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Biomedical subjects

P Kryger

Publications and source records attributed to P Kryger.

At least 55 records · Page 3Linked to original sources
PubMed1982

Light microscopic morphology of acute hepatitis non-A, non-B. A comparison with hepatitis type A and B.

Liver biopsies from a total of 240 patients with acute hepatitis A (86 patients), B (78 patients) and non-A, non-B (76 patients) were blindly evaluated for quantitative and qualitative light microscopic differences. No qualitative differences separate the three types of hepatitis, but the frequency and degree of some histological features seem to be characteristic of acute human non-A, non-B hepatitis. The degree of focal necrosis and portal inflammation was less pronounced in the non-A, non-B group as compared to the hepatitis A and B groups (P less than 0.01). Twenty-six percent of the non-A, non-B liver biopsies showed steatosis as compared with 10% and 6% in the hepatitis A and B groups, respectively (P less than 0.01). Bridging necrosis only occurred in liver biopsies from patients with non-A, non-B and B hepatitis. Abnormal bile ducts were detected in a total of five patients, three of whom were found in the non-A, non-B group. A comparison between histological findings in non-A, non-B patients with and without a possible intravenous exposure revealed that steatosis, cholestasis, large piecemeal necrosis and confluent necrosis occurred with the highest incidence in the patients without intravenous exposure, indicating that non-A, non-B hepatitis may be caused by more than one etiological agent.

Adolescent↗
PubMed1982

Viral hepatitis in Danish children. Disappearance of an infection from its previous reservoir.

Two hundred and eighty-five healthy Danish children aged between 7 and 17 years were studied for hepatitis B antigen and antibodies to hepatitis A and B. A positive response to each of these infections was found in 0.7% of them. During a 5-year period 40 children were admitted to hospital with viral hepatitis, 30 of whom had hepatitis A. Eighty-three per cent of these cases of hepatitis A were secondary to adult cases, or had resulted from foreign travel. Hepatitis A is no longer endemic in Danish children, and morbidity from hepatitis B or non-A non-B is negligible.

Adolescent↗
PubMed1982

Hepatitis B and A virus antibodies in alcoholic steatosis and cirrhosis.

Sera from 74 alcoholics with cirrhosis and 63 alcoholics with steatosis were tested for antibody to hepatitis B surface antigen, to hepatitis B core antigen, and to hepatitis A virus by radioimmunoassay or enzyme-linked immunosorbent assay. No significant difference between the two groups of alcoholics could be found concerning the prevalence of these antibodies. The total group of patients had antibody to hepatitis B surface antigen or hepatitis B core antigen, or both, significantly (p less than 0.001) more often (26%) than sex- and age-matched controls (4%). No significant difference was found between patients and controls concerning the prevalence of antibody to hepatitis A virus (46% v 40%). In patients with cirrhosis, no correlation between wedged hepatic vein pressure or wedged-to-free hepatic vein pressure and any of the viral antibodies could be established. The present results suggest that hepatitis B virus does not play a major role in the progression of alcoholic liver disease, but longitudinal studies are needed to solve this problem. The reason for the increased prevalence of antibodies to hepatitis B virus in these patients is unknown.

Adult↗
PubMed1981

IgM antibody to hepatitis B core antigen (anti-HBc IgM) in "healthy" HBsAg carriers: a longitudinal study of 75 cases.

In 75 healthy HBsAg carriers with normal liver tissue who were followed over a four years period, anti-HBc IgM was determined by ELISA. 61 HBsAg carriers (81%) were positive for anti-HBc IgM at first investigation. 54 individuals demonstrated persistence of anti-HBc IgM, 7 became anti-HBc IgM-negative within the observation period. 12 persons were persistent anti-HBc IgM of low quantities. 3 of 4 individuals with HBsAg clearance demonstrated a considerable decrease of anti-HBc IgM concentration. Although signs of liver damage or development of chronic liver diseases were not observed at the time of control biopsy the existence of anti-HBcIgM indicates that there exists also in healthy HBsAg carriers a persistent stimulation by HBcAg, inducing the production of anti-HBc IgM as a sign of permanent ongoing virus B replication. These results require a new and critical review of the "healthy" HBsAg carrier state.

Antibodies, Viral↗
PubMed1981

Viral hepatitis in southeast Asian refugees.

Five hundred sixty-four Vietnam refugees were studied for past or present infection with hepatitis A and B virus (HAV and HBV) by sensitive serological assays for hepatitis B surface and e-antigen and antibodies to HBsAg, HBeAg, HBcAg, and HAV. Fifteen percent of the men and 6% of the women were HBsAg-positive. Of these 66% were also positive for HBeAg. Serum transaminase values did not effectively differentiate between the infectious HBeAg carriers and the less infectious anti-HBe carriers. The HBsAg carrier rate did not increase by age after infancy, and among children, carriers clustered around HBsAg carrier mothers only. In contrast, the distribution of antibodies to the three HBV-associated antigens suggested continuous exposure throughout childhood, and a 90% prevalence rate was found at the age of 20 years. Screening for HBeAg in this new population group is necessary if appropriate precautions are to be taken, and if medical management of these patients is to be optimal. The prevalence of antibody to hepatitis A increases with age to 90% at 15 years. Among anti-HAV-positive children and adults IgM- anti-HAV was found in 8% of the children and none of the adults, indicating that only a few children may be in an infectious stage at the time of study, and therefore no specific prophylactic precautions are necessary.

Adolescent↗
PubMed1981

The significance of serologic, histologic, and immunohistologic findings in the prognosis of 88 asymptomatic carriers of hepatitis B surface antigen.

Eighty-eight asymptomatic carriers of hepatitis B surface antigen (HBsAg) were followed with biochemical, serologic, histologic, and immunohistologic studies over a period of four years. None of the 78 HBsAg carriers with normal or minimally changed liver tissue, antibody to hepatitis B e antigen (HBeAg) in serum, and no intranuclear hepatitis B core antigen (HBcAg) developed a chronic inflammatory liver disease. Four individuals lost circulatory HBsAg, and at least two individuals terminated their HBsAg carrier state. Seven asymptomatic HBsAg carriers with chronic hepatitis were characterized by HBeAg in serum and intranuclear HBcAg. However, three HBsAg carriers with chronic hepatitis and an absence of intrahepatocellular HBcAg were positive for antibody to HBeAg over the observation period. The mechanism that leads to chronic hepatitis in these patients remains to be determined.

Adult↗
PubMed1981

Anti-HBc of IgM-class, HBeAg and anti-HBe in acute and chronic hepatitis B.

The presence and persistence of IgM antibody against hepatitis B core antigen (anti-HBc IgM) and the correlation with other HBV markers were studied in 42 patients, all of whom had acute HBsAg-positive hepatitis but whose subsequent diseases differed. All patients initially had anti-HBc IgM. In 13 out of 15 patients with uncomplicated acute hepatitis, anti-HBc IgM disappeared within 6 months after onset of the disease. In five out of 12 patients, who in spite of transient HBsAg developed chronic liver disease, the anti-HBc IgM persisted for more than 2 years. Among 15 patients with persistent HBsAg, anti-HBc IgM was present from 7 months to more than 8 years. Seroconversion from HBeAg to anti-HBe was observed in seven patients and in five of these anti-HBc IgM disappeared during the follow-up period. These results indicate that anti-HBc IgM can be used as a serological marker of recent or ongoing HBV infection.

Adolescent↗
PubMed1981

Enzyme-linked immunosorbent assay for detection of immunoglobulin M antibody to hepatitis B core antigen.

An enzyme-linked immunosorbent assay for detection of specific immunoglobulin M (IgM) antibodies against the core antigen of the hepatitis B virus (anti-HBc IgM) is described. The interference of IgM rheumatoid factor was evaluated quantitatively. In the anti-HBc IgM test, the rheumatoid factor gave false-positive results when the concentration exceeded 20 IU/ml. The rheumatoid-positive sera were disclosed by a control and retested for anti-HBc IgM after absorption of rheumatoid factor with latex particles aggregated with human IgG. In five of seven selected patients with acute hepatitis B followed to biochemical and clinical recovery, anti-HBc IgM was present transiently until antibodies against hepatitis B surface antigen (anti-HBs) appeared. Two patients had persistent anti-HBc IgM during the follow-up period. Four patients with hepatitis B surface antigenemia and progression to chronic liver disease did not clear their anti-HBc IgM in the period of observation (11 to 24 months). Anti-HBc IgM could not be demonstrated in 223 of 225 Danish blood donors. The two donors found positive for anti-HBc IgM also had anti-HBs. Twenty patients with acute A or non-A non-B hepatitis were negative for anti-HBc IgM. The enzyme-linked immunosorbent assay for anti-HBc IgM described here has a high specificity and sensitivity. The diagnostic relevance needs further evaluation, including quantitation of anti-HBc IgM, but the results presented indicate that anti-HBc IgM may be helpful in differentiating between prior and recent or ongoing hepatitis B infection.

Antibodies, Viral↗
PubMed1980

Acute non-A, non-B hepatitis--clinical, epidemiological and histological characteristics.

Among 73 consecutive patients with biopsy documented acute non-toxic hepatitis, half of the patients (49%) had acute type B hepatitis, while 27 patients (37%) had acute type A infection. One patient had a significant rise in antibodies against cytomegalovirus. The remaining 10 patients (14%) fulfilled the criteria of hepatitis type non-A, non-B. The main type of exposure for hepatitis A was visit to endemic hepatitis areas (41%), and for type B it was drug addiction (46%). Half of the patients with hepatitis non-A, non-B had no known hepatitis exposure while some had visited endemic hepatitis areas or were drug addicts. The patients with non-A, non-B hepatitis had significantly less biochemical changes as compared to the patients with hepatitis B. In contrast, the histological findings showed the greatest activity in the biopsies from patients with hepatitis B and non-A, non-B. Follow-up liver biopsies in half of the patients with non-A, non-B hepatitis showed no signs of chronic active liver disease. It is concluded that hepatitis type non-A, non-B is a significant problem in Denmark.

Acute Disease↗
PubMed1978

Left ventricular function after myocardial infarction: relation between systolic time intervals and quantitative ischaemic ECG changes.

Twentyfour male patients with sustained myocardial infarction (MI) were studied with 12-lead ECG and systolic time intervals (STI) 5 months after the acute episode. From the ECGs were calculated the summed voltages of the R wave (sigma R), the Q wave (sigma Q), and the ST segment deviation (sigma ST). These ischaemic ECG variables were correlated with the STI parameters of left ventricular function: LVETI, PEP and PEP/LVET. Statistically significant regression equations relating the ECG changes to the STI variables were found in anterior MI, for sigma ST in the entire series, but not in inferior MI. Thus a simple and rapid inspection of the resting 12-lead ECG gives an indirect but reliable quantitative estimate of left ventricular function in patients with a sustained myocardial infarction.

Aged↗
PubMedDate not supplied

Presence and meaning of anti-HBc IgM as determined by ELISA in patients with acute type B hepatitis and healthy HBsAg carriers.

To evaluate the clinical implication of IgM antibody against hepatitis B core antigen (anti-HBc IgM), a consecutive series of 87 patients with acute type B hepatitis and 16 healthy carriers of hepatitis B surface antigen (HBsAg) were studied by a newly developed reverse ELISA technique. Anti-HBc IgM was present for at least 2 months in 81 of the 82 patients with HBsAg at the time of admission. Seroconversion from HBsAg to anti-HBs was observed in 38 patients during the time of observation, and in all patients, anti-HBc IgM was present until clearance of HBsAg. Thirty-three of the 38 patients remained anti-HBc IgM positive, at least until the appearance of anti-HBs. Quantitation of anti-HBc IgM by ratio unit (RU) values revealed that 3 of 8 patients with RU values greater than or equal to 5 for more than 6 months subsequently developed chronic liver disease, as compared to 1 of 72 patients with anti-HBc IgM above this level for less than 6 months. Anti-HBc IgM was demonstrated in 3% of 5 patients with total anti-HBc titer above 1:100 despite the presence of anti-HBs. In these patients, anti-HBc IgM steadily decreased after the onset of illness indicating a recent acute hepatitis B infection. Anti-HBc IgM was present in 12 of 16 healthy HBsAg carriers (75%). However, these 12 carriers had RU values between 2.5 to 5.5, compared with RU values above 5 (mean RU value 11.3) at the onset of illness in 80 of 82 HBsAg-positive patients with acute hepatitis. Anti-HBc IgM seems to be a specific serological marker for recent or ongoing hepatitis B infection which may be useful in differentiation between hepatitis B infection with or without HbsAg and acute non-A, non-B hepatitis.

Acute Disease↗
PubMedDate not supplied

Acute type B hepatitis among HBsAg negative patients detected by anti-HBc IgM.

A consecutive group of 169 patients with acute hepatitis found negative for hepatitis B surface antigen (HBsAg) and negative for IgM antibody against hepatitis A (anti-HAV IgM) was studied for presence of IgM antibody against hepatitis B core antigen (anti-HBc IgM) by ELISA. Anti-HBc IgM was found in a total of 34 of 60 patients with detectable total anti-HBc. One hundred and nine patients had no detectable anti-HBc IgM and no total anti-HBc and were thus considered as having acute non-A, non-B hepatitis. Among the 34 patients with anti-HBc IgM in their first serum sample, 23 were anti-HBs negative and all had high and steadily decreasing ratio unit (RU) values for anti-HBc IgM (mean RU value 17.1). Twelve of the 23 patients showed seroconversion to anti-HBs during the follow-up, indicating an actual hepatitis B virus infection. Eleven of the 34 anti-HBc IgM positive patients had anti-HBs in their first serum sample. In this group, the RU values for anti-HBc IgM were high and steadily declining and the initial values were significantly lower (mean RU value 9.9) (p less than 0.05) than in the anti-HBs negative group. Evidence is provided that anti-HBc IgM in serum from patients with HBsAg negative hepatitis with or without anti-HBs indicates an actual hepatitis B virus infection. According to generally accepted criteria, the demonstration of anti-HBc IgM identified 20% of the 169 patients with acute non-A, non-B hepatitis as having an actual hepatitis B infection.

Acute Disease↗
PubMedDate not supplied

Chronic persistent hepatitis: serological classification and meaning of the hepatitis B e system.

In order to evaluate the prognostic implications of the hepatitis B e system in patients with chronic persistent hepatitis (CPH), 53 consecutive patients were studied. Fourteen of 16 patients with HBsAg and HBeAg were followed from 12 to 120 months (mean, 38 months). Eleven of the 14 patients were persistently HBeAg positive and five of these developed chronic active hepatitis (CAH) or cirrhosis. A further nine patients were HBsAg positive but HBeAg negative at time of CPH diagnosis (mean follow-up, 47 months). One of these nine patients developed CAH during follow-up. The remaining 28 patients were all HBsAg negative, and only 2 or the 28 patients progressed to CAH or cirrhosis during the time of follow-up (mean, 43 months). It is concluded that the persistence of HBeAg in patients with CPH indicates a serious prognosis with a frequent transition to CAH or cirrhosis.

Adult↗
PubMedDate not supplied

Hepatitis B virus DNA in serum from patients with acute hepatitis B.

Sera from 77 consecutive patients with acute type B hepatitis were examined for hepatitis B virus DNA (HBV DNA) by a spot hybridization method. The median follow-up time was 8 months (range, 1 week to 3 years). HBV DNA was detected in 26 (34%) patients on admission to the hospital. A significant positive correlation was found between short duration of symptoms and the presence of HBV DNA (p less than 0.025). Twenty-four (46%) of 52 HBeAg-positive patients were HBV DNA positive compared to 2 HBV DNA-positive patients of 25 HBeAg-negative patients (8%) (p less than 0.001). Four HBeAg-negative patients had serum HBV DNA initially or during follow-up; three had anti-HBe. Six of 77 patients with acute type B hepatitis (8%) became chronic HBsAg carriers, and HBV DNA was detectable from 5 months to more than 3 years after onset of symptoms. The presence of serum HBV DNA for more than 8 weeks after initial symptoms may predict development of a chronic HBsAg carrier state. In none of the chronic carriers was serum HBV DNA present after clearing of HBeAg.

Adolescent↗