Preliminary results from epidemiological and laboratory studies on the new H1N1 influenza virus show that the 7-20 years age group suffered the highest morbidity; some adults over 20 years of age were also affected. The influenza epidemic caused by the H1N1 virus was characterized by slow spread, unevenness of attack rates, and the occurrence of many mild cases and inapparent infections. At least up to the end of 1977 there was concurrent persistence and spread of both H1N1 and H3N2 viruses. The H and N antigens of the new H1N1 virus, as well as its behaviour toward nonspecific inhibitors, were found to be closely similar to the old H1N1 virus prevalent during the first half of the 1950s. Most of the new H1N1 isolates in eggs were found to be temperature sensitive.

Adolescent↗

PubMedDate not supplied

Chronic lobular hepatitis: a clinicopathological and prognostic study.

A series of 80 patients with chronic lobular hepatitis (CLH) was reviewed clinically and histologically to demonstrate etiology, clinical presentation, course, and prognosis of this disorder. Data from our study indicate that CLH in Taiwan is a disease of viral origin, mostly hepatitis B (67.5%) and some non-A, non-B. It occurs predominantly in young males (81.3%); frequently commences as acute viral hepatitis (57.5%); and has clinical and laboratory features similar to convalescent viral hepatitis or even indistinguishable from full-blown acute viral hepatitis. Clinical and histological follow-up study indicate that CLH may extend for several years with remissions and relapses. No evidence of progression to cirrhosis was observed at least in a 4 1/2-year period of follow-up. It is concluded that CLH is a persistent but nonprogressive disease although the number of non-A, non-B CLH is too small to ascertain its nonprogressive course. The prognosis is generally good, and no specific therapy is required.

Adolescent↗

PubMedDate not supplied

Sex difference in chronic hepatitis B virus infection: an appraisal based on the status of hepatitis B e antigen and antibody.

Hepatitis B e antigen (HBeAg) and antibody (anti-HBe) were studied by radioimmunoassay in consecutive series of 145 asymptomatic hepatitis B surface antigen (HBsAg) carriers, 389 patients with HBsAg-positive chronic liver disease and 194 patients with HBsAg-positive hepatocellular carcinoma, and compared between male and female subjects. The male to female ratio increased from 1.2 in asymptomatic carriers to 6.3 in chronic liver disease and 9.8 in hepatocellular carcinoma. Abnormal SGPT was much more frequently seen in male carriers than in females (p less than 0.01). Contrary to female patients with chronic liver disease, the positive rate for HBeAg in males is lower and tended to decrease with increasing age. It is postulated that male patients with chronic hepatis B virus infection might have higher HBeAg clearance ability that resulted in more frequent hepatitis B virus DNA integration and subsequent development of hepatocellular carcinoma. However, the ultimate mechanism regulating this difference awaits further study.

Adolescent↗

PubMedDate not supplied

The window period between hepatitis B e antigen and antibody in chronic type hepatitis.

To examine the period between disappearance of hepatitis B e antigen (HBeAg) and appearance of anti-HBe, 48 patients with clinicopathologically verified chronic B hepatitis were followed every 1 to 3 months after HBeAg clearance. Sera were tested by radioimmunoassay for HBeAg and anti-HBe. Anti-HBe appeared in days to years, mostly (78.7%) within 1 year, after disappearance of HBeAg. Only 40.5% of patients had an "e-window" shorter than 1 month. Clinical and histological exacerbation preceding HBeAg clearance precipitated or accelerated appearance of anti-HBe. Since the patients in the "e-window" period were positive for DNA polymerase, it is suggested that the "e-window" reflects relative insensitivity of the radioimmunoassay rather than absence of HBeAg/anti-HBe. Therefore, HBeAg can reappear and clinical activity can relapse particularly during immunosuppressive therapy.

Adult↗

PubMedDate not supplied

White count, pH and lactate in ascites in the diagnosis of spontaneous bacterial peritonitis.

In order to evaluate the diagnostic accuracy of ascitic pH and lactate for early confirmation of spontaneous bacterial peritonitis (SBP), 109 consecutive patients with ascites were studied. The mean ascitic leukocyte [white blood cell (WBC)] and polymorphonuclear cell (PMN) counts, pH and lactate levels in 42 patients with sterile "normal" ascites were 124 +/- 157 per mm3, 41 +/- 77 per mm3, 7.502 +/- 0.097 and 11.1 +/- 7.9 mg per dl, respectively. Mean ascitic WBC and PMN counts were significantly increased in 10 patients with SBP (10,452 +/- 8,091 and 9,522 +/- 7,470 per mm3), in 10 patients with bloody ascites (2,591 +/- 4,284 and 1,057 +/- 1,494 per mm3) and in 11 patients with cytology positive malignant ascites (1,529 +/- 2,071 and 868 +/- 1,601 per mm3) (p less than 0.001). Mean ascitic pH was significantly reduced in SBP (7.335 +/- 0.048), in bloody ascites (7.384 +/- 0.037) and in cytology positive malignant ascites (7.355 +/- 0.167) (p less than 0.001). Mean ascitic lactate was also significantly elevated in these three groups of patients (36.8 +/- 17.0, 42.8 +/- 35.8 and 24.0 +/- 17.5 mg per dl, respectively; p less than 0.001) as well as in patients with bacteremia (51.6 +/- 78.0 mg per dl, p less than 0.005). However, ascitic pH less than 7.31, ascitic lactate greater than 33 mg per dl were observed only in three of the patients with SBP.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascitic Fluid↗

PubMedDate not supplied

Natural history of chronic hepatitis B virus infection in Taiwan: studies of hepatitis B virus DNA in serum.

Hepatitis B virus DNA (HBV DNA) in serum was measured by a Spot hybridization technique in a consecutive series of 79 cases with chronic HBV infection from Taiwan. HBV DNA was found in 96.3% (52/54) of HBeAg-positive, 66% (2/3) with neither HBeAg or anti-HBe and in 63.6% (14/22) of anti-HBe positive patients. The levels of HBV DNA in the HBe-Ag-positive patients were significantly higher than in the anti-HBe positive patients (median, 944 vs. 58 pg per ml, p less than 0.001). The mean ages increased from 28.7 years for the cases with high levels of HBV DNA, to 34.7 years for those with low levels (p less than 0.01) and to 41.0 years in those without HBV DNA in serum (p less than 0.05 when compared with those with low level of HBV DNA). Ninety per cent of patients (27/30) with high levels of HBV DNA showed only minor hepatic inflammatory activity, as did 91% (10/11) of those without HBV DNA. In contrast, histologic signs of chronic active hepatitis or chronic lobular hepatitis were demonstrated in 76% of cases (29/38) with low levels of HBV DNA. These data are consistent with the hypothesis that liver damage occurs during the period of clearance of hepatocytes supporting HBV replication, and are inconsistent with the view that HBV may be directly cytopathic. Thus, the natural history of chronic HBV infection may be divided into three phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Changes of serum hepatitis B virus DNA in two types of clinical events preceding spontaneous hepatitis B e antigen seroconversion in chronic type B hepatitis.

Two types of clinical events, acute exacerbation and uneventful course, precede spontaneous HBeAg seroconversion to its antibody (anti-HBe) in chronic type B hepatitis. To examine the possible mechanism responsible for these two types of clinical events, serial serum specimens from 75 patients who underwent spontaneous HBeAg seroconversion were assayed for hepatitis B virus DNA by slot blot hybridization with 32P-labeled cloned hepatitis B virus DNA as probe. Of these 75 patients, 47 (62.7%) had episodes of acute exacerbation (ALT greater than 300 IU per liter) within 3 months prior to HBeAg seroconversion. All of these 47 patients had high hepatitis B virus DNA levels (greater than 1,000 pg per ml) at the onset of acute exacerbation. Their serum hepatitis B virus DNA disappears shortly before or simultaneously with the HBeAg clearance in 27 patients (57.4%) and persisted but with decreasing levels for 2 to 40 months in 20 patients. Most of these patients had high alpha-fetoprotein levels or evidence of bridging hepatic necrosis. In contrast, the serum hepatitis B virus DNA was undetectable for a minimum of 3 (3-17) months in the 28 patients who had an uneventful course before HBeAg seroconversion. Twenty of these 28 patients had well-documented episodes of acute exacerbation with high hepatitis B virus DNA levels, but with normal alpha-fetoprotein and little evidence of extensive necrosis as far back as 6 to 27 months before HBeAg seroconversion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Acute exacerbation in chronic type B hepatitis: comparison between HBeAg and antibody-positive patients.

The incidence, clinicopathological features and etiology of acute exacerbation occurring in patients with chronic type B hepatitis were assessed prospectively among 385 patients who had HBeAg and 279 who had anti-HBe in serum. During an average follow-up of 23.5 months, acute exacerbations occurred in 197 HBeAg-positive patients and in 56 anti-HBe positive patients, with a calculated annual incidence of 28.6 and 10.3%, respectively (p less than 0.001). The clinical and laboratory findings of acute exacerbations were similar in the HBeAg-positive and anti-HBe positive patients. The mean serum bilirubin and alpha-fetoprotein levels were higher in anti-HBe positive patients (p less than 0.01), but actual differences were small. The histologic features of acute exacerbations were also similar in the HBeAg-positive patients and anti-HBe positive patients. Lobular alterations were the main histologic findings; in addition, one-fourth of patients had bridging necrosis and one-fourth had piecemeal necrosis. Spontaneous reactivation of hepatitis B was the major cause of these exacerbations in both HBeAg-positive patients (91.5%) as well as anti-HBe positive patients (62.5%). Hepatitis delta virus superinfection accounted for a higher percentage of exacerbations in anti-HBe positive patients (14.3%) than in HBeAg-positive cases (6.5%). Hepatitis A and possibly non-A, non-B virus superinfections also contributed to some episodes of exacerbation. Thus, acute exacerbations of disease occurred more frequently in HBeAg-positive patients than in anti-HBe positive patients with chronic type B hepatitis, but the clinicopathological features and etiologies were similar.

Acute Disease↗

PubMedDate not supplied

The development of cirrhosis in patients with chronic type B hepatitis: a prospective study.

The incidence and contributing factors of cirrhosis developing in patients with chronic type B hepatitis were assessed prospectively in 684 clinicopathologically verified patients, of which 509 were HBeAg positive and 175 were anti-HBe positive at entry into the study. During an average follow-up period of 35.3 months, cirrhosis occurred 6 to 64 months after entry in 35 HBeAg-positive and 7 anti-HBe positive patients with a calculated annual incidence of 2.4 and 1.3%, respectively (p greater than 0.05). The incidence increased significantly with the increasing age at entry. Patients who had experienced (a) hepatic decompensation, (b) repeated episodes of severe acute exacerbation (with alpha-fetoprotein greater than 100 ng per ml and/or bridging hepatic necrosis), (c) severe acute exacerbation not accompanied by subsequent HBeAg seroconversion and (d) hepatitis B virus reactivation (particularly those with HBeAg reappearance) were found to develop cirrhosis much more frequently (p less than 0.001). Contrary to general belief, patients who had hepatitis delta virus superinfection and patients with chronic active hepatitis were not particularly prone to develop cirrhosis. We conclude that in addition to age factor, the extent, severity, duration, frequency and etiology of the hepatic lobular alterations are important factors for the development of cirrhosis in patients with chronic type B hepatitis.

Adolescent↗

PubMedDate not supplied

HLA class I antigen display on hepatocyte membrane in chronic hepatitis B virus infection: its role in the pathogenesis of chronic type B hepatitis.

It has been suggested that cytotoxic T cells are involved in the recognition and lysis of the infected hepatocytes in chronic hepatitis B virus infection, and that the target antigen is probably HBcAg which is displayed on the hepatocyte membrane during active viral replication. However, studies in other viral infection have demonstrated that cytotoxic T cells recognize viral antigen on the infected cells only in the context of HLA class I antigens. To test whether this mechanism is also operative in chronic hepatitis B virus infection, we studied the expression of HLA class I antigens in livers from 35 patients with chronic hepatitis B virus infection by indirect immunofluorescence using monoclonal antibody against HLA class I antigens. The blocking effect of monoclonal antibody against HLA class I antigens on the in vitro T cell cytotoxicity to autologous hepatocytes was also studied. The results revealed that HLA class I antigen was undetectable on the hepatocyte membrane in all of 10 HBeAg-positive carriers with minor hepatitic activity, whereas it was demonstrated in 15 (88%) of the 17 HbeAg-positive patients with chronic active liver disease and in 7 (87%) of the 8 anti-HBe-positive "normal" carriers. The in vitro T cell cytotoxicity to autologous hepatocytes in six HBeAg-positive patients with chronic active liver disease was significantly inhibited by preincubation of hepatocytes with monoclonal antibody (10 to 40 micrograms per ml) against HLA class I antigen, but not by monoclonal antibody against HLA class II antigens and non-HLA-associated surface molecules (Leu 11).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗

PubMedDate not supplied

The incidence of fulminant hepatic failure in acute viral hepatitis in Taiwan: increased risk in patients with pre-existing HBsAg carrier state.

The incidence of fulminant hepatitis in Taiwan was studied in a series of consecutive 523 patients with acute viral hepatitis including 11 with acute hepatitis A, 67 with acute hepatitis B, 124 with acute hepatitis NANB and 321 acute hepatitis in HBsAg carriers (patients who were HBsAg positive but anti-HBc IgM negative). Thirty-eight (7.3%) were recognized as fulminant hepatitis. The incidence of fulminant hepatitis was relatively low in patients with acute hepatitis A, B or NANB (2.0% or 4 out of 202), but was much higher in HBsAg carriers with acute hepatitis (10.6% or 34 out of 321). The incidence of fulminant hepatitis correlated significantly with the pre-existing HBsAg carrier state after adjustment of the confounding effect of age. The incidence of fulminant hepatitis in HBsAg carriers with acute hepatitis showed no significant difference in relation to sex or to the presence of anti-delta in serum, but it increased proportionally with age. We concluded that the pre-existing HBsAg carrier state was a major risk factor for development of fulminant viral hepatitis. The etiology of superimposed acute hepatitis leading to fulminant hepatic failure might be varied according to the different geographic origins.

Acute Disease↗

PubMedDate not supplied

Acute hepatitis C virus superinfection followed by spontaneous HBeAg seroconversion and HBsAg elimination.

Acute hepatitis C virus superinfection followed by spontaneous hepatitis B e antigen seroconversion and hepatitis B surface antigen clearance in a patient with chronic type B hepatitis is described. The observations suggests that HCV may exert a suppressive effect on hepatitis B virus.

Acute Disease↗