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C Crivellaro

Publications and source records attributed to C Crivellaro.

52 records · Page 3Linked to original sources

Chronic hepatitis in childhood: the spectrum of the disease.

During a multicentre study of chronic hepatitis in childhood diagnosed by biopsy, the spectrum of the disease has been evaluated in 196 consecutive patients, including 157 from Northern Italy and 39 from Southern Italy. Only 31% of patients in the former group and 27% in the latter were symptomatic when first seen: the majority of cases being seen after familial screenings for hepatitis B virus (HBV) markers or during intercurrent infections, thus suggesting that the frequency of chronic hepatitis in childhood might be largely underestimated in our area. In Southern and Northern Italy 83% of symptomatic and 95% of asymptomatic patients were hepatitis B surface antigen (HBsAg) positive in serum; only 15 (8.3%) of these children were born to mothers known to be HBsAg positive at delivery, but a high circulation of HBV was found in their families: in fact more than 65% of household contacts in Northern Italy and more than 90% in Southern Italy had serological evidence of past or ongoing HBV infection. These data indicate that, although familial screenings for HBV could have enhanced the percentage of HBsAg positive asymptomatic cases, chronic hepatitis in Italian children is mainly caused by HBV infection acquired in the familial setting through horizontal transmission. Such findings also emphasise the importance of mass vaccination of infants as the most effective means to prevent chronic type B hepatitis in childhood in our area. Among HBsAg positive children 55% had histological features of chronic active hepatitis and 85% were hepatitis Be antigen (HBeAg) positive in serum. Anti-HBe positive hepatitis was significantly more frequent in Southern than in Northern Italy in parallel with the significantly higher prevalence (17%) of hepatitis delta virus infection in that area. Of the 16 HBsAg negative cases included in the study three had autoimmune hepatitis, three Wilson's disease, one alpha1 antitrypsin deficiency, and nine had cryptogenic hepatitis, often associated to mild liver lesions resembling those seen in our adult patients with chronic non-A, non-B hepatitis unrelated to percutaneous exposure.

Adolescent↗

IgM antibody to hepatitis B core antigen in children with chronic type B hepatitis.

IgM antibody to hepatitis B core antigen (anti-HBc IgM) was investigated by an antibody-capture radioimmunoassay (serum dilution 1:4000) in serum samples from 31 untreated children with chronic hepatitis B who were followed prospectively for 1-7 years. At the start, all patients were positive for hepatitis B e antigen (HBeAg), and anti-HBc IgM was detected in 23 cases, including 15 out of 16 with chronic active hepatitis and 7 out of 14 with chronic persistent hepatitis. A significant positive correlation was found between anti-HBc IgM levels and severity of liver damage (P less than 0.05), while an inverse relationship was found between anti-HBc IgM levels and distribution of hepatitis B core (HBcAg) antigen in the liver as detected by immunofluorescence. In fact 75% of anti-HBc IgM positive patients showed a focal HBcAg pattern (less than 40% positive nuclei), whereas 87% of antibody negative cases exhibited a diffuse HBcAg expression (more than 60% stained nuclei). During follow-up, seroconversion from HBeAg to anti-HBe with subsequent remission of liver disease occurred in 82% of patients presenting with detectable levels of anti-HBc, including three out of seven cases with chronic persistent hepatitis, but in none of the cases that were initially negative (P less than 0.01). These results indicate that during the natural course of chronic hepatitis B in children, anti-HBc IgM levels in serum reflect the degree of host immune response to infected hepatocytes. The close correlation between anti-HBc IgM seropositivity and seroconversion from HBeAg to anti-HBe suggests that anti HBc IgM may have a prognostic value during the follow-up of children with chronic HBeAg positive hepatitis B.

Adolescent↗

Plasma carnitine and acetyl-carnitine levels at different times of the day.

An interest in both biochemical and clinical carnitine investigation has recently developed. A more complete and extensive study is obtained if acetyl-carnitine as well as carnitine are investigated. This research, using an improved and simplified method for carnitine and acetyl-carnitine determination in the same sample (1 ml) without radioisotopic tracer use, investigates if there are the same differences in their plasma levels at different times of the day. The sample was eluted in a chromatographic column (55 X 15 mm) containing Sephadex G-25M with phosphate buffer (25 mmol/l, pH 7.4). The fraction containing acetyl and free carnitine was divided and employed separately for two assays. The carnitine assay uses an enzymatic reaction catalyzed by carnitine acetyl-transferase (CAT) and measurements are carried out spectrophotometrically. The calibration curve shows r = 0.987 and sensitivity at 5 mumol/l (reference plasma values: 38 +/- 3 mumol/l in 9 subjects). The acetyl-carnitine assay is carried out concentrating the sample by lyophilization and then measuring the enzymatic coupled reactions catalyzed by CAT, malate dehydrogenase and citrate synthase fluorimetrically. The calibration curve gives r = 0.991 and sensitivity at 1.4 mumol/l (reference plasma values: 2.8 +/- 0.3 mumol/l in 9 subjects). Both assay methods are measured at the end point. The carnitine and acetyl-carnitine measured in the plasma of 6 normal subjects at different times of the day vary respectively from 28 to 37 mumol/l and from 1.1 to 5.2 mumol/l in agreement with plasma free fatty acid (FFA) variation from 230 to 779 microEq/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcarnitine↗

Changes in hepatitis Be antigen/antibody system in children with chronic hepatitis B virus infection.

The long-term changes in the HBeAg/anti-HBe system were examined in 55 children with chronic type B hepatitis (52 patients) or cirrhosis (three patients) during a follow-up period of two to 10 years. At the time of presentation, positive reactions to HBeAg were seen in 46 children, and to anti-HBe in nine. Spontaneous seroconversion from HBeAg to anti-HBe occurred in 13 of 38 patients (average annual rate 16%), mainly those with acute onset of hepatitis B or with features of active liver disease at presentation and with a focal distribution pattern of hepatitis B core antigen in the liver. Normalization of transaminase activity and disappearance of histologic features of activity were the rule in patients in whom seroconversion occurred, but the exception in those who maintained persistently HBeAg-positivity. In contrast to the favorable evolution of illness observed in children showing anti-HBe seroconversion, three of nine patients who had anti-HBe-positive reactions at presentation were found to have liver cirrhosis, and a fourth patient had features of active hepatitis throughout the observation period. Because delta antigen was detected in the liver in two of these patients, it is conceivable that etiologic cofactors could have influenced their course of chronic hepatitis.

Adolescent↗

Cellular immunity to the hepatitis B virion in acute hepatitis type B.

Ten patients were studied serially during acute hepatitis type B for lymphocyte sensitization to the hepatitis B surface antigen (HBsAg) and to the complete hepatitis B virion (Dane particle). Using the lymphocyte transformation test, sensitization to purified HBsAg was not observed during the first 10 days of illness but became detectable later, being particularly evident during convalescence, while sensitization to antigens of the complete virion, other than HBsAg, was demonstrable as soon as at the onset of symptoms, often at the time of maximum liver cell damage. These results indicate that in the course of acute hepatitis type B, lymphocyte sensitization to other antigens of the complete virion precedes that to HBsAg and may be of greater pathogenetic importance.

Acute Disease↗

Virologic features of chronic hepatitis B virus infection in childhood.

Hepatitis B virus markers were studied in serum and liver of 24 children with chronic hepatitis. All patients had evidence of active virus replication, as shown by hepatitis B core antigen in the liver cell nuclei, independently of the severity of histologic lesions. Furthermore, 19 of 24 patients had hepatitis B e antigen in serum, and most patients showed a diffuse pattern of HBcAg distribution in the liver. In all 24 children, the presence of immunoglobin G bound to the liver cell surface paralleled the activity of virus replication, but it did not correlate with the severity of liver lesions. During a follow-up period of two to four years, the virus replication persisted in all eight patients receiving immunosuppressive therapy, whereas in 5 of 16 untreated patients we observed a seroconversion to antibody to HBeAg, which is currently regarded as a favorable event for the prognosis of the disease.

Child↗

Virological changes in chronic hepatitis type B treated with levamisole.

8 children, known to have been hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive for more than 6 months and with chronic active hepatitis on biopsy, received 2.5 mg levamisole/kg/day, 2 days a week for 6-18 months. In 6 of the 8 children transaminases normalized within 4-18 months of therapy, with seroconversion to antibody to HBeAg (anti-HBe) and disappearance of HBV-DNA polymerase from serum and of hepatitis B core antigen (HBcAg) from liver. In these cases liver biopsies taken after treatment showed histological regression to chronic persistent hepatitis. Two distinct patterns of response to levamisole were noted: patients having higher pretreatment transaminase levels and lower expression of HBcAg in the liver showed an early transaminase normalization and anti-HBe seroconversion with therapy, while in patients with less active disease and more diffuse HBcAg positivity in pretreatment liver biopsies, longer treatment periods were necessary to achieve these effects. Our results suggest that long-term levamisole therapy may be beneficial in HBeAg-positive chronic hepatitis type B.

Adolescent↗

Chronic hepatitis type B in childhood: longitudinal study of 35 cases.

Clinical, virological, and histological features of hepatitis B virus infection have been examined in 35 children, aged 1 to 11 years, known to be hepatitis B surface antigen (HBsAg) carriers for at least six months when entering the study. Only 10 patients had a history of acute unresolved hepatitis: in the remaining cases the detection of HBsAg had been an occasional finding. Although 77% of the patients were asymptomatic, all had evidence of hepatic involvement and liver history showed the features of chronic persistent hepatitis in 18 cases and of chronic active hepatitis in 16 cases, with associated cirrhosis in two of them. One patient had only minimal histological changes. A high percentage of children with both chronic persistent and chronic active hepatitis had evidence of active virus replication throughout the observation period. During the follow-up study of one to eight years (mean 3.1 +/- 1.7 years), transaminase levels became consistently normal in five patients with chronic persistent hepatitis, and inflammatory infiltrates disappeared in three of them. However, only one of these children cleared HBsAg from serum. Eleven of 16 patients with chronic active hepatitis received immunosuppressive treatment but only one of them achieved a complete and protracted remission, although active viral replication persisted. On the other hand, two of five untreated patients reached complete remission after two and three years of follow-up respectively and one of them cleared HBsAg three years later. These results would suggest the possibility of a spontaneous complete remission of HBsAg positive chronic active hepatitis in children but also raise doubts about the usefulness of immunosuppressive therapy in such patients.

Carrier State↗

Epidemiological aspects of acute viral hepatitis in drug abusers.

The epidemiological features of acute symptomatic viral hepatitis were examined in 151 consecutive, hospitalized drug abusers. Hepatitis B was diagnosed in 101 patients (66.8%), hepatitis A in 13 (8.6%) and non-A, non-B hepatitis in 35 (23.1%). Non-A, non-B hepatitis was significantly more prevalent among drug abusers than in an age-matched control population of non-drug abusers. Moreover, the mean duration of parenteral drug abuse was significantly lower among non-A, non-B cases than in patients with hepatitis A or B. These results suggest a wide circulation of both hepatitis B virus and non-A, non-B agent(s) among drug abusers in our area. These patients most likely represent a main reservoir of non-A, non-B infection due to the high rate of chronicity reported for non-A, non-B hepatitis.

Adolescent↗

Chronic evolution of acute hepatitis type B: prevalence and predictive markers.

During a prospective study of acute symptomatic viral hepatitis, started in 1978, 664 consecutive adult patients, including 223 drug abusers, fulfilled the diagnostic criteria (anti-HBc IgM positivity) for acute type B hepatitis. In order to evaluate the outcome of the disease, 443 patients were followed for up to 12 months after the onset. 2.4% of the infections became chronic; the rate did not significantly differ between drug addicts and non-drug abusers, suggesting that chronic hepatitis is a rare complication of acute symptomatic hepatitis type B. Ongoing liver damage after clearance of HBsAg from serum was observed in drug abusers only (14% of the cases). Clinical, biochemical and virological features of the acute phase in patients with ongoing infection were compared with those of uncomplicated cases. Anicteric hepatitis and lower transaminase values were significantly (p less than 0.05) associated to a chronic evolution of the disease, as well as a higher prevalence of HBV-DNA, DNA polymerase and HBcAg positivity in serum. Testing HBV-DNA and DNA polymerase early in the course of the infection appeared to be of high predictive value for the subsequent outcome of the illness.

Acute Disease↗

The changing epidemiology of acute type B hepatitis: results of an 11-year prospective study in Padua (northern Italy).

The epidemiological pattern of acute type B hepatitis has been investigated in 1,107 consecutive patients during an 11-year prospective study conducted in Padua (Northern Italy) between 1978 and 1988. Remarkable changes were observed: 1) the attack rate of the disease increased significantly (p less than 0.05) between 1978 (18/10(5) inhabitants) and 1982 (29/10(5) inhabitants), particularly in male subjects and in the 15-19-year age group. The proportion of drug addicts also increased from 8.8 to 42% (p less than 0.05). These changes coincide in time with the spread of parenteral drug abuse in our area; 2) the attack rate dropped significantly (p less than 0.05) between 1983 and 1988 reaching the lowest levels ever observed before (4.7/10(5) inhabitants). The proportion of drug addicts decreased significantly (p less than 0.05), although the number of subjects starting narcotic abuse did not decline in recent years. Two major events could explain this pattern: a partial exhaustion of the susceptible population after spread of infection among drug abusers and, later on, the changing risk behaviours observed in our drug abusers after the AIDS prevention campaign. Other factors, including vaccination of some high risk groups, could have contributed to these changes.

Adolescent↗

Acute non-A, non-B hepatitis in Italy: a 16-year prospective epidemiological study. The possible role of hepatitis C virus.

During a survey of acute symptomatic viral hepatitis conducted in Padua over the last 16 years, 404 (20%) cases of non-A, non-B hepatitis were observed, including 55% with overt parenteral exposure (35% drug abusers) and 45% with unknown exposure. Between 1978 and 1982 the attack rate of the disease increased significantly (p < 0.01) in males, (from 3.8 to 17.3/10(5) inhabitants), in adolescents and in youths. The prevalence of drug abusers rose up to 58% in 1982 suggesting the occurrence of an outbreak in this risk group. In subsequent years the attack rate returned to initial levels in males, although drug abuse still remains the single most important route of infection, and declined in females, especially after the disappearance of post-transfusion hepatitis since 1991. Retrospective anti-HCV testing of patients seen up to 1990 and prospective investigation of patients hospitalized later have shown an antibody prevalence of 88% among parenterally transmitted cases, and of 29% in the other patients, without significant differences between the prospective and the retrospective study. These findings suggest that an outbreak of hepatitis C occurred in our area in the early eighties and that drug abuse is still the most important mode of transmission of acute hepatitis C.

Acute Disease↗

Acute non-A, non-B hepatitis in childhood.

A prospective study of acute symptomatic viral hepatitis in childhood was started at the Department of Infectious Diseases of Padua (Italy) in 1978. During an 8-year period, 93 consecutive patients (aged 3 months to 12 years) fulfilled the diagnostic criteria, including five (5.5%) cases classified as non-A, non-B hepatitis. This figure is lower than that generally reported in adult patients, probably because of a lower exposure of children to blood and contaminated materials. Two of the five children with non-A, non-B hepatitis had received blood transfusions, while three had no history of parenteral exposure. Although the outcome of the illness was favorable in all five patients, a variety of clinical features could be observed: two children had a mild, short-lasting disease, anicteric in one case, while three had a polyphasic pattern of transaminases with delayed biochemical resolution, including one patient with deep jaundice and severe early phase features. These findings suggest that in children, as well as in adults, non-A, non-B hepatitis is probably a heterogeneous entity induced by different agents with different modes of transmission.

Acute Disease↗