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Biomedical subjects

E Sagnelli

Publications and source records attributed to E Sagnelli.

At least 73 records · Page 4Linked to original sources

Infection with the delta agent in chronic HBsAg carriers.

To establish the mechanism of progression to chronicity of the HBsAg-associated delta infection, serum hepatitis B virus and delta markers were tested in five babies born to HBsAg-positive mothers with anti-delta, in 42 follow-up patients with acute hepatitis B virus and delta hepatitis, and in collections of sera from 8 HBsAg carriers with anti-delta. Evidence of delta infection was found in the baby born to a mother with serum HBeAg and in none of the four babies born to mothers with anti-HBe. Hepatitis was self-limited in the 42 patients acutely infected by hepatitis B virus and delta agent; none developed persistent HBs-antigenemia and the majority displayed transient anti-delta of IgM class. In seven HBsAg carriers high titers of anti-delta developed during the follow-up; coincident with the rise of the antibody, aminotransferase elevation occurred in five previously asymptomatic carriers and persisted in three of them. No sign of infectious hepatitis B virus replication was detected in five of the carriers throughout the follow-up, and all of them had anti-HBe before the rise of anti-delta and of aminotransferase. HBsAg carriers with diminished hepatitis B virus synthesis appear to be at high risk of developing chronic delta infection and disease when exposed to the delta-infectious serum of other carriers.

Adult↗

[Maternal-fetal transmission of hepatitis B virus. Follow-up study of 21 infants born to HBSAG-positive mothers, and 6 born to HBSAG-negative mothers with anti-HBV antibodies].

Vertical transmission of hepatitis B virus (HBV) was studied in 21 mother-infant pairs. A transient HBs-antigenemia was observed in 60% of the 10 children born to HBsAg healthy carrier mothers and 91% of the 11 babies born to mothers with HBsAg-positive CAH. Among the 16 children showing HBs-antigenemia, 3 developed acute viral hepatitis two of whom showed progression to chronicity.

Antibodies, Viral↗

Serum levels of hepatitis B surface and core antigens during immunosuppressive treatment of HBsAg-positive chronic active hepatitis.

One of the following treatments was randomly assigned to 101 consecutive patients with biopsy-proven chronic active hepatitis: prednisone 20 mg daily, azathioprine 100 mg daily, prednisone 20 mg and azathioprine 50 mg daily, or B vitamins 2 tablets daily (control group). Patients were observed at the beginning of the study, then at 2, 6, and 12 months after treatment. At each visit levels of HBsAg and Dane-particle-associated core-antigen (HBcAg) and their corresponding antibodies were determined. 42 patients were HBcAg positive at the beginning of the study. Of these 42 patients, the 34 who were under treatment remained HBcAg positive and showed a rise in HBcAg titre, while the 8 who were not treated had a fall in HBcAg titre (6 patients) or became HBcAg negative (2 patients) in 6 months. Among 59 patients who were HBcAg negative at the beginning of the study, this antigen became persistently detectable in 40% of the 42 patients who were treated, and was transiently present in 2 (12%) out of the 17 untreated patients (p < 0.05). Our data indicate that long-term prednisone and/or azathioprine treatments favour the replication of hepatitis-B virus in patients with HBsAg-positive chronic active hepatitis.

Chronic Disease↗

The growth-hormone in long-term steroid-treated patients with chronic active hepatitis.

To determine whether the hypothalamo-pituitary axis (HPA) became suppressed in patients with chronic active hepatitis (CAH) treated with prednisone or long-activity synthetic corticotrophin (L.A.S.C.) for at least 12 months 36 patients with CAH were assessed for growth hormone release following insulin hypoglycemia test (IHT). Sixteen out of the 36 patients were treated with steroids, 11 with L.A.S.C. and 9 were untreated. Sixteen patients were less than 12 years old of whom 8 were treated with prednisone and 5 with L.A.S.C. and 3 untreated. Suppression of HPA was observed only in two patients of whom one was treated with prednisolone for 24 months and the other one received L.A.S.C. for 23 months. Normal HPA was observed in all the other 34 patients. Two patients aged 6 and 8 years were treated with steroids for 3 and 6 years respectively and showed impairment of the growth in height and remained permanently stunted even when steroids had been discontinued. Our data suggest that both steroids and L.A.S.C. treatment does not impair HPA in patients with CAH when administered for less than two years.

Adolescent↗

Abnormal steroid sulfate in plasma of women with intrahepatic cholestasis of pregnancy.

Concentrations of numerous sulfate steroids were checked in the plasma of 10 women in normal pregnancy (NP), 21 women with intrahepatic cholestasis of pregnancy (ICP) and 10 pregnant women suffering from viral hepatitis with jaundice (VHP). A considerable increase in 5 alpha pregnane and 5 beta pregnane 3 alpha, 20 alpha diols, mono- and disulfates and in 5 alpha pregnane 3 beta, 20 alpha diols disulfates was observed only in ICP and not in VHP. This observation permits us to hypothesize that these hormone changes can have a causative role in the pathogenesis of ICP.

Alanine Transaminase↗

The significance of the Australia antigen (HBsAg) persistent healthy carrier "status": a long-term follow-up study of 34 cases.

Thirty-four persistent healthy carriers of HBsAg (serum HBsAg detectable for longer than 3 months with normal liver function tests and normal liver histology or slight aspecific abnormalities) were discovered by routine testing of household relatives of B virus hepatitis patients. The carriers were followed-up for 11 to 37 months by clinical control, liver function tests and liver needle biopsy. None carrier had previous jaundice. During the follow-up period, in 17 of the 34 subjects, was there no evidence of deterioration in either clinical state, liver function of pathological findings. In 5 of the 34 carriers, HBsAg disappeared from serum after a period ranging from 6 to 12 months. The remaining 12 cases developed clinical and histological picture of acute viral hepatitis after 6 to 29 months (mean 12 months). Of these 12 patients, 6 recovered and become HBsAg; 2 remained HBsAg healthy carriers despite normalization of biochemical and histological abnormalities; 3 progressed from the acute stage to antigen positive CAH. The remaining one case could not be followed-up after the acute hepatitis. Our data indicate that the outcome of the HBsAg carrier state is unpredictable and stress the need of long-term follow-up surveillance.

Adolescent↗

Dane particles-associated hepatitis B core antigen in patients with HBsAg-positive chronic hepatitis.

Dane particles-associated hepatitis B core antigen (HBcAg) was determined by radioimmunoassay in 61 patients with hepatitis B surface antigen (HGsAg)-positive chronic hepatitis. HBc antigenemia was observed in 61% of patients, especially in those with epidemiological risk factors. Patients with chronic active hepatitis as well as those with chronic persistent hepatitis may have HBc antigenemia. The highest levels of HBcAg were observed in male homosexuals. Follow-up determinations indicate the general tendency of HBcAg to decrease or disappear. HBcAg-positive patients with chronic active hepatitis had a poor prognosis, whereas HBcAg-negative patients frequently had a favorable clinical course of the disease (P less than 0.001). The assay of HBcAg in the serum of patients with HBsAg-positive chronic active hepatitis is a useful parameter with both clinical and epidemiological importance.

Adult↗

Treatment of chronic active hepatitis with either prednisolone or corticotrophin: a controlled trial.

A total of 54 patients hospitalized for chronic active hepatitis were randomly treated, 29 with prednisolone (maintenance dose 15 mg/day) and 25 with depot synthetic corticotrophin (maintenance dose 1 mg/week, i.m.) and were followed up for 6 to 24 months or longer. In this series, young males predominated, the incidence of serum HBsAg positivity approached 80% in both treatment and no patient had initial evidence of cirrhosis or had autoimmune associated diseases. With either drug SGOT levels showed a decrease during the initial 12 months of therapy (p less than 0.05); initial jaundice, when present, had disappeared by the 3rd month of treatment. With both treatments globulins and gamma-globulins decreased significantly after 12 to 24 months of therapy. Serum HBsAg persisted in all but two cases. Serum liver biopsies showed the following evolutions of histological activity: 12 cases (22%) improved to the "inactive phase" (8 with prednisolone and 4 with corticotrophin); 19 (35%) improved to a lesser extent (8 with prednisolone and 11 with corticotrophin); 17 (32%) remained unchanged (11 with prednisolone and 6 with corticotrophin); 6 (11%) worsened (2 with prednisolone and 4 with corticotrophin). Morphological features of cirrhosis appearently developed in 15 patients (8 treated with prednisolone and 7 with corticotrophin) of whom 7 achieved improvement of histological aggressiveness concurrently. Differences between treatments were not significant. Side effects suggesting drug discontinuation occurred only in 6 cases.

Adolescent↗

Liver histology in 34 "HPsAg long-term healthy carriers.

Thirty four out of 45 HBsAg long-term carriers with normal liver function tests, discovered among family members of patients with HBsAg positive liver diseases, have been investigated by liver biopsy. Of these 34, 12 had normal liver tissue and 8 mild non specific changes, such as focal Kupffer cell hyperplasia or mild lymphocytic infiltrates in the portal tracts on liver biopsy. Two subjects showed multiple histioid granulomata scattered in normal liver parenchyma. Of the remaining 12 cases, 8 showed some areas of pin-head necrosis and mild portal tracts infiltration and 4 showed some areas of focal parenchymal infiltration associated with portal tracts inflammation. We consider that these histological changes are very mild lesions within the spectrum of hepatitis. None of our cases had histological picture of Chronic liver disease. Consequently it appears that normal liver function tests may be of some values to exclude severe histological abnormalities.

Adolescent↗

Acute viral hepatitis in Italy. Results of a collaborative study.

The etiological and clinical aspects of viral hepatitis were evaluated by a retrospective survey of patients hospitalized in 1972, 1973 and 1974 in 12 specialized medical centers scattered throughout Italy. The data refer to 2788 patients suffering from acute viral hepatitis who were hospitalized during the initial 10 days of jaundice. The majority of patients (90%) had not been treated with steroids. For each case, the clinical and biochemical data were recorded, coded, computerized and statistically analyzed. In our patient population viral hepatitis was more frequent among younger patients. We observed a high frequency of HBsAg positive hepatitis (40.7%) which was seldom associated to a history of parenteral exposure and showed an irregular geographical distribution. HBsAg positive hepatitis was similarly distributed between males and females. It was more frequent in patients older than 30 (60%) than in children (18-23%) and younger patients (42%). In our series, the frequency of HBsAg hepatitis found in surgeons (81.8%) and nursing personnel (66.3%), but not in physicians (41.2%), was greater than that of the entire sample due to their exposure to blood.

Adolescent↗

Familial clustering of hepatitis B antigen and liver diseases in families with a high incidence of viral hepatitis.

In each of 23 families in which two or more cases of acute hepatitis-like jaundice (index cases) occurred, all family members were studied to evaluate HBAg clustering and the incidence of asymptomatic liver disease. There were 49 "index cases" of hepatitis-like jaundice: 38 cases of acute viral hepatitis, 5 of chronic agressive hepatitis and 6 of active cirrhosis. The overall number of members in these families (excluding index cases) was 170 and 155 of which were tested by clinical examination, laboratory tests and needle liver biopsy. In 27 out of the 155 subjects there was evidence of liver diseases (10 non icteric hepatitis cases, 12 CAH cases and 5 cirrhosis cases). HBAg was present in the serum of 19 of these patients, and twof the cirrhotic patients were positive. Furthermore, 33 of the 155 cases were healthy HGAg carriers showing no abnormality in liver function tests. In the majority of these carriers liver histology showed slight damage (pin-head necrosis or portitis) sometimes compatible with resolving viral hepatitis. A long-term follow-up of the HGAg carriers showed that three of these subjects progressed to acute viral hepatitis.

Acute Disease↗

Differential diagnosis between benign and malignant biliary tract obstruction: discriminative usefulness of some clinical and laboratory data.

The data of 26 patients with obstructive jaundice caused by biliary tract stones were compared to those of patients with malignant obstructive jaundice in order to evaluate the diagnostic effectiveness of some laboratory tests in the differential diagnosis between these two conditions. The Fisher's discriminant analysis was employed. The combined evaluation of serum albumin and haptoglobin appeared to have the most satisfactory discriminative effectiveness, yielding a 54% rate of correct diagnosis, with a safety margin of 95%.

Alanine Transaminase↗

The differential diagnosis between intrahepatic cholestatic jaundice and viral hepatitis during pregnancy.

Clinical and laboratory findings from 15 patients with icteric viral hepatitis during pregnancy (VHP) and from 22 patients with intrahepatic cholestasis during pregnancy (CJP) were evaluated statistically in order to find out which parameters might help in order to find out which parameters might help in differentiating the two diseases. Diagnosis was established by needle liver biopsy in all cases. The following data were considered: history, physical examination, erythrocyte sedimentation rate (ESR) serum cholesterol, prothrombin time, total serum bilirubin, SGOT, SGPT, serum alkaline phosphatase, serum protein, serum flocculation tests, BSP blood clearance and serum HB Ag. Vomiting, high GOT and GPT serum levels, and serum HB Ag positivity suggest VHP diagnosis. Otherwise a severe itching with scratching lesions, high ESR, elevated total cholesterol and serum alkaline phosphatase values mainly if occurring in the later stage of pregnancy are consistent with CJP diagnosis. When clinical and laboratory data from a jaundiced pregnant female do not allow diagnosis, this can be established only on the basis of needle liver biopsy.

Alanine Transaminase↗

Effect of immunosuppressive therapy on HBsAg-positive chronic active hepatitis in relation to presence or absence of HBeAg and anti-HBe.

Two hundred and four patients with biopsy-proven HBsAg-positive chronic active hepatitis were treated for at least 2 years with azathioprine, prednisolone or a combination of both, or were untreated. Prevalences of HBeAg, anti-HBe, and anti-HBc were 26, 58, and 100%, respectively. Criteria for improvement or progression of disease were based on clinical, biochemical, and morphologic parameters. Prednisolone therapy and combination therapy did not modify the course of the disease in HBeAg-positive patients; azathioprine therapy may have been deleterious for these patients. Among HBeAg-negative patients, deterioration or death occurred more frequently in those who were untreated than in those who received the combination of azathioprine and prednisolone. Prednisolone therapy was of moderate effect, whereas azathioprine did not influence the outcome.

Adolescent↗

Interaction between HDV and HBV infection in HBsAg-chronic carriers.

We studied the interaction between HBV and HDV infection in 149 consecutive subjects with HBsAg positive chronic hepatitis and in 22 chronic HBsAg healthy carriers. Liver HBcAg was detected in 52 (30.4%) of the 171 subjects. Of these 52, 35 were HBV-DNA and HBeAg positive, 11 HBV-DNA positive only; two HBeAg positive only and four were negative for both HBeAg and HBV-DNA. None of the 119 HBcAg-negative subjects had detectable HBV-DNA in serum. HD-Ag in hepatocytes was detected in 31 of the 171 subjects (18%); it was detectable in none of the 22 HBsAg healthy carriers, in four of the 56 patients with chronic persistent hepatitis (7.2%), in six of the 24 patients with chronic lobular hepatitis (25%), in 16 of the 40 patients with chronic active hepatitis (40%) and in five of the 29 with cirrhosis (17%). A presence of anti-HD in serum in the absence of liver HD-Ag was found in 54 of the 171 subjects (32%). This condition was observed not only in patients with a progressive disease (37.7% of chronic active hepatitis or cirrhosis and 33% of chronic lobular hepatitis), but also in healthy carriers (36%) and in chronic persistent hepatitis patients (21.4%). Liver HBcAg was detected in 6.4% of the 31 HD-Ag-positive patients, in 12.9% of the 54 HD-Ag-negative/anti-HD positive, but in 50% of the 86 with no marker of HDV infection. HDV appears to inhibit HBV genome and such inhibition may persist even when anti-HD is the only HDV marker detectable.

DNA Replication↗