗
PubMed1992

Treatment of chronic hepatitis B with beta interferon given intramuscularly: a pilot study.

In a pilot study aimed to test the therapeutic potential of beta interferon (IFN) given intramuscularly we treated 4 patients with HBeAg positive chronic hepatitis B with a progressively increased dosage of beta IFN (from 5 to 9 million units daily) for 1 month and with 9 million units for 5 additional months, thrice weekly. In 3 of the 4 patients, serum HBV-DNA decreased during therapy and remained undetectable in 2 who seroconverted from HBeAg to anti-HBe while in 1 patient viraemia rebounded to pretreatment levels during the follow-up. In the remaining patient serum HBV-DNA fluctuated during treatment. These results suggest that beta IFN given intramuscularly has a potential therapeutic efficacy in patients with chronic hepatitis B and prompt further clinical trials in a larger number of patients.

Adult↗
PubMed1992

Treating chronic liver disease: lessons from a day hospital.

The relationship between the professional background of the physician requesting the biopsy procedure (whether non-specialist or specialist in hepatology/gastroenterology) and the subsequent decision of treatment of the patients was analyzed. Treatment was divided into two categories named arbitrarily "no therapy" (general supportive measures) or "therapy" (causal treatment based on active drugs or measures aimed at affecting the cause of the disease). Of the 204 cases of outpatient needle biopsies available for study, 157 were made by specialist request and 47 were made by a non-specialist request. Sixty-eight (43%) of the former, but only 3 (2%) of the latter had "therapy" (p = 0.0001). Also, patients in which histology showed chronic active liver disease had "therapy" more frequently (49 of 109, 44.9%) than those without chronic active liver disease (22 of 95, 23%) with p less than 0.01. However, patients with histological active chronic disease were not more frequent among specialist requests (56.6%) than among the non-specialist requests (42.5%). But among patients attended by the specialist, there were more patients (31.8%) with positive serum markers of Hepatitis B virus infection than among those sent by others (12.7%) with p less than 0.01. We conclude that at least in the premises in which this study was carried out, blind liver biopsies will lead to active treatment more often in patients treated by a specialized physician, because these patients are more likely to have a virus identified as the cause of their liver disease and consequently will receive antiviral treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Wild-type and e antigen-minus hepatitis B viruses and course of chronic hepatitis.

Using an oligonucleotide hybridization assay, we studied the clinical implication of wild-type hepatitis B virus (HBV) and a HBV mutant that is unable to secrete hepatitis B e antigen (HBeAg) because of a translational defect due to a stop codon in the pre-C region in 106 hepatitis B surface antigen-positive patients with chronic hepatitis B. Wild-type HBV was detected in 31 of 42 (73.8%) HBeAg-positive patients, whereas a mixed viral population was present in 10 (23.8%). Significant differences in the severity and outcome of liver disease were not observed in the two groups of patients. However, the emergence of HBeAg-minus HBV in wild-type HBV carriers was associated with an exacerbation of liver disease and was followed by the presence of antibodies against HBeAg (anti-HBe) in serum in 50% of the cases. In 61 of 64 (95.3%) anti-HBe-positive patients, HBeAg-minus HBV was the predominant virus: HBeAg-minus HBV was detected in 42 patients (65.6%), whereas both wild-type and HBeAg-minus HBV were present in 19 (29.7%). HBeAg-minus HBV was associated with a course of hepatitis characterized by flare-ups of liver cell necrosis interspersed with periods of asymptomatic HBV carriage (P less than 0.01). These data support the hypothesis that genetic heterogeneity of HBV significantly influences the course and outcome of chronic hepatitis B. Wild-type HBV secreting HBeAg induces immunologic tolerance and causes chronic infection. HBeAg-minus HBV might be unable to induce chronic infection without the helper function of wild-type HBV, but it appears to be more pathogenic. Once chronic infection is established, HBeAg-minus HBV variants may prevail and displace wild-type virus.

Adolescent↗
PubMed1991

Antibodies to Mycobacterium paratuberculosis in patients with Crohn's disease.

IgG antibodies against Mycobacterium paratuberculosis protoplasmic antigen were looked for by an enzyme immunosorbent assay in patients with Crohn's disease, Ulcerative colitis, active pulmonary tuberculosis, past pulmonary tuberculosis, and in healthy controls. Serum reactivity for these antibodies was not correlated to PPD skin test positivity without history of mycobacterial disease. A cutoff based on the mean absorbance value of a pool of healthy blood donors was chosen. Positive values were found in 12/24 (50%) patients with active pulmonary tuberculosis and 2/10 (20%) skin-test-positive subjects with past pulmonary tuberculosis as expected, because antigenic sharing is common among different mycobacteria. The control group of blood donors showed borderline positivities in 3/149 cases (2.01%). Positive values were found in 4/108 (3.70%) patients with Crohn's disease and 2/40 (5%) with ulcerative colitis. We conclude that our data do not support a causal relationship between the M. paratuberculosis and Crohn's disease, but occasional patients with inflammatory bowel diseases show unexpected positivities for these mycobacterial antibodies.

Adolescent↗
PubMed1991

Role of hepatitis delta virus infection in hepatocellular carcinoma.

Hepatitis B virus (HBV) DNA integrates into the host DNA and shows a series of potentially oncogenetic properties, but HBV is not an acutely transforming virus, because HCC develops decades after infection. Other factors, namely cirrhosis, inflammation, alcohol intake, and viral superinfections, could promote the oncogenetic process induced by HBV-DNA integration. We studied the impact of HDV infection in the pathogenesis of HCC in 62 consecutive patients. Their mean age was 59 years (range 25-75 years), 54 were male and eight female; 58 had cirrhosis. The findings suggest that HBsAg-positive patients with HDV superinfection developed cirrhosis and HCC at an earlier age than HBsAg carriers without HDV infection. HDV appears to represent a "promotion" factor for HCC in subjects with an oncogenic risk induced by HBV. A long-lasting necroinflammatory lesion of the liver substained by productive HBV and HDV infections may be a major pathogenetic mechanism.

Carcinoma, Hepatocellular↗
PubMed1991

Chronic active hepatitis B. Interferon-activated natural killer-like cells against a hepatoma cell line transfected with the hepatitis B virus nucleic acid.

In a rapid 51Cr release assay, peripheral blood mononuclear cells from 12 healthy donors did not lyse the hepatitis B virus deoxyribonucleic-acid-transfected human hepatoma cell line 2.2.15, but under the same experimental conditions they did lyse K562 cells. Peripheral blood mononuclear cells from 10 out of 16 patients with chronic active hepatitis B exhibited cytotoxic activity against 2.2.15 cells in the presence of a relatively reduced natural killer cell activity to the K562 cell target. Enhancement of the cytotoxic activity to 2.2.15 cells was statistically significant in the group of patients being treated with leukocyte alpha-interferon. The activity was not influenced by the degree of human leukocyte antigen type matching between effector and target, and was enhanced by depletion of T-cells and by in vitro interferon treatment. These results therefore support the concept of a natural killer-like cell activated by clinical administration of interferon in chronic active hepatitis B patients. This cell effector was lytic for the virus B negative HEP-G2 cells also. However, T-cells purified from a few patients failed to lyse the HEP-G2 while lysing the 2.2.15 target, thus indicating that a preferential recognition of the virus-infected target may be exerted by certain T-lymphocyte subsets. The use of the human leukocyte antigen type defined, highly differentiated, hepatitis B virus releasing 2.2.15 cell line as target for fresh lymphocytes in this cytolytic assay did not disclose cytolytic T-cells in an obvious way. Further manipulation of this system perhaps using T-cell clones may be the next step to exploit the investigative possibilities offered by the availability of the 2.2.15 cell target.

Adult↗
PubMed1991

[Intrahepatic cholestasis in hyperthyroidism].

Three cases of cholestatic liver disease related to hyperthyroidism are reported. Features indicative of a role of the endocrine disease in the pathogenesis of the cholestatic syndrome were the appearance of liver damage in temporal relation with the clinical onset of thyroid hyperfunction and its disappearance with the amelioration of the hyperthyroidism; the absence of congestive heart failure and of infectious, toxic or obstructive agents of liver damage; the pathological and biochemical findings of intrahepatic cholestasis. Hyperthyroidism can be rarely complicated by a severe cholestatic syndrome that may dominate the clinical presentation and course.

Biopsy↗
PubMed1991

Hepatitis B virus replication modulates pathogenesis of hepatitis D virus in chronic hepatitis D.

Hepatitis D virus and hepatitis B virus nucleic acids were detected by Northern and Southern blot hybridization in the sera and livers of 85 chronic carriers of HBsAg and anti-hepatitis D followed up for a mean of 10 yr. We identified three subsets of patients: 13 with hepatitis D virus and hepatitis B virus viremia, 53 with serum hepatitis D virus RNA, but without hepatitis B virus DNA and 19 negative for both nucleic acids. Genomic and subgenomic forms of hepatitis D virus RNA were detected only in patients with hepatitis D virus and hepatitis B virus viremia. Histological findings and disease activity at admission were comparable in the three groups of patients, but the outcome was significantly worse in patients with active replication of both viruses; two of them died of terminal liver failure and hepatocellular carcinoma developed in two; the remaining patients had an uneventful course. These results suggest that active hepatitis B virus replication represents an important previously unrecognized determinant of severe liver damage in patients with chronic hepatitis D virus infection. Since hepatitis B virus provides the means for hepatitis D virus secretion and release from infected cells, active hepatitis B virus multiplication favoring the spread of hepatitis D virus from cell to cell may increase the pathogenetic potential of the defective agent.

Adolescent↗
PubMed1990

A new hepatitis B virus strain in patients with severe anti-HBe positive chronic hepatitis B.

In hepatitis B virus carriers who are anti-HBe positive despite ongoing viral replication (HBcAg in liver and HBV-DNA in serum) the natural course of hepatitis is severe and the response to interferon is low. We investigated whether a new hepatitis B virus (HBV) strain could be involved. A translational termination codon at the carboxyterminal end of the pre-C region responsible for the lack of HBeAg secretion was found in 18 of 19 HBV clones isolated from seven pedigreed patients with this clinical syndrome. The same findings were confirmed by direct sequencing. One of these patients underwent a liver transplant and HBV infection of the new liver resulted in high titered viremia and intrahepatic expression of HBcAg, without detectable HBeAg in serum. Another patient was superinfected by hepatitis delta virus (HDV) and developed high titres of total and IgM anti-HD. In spite of this, chronic hepatitis remained unchanged during 7 years of follow-up. These data strongly suggest that a viable precore minus mutant of hepatitis B virus is responsible for the lack of HBeAg in the serum of these patients. The HBV variant may explain the peculiar geographic distribution of anti-HBe positive hepatitis. The variations in the virus genome sequence may cause the more severe form of liver disease and modify the pathogenicity in the case of HDV superinfection.

Adult↗
PubMed1990

Endoscopic ultrasonography in eosinophilic infiltration of gastric wall.

The case of a young man with eosinophilic gastroenteritis with primary muscularis propria involvement in the antrum and distal ileum is presented. Initial diagnosis was based uniquely on indirect clinical and radiological findings since endoscopic and histologic data had been misled by the depth of eosinophilic infiltration. In order to directly prove the diagnosis, full-thickness operative biopsy would have been necessary but was avoided on ethical grounds. Valuable information was gained through Endoscopic Ultrasonographic (EUS) study of the antrum which showed an asymmetrical thickening of the outer hypoechoic layer of the wall corresponding to the muscularis propria. The overall thickness of the antrum amounted to 0.6 cm, clearly distinct from the 0.2 cm value in uninvolved areas. Subserosal involvement was also appreciated in spite of the absence of ascites; superficial layers, mucosa and submucosa, appeared uninvolved. The patient was restudied 6 months later when symptom-free: at this time, blood eosinophilia persisted and the EUS picture was unchanged. These observations suggest that peripheral blood eosinophilia along with eosinophilic infiltration of the gastric wall are stable conditions, unrelated to symptoms. Endoscopic ultrasonography is of value in ascertaining muscular involvement in eosinophilic gastroenteritis.

Adult↗
PubMed1990

Immunohistochemical research of HDV infection in Chinese patients with chronic liver disease.

The prevalence of HDAg in the liver of Chinese patients with chronic hepatitis and hepatocellular carcinoma was determined using direct immunofluorescence and immunoperoxidase. Overall, 6 patients (6.31%) out of 95 HBsAg carriers with inflammatory liver disease and neoplasia were found to be HDAg positive. HDAg was detected in the livers of 6 (7.59%) out of 79 chronic hepatitis patients. The relative frequency of HDAg in cirrhosis-B, CAH-B and CPH-B was 14.3%, 7.1%, and 5.89%, respectively. These results suggest that a sizeable number of HBsAg carriers are also carriers of HDV. In view of the large number of HBV carriers in China, the relatively minor but distinct presence of HDV represents an important health problem.

Carcinoma, Hepatocellular↗
PubMed1989

Natural course and response to interferon of chronic hepatitis B accompanied by antibody to hepatitis B e antigen.

The course of chronic hepatitis B was studied in 30 patients who had antibody to hepatitis e antigen and hepatitis B virus DNA in the serum and hepatitis B core antigen in the liver. Over a 2-year period, no patient experienced a sustained spontaneous remission of disease, and follow-up liver histology revealed worsening of the disease in four patients. After 2 years of observation, 24 patients were allocated randomly to one of two groups: 12 patients served as untreated controls and 12 received recombinant human alpha-interferon-2a in a dose of 9 million units intramuscularly three times weekly for 16 weeks. Patients who remained viremic after 16 weeks received 3 million units three times weekly for an additional 8 weeks. Abnormal amino-transferases and serum hepatitis B virus DNA persisted without appreciable changes in all untreated patients. Hepatitis B virus DNA rapidly became undetectable and serum aminotransferases fell to normal in eight treated patients. After the end of treatment, hepatitis B virus DNA became detectable once again in seven patients, in six of whom a peak of aminotransferases (range: 256 to 850 units per liter) ensued; subsequently, hepatitis B virus DNA disappeared, and serum aminotransferases again fell to normal in two of the seven. Overall, hepatitis B virus DNA was no longer detectable in serum and liver histology improved in three treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗