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Biomedical subjects

B Berris

Publications and source records attributed to B Berris.

At least 19 recordsLinked to original sources
PubMed1995

Accelerated nodulosis in a patient with psoriasis and arthritis during treatment with methotrexate.

A 66-year-old woman with longstanding psoriasis involving the skin presented with asymmetrical polyarthritis. Methotrexate (MTX) was given initially intramuscularly and orally. Intramuscular MTX was discontinued, and a few months after she had been taking only oral MTX she developed nodules, first in surgical incisions, and subsequently in her buttocks, thighs, legs, and arms. Reduction of the dose of oral MTX was followed by gradual diminution in size of the nodules and then total disappearance.

Administration, Oral↗
PubMed1992

Effects of interferon-alpha therapy on serum and liver HBV DNA in patients with chronic hepatitis B.

The aim of this study was to evaluate the effect of interferon-alpha therapy on serum and liver HBV DNA in 20 patients with chronic hepatitis B and to correlate the presence or absence of HBV DNA with the clinical response. There were 11 responders and all lost HBV DNA from the serum. Ten of the 11 were followed for 36 months following IFN treatment and remained well with absence of HBeAg and HBV DNA from the serum and with normal ALT. Five also lost HBsAg. HBV DNA became undetectable in the liver of nine of 10 of these patients in whom liver tissue was available for study. HBV DNA persisted in the liver of seven of nine nonresponders and was not detected in two in spite of the presence of HBV DNA and HBeAg in the serum of these two patients. We conclude that IFN may induce long remissions in patients with chronic hepatitis B with loss of HBV DNA from the serum and that occasionally HBV DNA may persist in the liver of such patients.

Adult↗
PubMed1991

Anti-HCV in post-transfusion hepatitis: deductions from a prospective study.

Stored sera from 52 patients who developed post-transfusion hepatitis (PTH) during a prospective study of PTH in Toronto in 1984/85, sera from 111 donors whose blood was transfused into these patients and sera from 50 patients with chronic active hepatitis with a remote history of blood transfusion were tested for anti-HCV. In patients with PTH seroconversion occurred relatively early. Ten converted in less than 14 weeks after transfusion. Only three of the 34 patients (9%) whose hepatitis resolved developed anti-HCV compared to 11 of 18 (61%) whose hepatitis became chronic. Patients who seroconverted had higher alanine aminotransferase (ALT) values during the phase of acute hepatitis than those who did not seroconvert. Most of the patients who developed PTH received blood that was negative for anti-HCV. Four donors whose blood was positive for anti-HCV transmitted hepatitis. Three of the patients developed anti-HCV and chronic hepatitis. One of the recipients did not seroconvert and the hepatitis resolved. Forty-two of the 50 patients (84%) with chronic hepatitis and a remote history of blood transfusion were positive for anti-HCV. We conclude that anti-HCV-positive donors may transmit hepatitis C; that if anti-HCV is diagnostic of hepatitis C, most cases of acute PTH are either not due to hepatitis C or may represent cases of hepatitis C in which the anti-HCV test was undetectable. On the other hand, most cases of PTH which progress to chronic hepatitis are caused by HCV.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1990

Parotid gland enlargement in HIV infection: clinical/imaging findings.

Parotid gland enlargement with or without facial paralysis may be the presenting clinical manifestation of AIDS. Submandibular involvement may occur as well. Failure to recognize this association may lead to inappropriate or unnecessary intervention in the investigation and treatment of the salivary gland enlargement. In this paper, we discuss the role of imaging techniques in the investigation of salivary gland enlargement, and identify the specific radiologic signs found in HIV infection. Demonstration of intraparotid or submandibular gland cysts with focal intraparotid mass lesion(s) on imaging may help to differentiate parotid gland enlargement due to HIV infection from the many other causes of parotid enlargement.

Adult↗
PubMed1989

Lactase deficiency in Singapore-born and Canadian-born Chinese.

Seventy-three of 77 adult Singapore-born Chinese (95%) and 48 of 49 Canadian-born adult Chinese (98%) were demonstrated to be lactase deficient using the lactose breath hydrogen test. The similar prevalence of lactase deficiency in the Singapore- and the Canadian-born Chinese despite a larger estimated amount of daily milk ingestion in the Canadian-born Chinese (430 ml vs 157 ml) supports the concept that lactase deficiency, which is transmitted genetically, does not have an adaptable component related to the quantity of lactose ingested. When the lactose breath hydrogen test performed with a dose of 0.5 g/kg of lactose was compared with the test using a standard dose of 50 g of lactose, there was very little loss of sensitivity. In spite of the presence of lactase deficiency, only 32% of the Singapore subjects and 23% of the Canadian subjects had gastrointestinal symptoms when milk was ingested in the daily diet. Peak breath H2 was higher in females than males, but the difference was more significant in the Canadian cohort.

Adolescent↗
PubMed1988

Posttransfusion hepatitis in Toronto, Canada.

Five hundred seventy-six consecutive patients from the surgical, obstetrical, and medical services who had received transfusions of volunteer blood were followed-up at regular intervals for 6 mo. Fifty-three (9.2%) developed acute posttransfusion non A, non B hepatitis. Forty-seven (89%) had an incubation period between 2 and 8 wk. The frequency was not related to the age or sex of the patient, the indications for transfusion, the type of surgery, anesthesia, the presence of perioperative hypotension, or the number of units of blood transfused. There were no cases of fulminant hepatitis. Nineteen of the 53 patients (36%) with acute posttransfusion hepatitis progressed to chronic hepatitis. Development of chronic hepatitis was not related to the age or sex of the patient, the incubation period of the preceding acute hepatitis, the presence of shock or malignancy, or the number of units of blood transfused. Patients with higher levels of alanine aminotransferase during the acute hepatitis were more prone to develop chronic hepatitis. The finding of 9.2% of transfusion-related hepatitis in recipients of hepatitis B surface antigen-screened blood from volunteer donors underscores the potential sequelae of blood transfusion, especially as a source of contribution to the pool of chronic liver disease.

Female↗
PubMed1988

Serum HBV-DNA (hepatitis B virus DNA) in acute and chronic hepatitis B infection.

HBV DNA was measured in the sera of 69 patients with hepatitis B virus infections. Sixteen patients had acute hepatitis B, 24 had chronic active hepatitis (CAH), 6 had chronic persistent hepatitis (CPH), 5 had cirrhosis without CAH and 18 were asymptomatic HBsAg carriers. In patients with acute hepatitis B who recovered, HBV DNA was present in the serum transiently early in the illness. HBV DNA persisted in the serum in the two patients who developed chronic hepatitis. Sera of 23 of 24 patients with CAH were persistently positive for HBV DNA. There was no relationship between the quantity of HBV DNA in the serum and the histological intensity of activity. Thirteen of the 24 patients with CAH had histological evidence of cirrhosis in addition to CAH and HBV DNA was detected in the sera of all 13. The sera of 2 of 6 patients with CPH were positive for HBV DNA. In one it was positive only where there was clinical evidence of reactivation of HBV infection. The other patient subsequently developed CAH. Sera of 5 patients with established HBsAg positive cirrhosis but without evidence of CAH were negative for HBV DNA. Two of these patients had hepatocellular carcinoma. Sera of 18 asymptomatic anti-HBe positive carriers with normal ALT were negative for HBV DNA. HBeAg and HBV DNA were not always found in the serum together. In acute hepatitis 5 patients with HBV DNA in the serum were HBeAg positive, but in 6 patients the sera were HBeAg positive inthe absenceof HBV DNA.

Acute Disease↗
PubMed1987

Hepatitis B virus DNA in asymptomatic HBsAg carriers: comparison with HBeAg/anti-HBe status.

Sera of 17 HBeAg positive and 104 anti-HBe positive asymptomatic HBsAg carriers from two cohorts were tested for HBV DNA. HBV DNA was found in 13 of 17 HBeAg positive carriers (76.5%) and in only 7 of 104 of anti-HBe positive carriers (6.7%). Eleven of the 17 HBeAg positive carriers were retested for HBV DNA over a period of 7 to 36 months after the initial test. HBV DNA disappeared from the serum in 2 patients in spite of persistence of the HBe antigen. Of the 104 anti-HBe carriers, 89 were retested for HBV DNA over a period of 6 to 52 months after the initial test. HBV DNA disappeared from the serum in 5 of the 7 who were previously positive for HBV DNA, and persisted in 2. These findings indicate that there is an inconstant relationship between the time of seroconversion of HBeAg to anti-HBe and the disappearance of HBV DNA. In one HBeAg positive patient, HBV DNA, which was absent in the serum on first testing, was present on retesting. This suggests that the presence of HBV DNA in the serum of some patients may be intermittent. The presence of HBV DNA in the serum of some anti-HBe positive carriers accounts for the finding that they may be infective. All but one of the HBV DNA positive anti-HBe carriers were born outside North America, most in Asia. HBV DNA were found more frequently in the serum of anti-HBe positive carriers who had biochemical and histological evidence of liver disease than in carriers without such evidence.

Antibodies, Viral↗
PubMed1986

Chronic viral diseases.

Until 20 years ago the only chronic viral diseases known were those considered to be confined to the nervous system. As a result of recent advances in epidemiology, molecular biology and immunology, new viral diseases have been recognized and their clinical features and pathogenesis elucidated. Chronic disease may result from infection with the hepatitis B and D viruses and whatever agent or agents cause hepatitis non-A, non-B, the herpesviruses, Epstein-Barr virus, cytomegalovirus and human T-lymphotropic virus type III. These diseases have common features, including long-term or even lifetime asymptomatic carriage, viremia, with virus free in the plasma or attached to circulating mononuclear cells, presence of virus in body secretions, irreversible tissue injury in target organs and oncogenic potential. New information on these diseases is reviewed. Other chronic diseases for which the cause is currently unknown may eventually prove to be due to viral infection. In addition, vaccines may be developed for prophylaxis of some chronic viral diseases and associated malignant diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1984

DNA: DNA hybridization method for the diagnosis of hepatitis B infection.

Hepatitis B viral (HBV) DNA was detected in a hepatoma cell line which produces hepatitis B surface antigen (HBsAg) and in patients with acute hepatitis B. The serum of one patient with acute hepatitis B was found to be infectious when injected i.v. into a chimpanzee up to a dilution of 10(-8). Hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were detectable in the same serum sample by radioimmunoassay up to a dilution of 10(-5) and of 10(-3), respectively. Using DNA: DNA hybridization on nitrocellulose membranes, HBV DNA sequences were detectable up to 10(-8) dilution corresponding to the infectivity level. Based on this finding, it appears that DNA: DNA hybridization is the most sensitive method for detecting hepatitis B virus (HBV) infection. In situations with low virus levels it may be the only indicator of the presence of infectious hepatitis B virus. The use of a tritium-labelled probe makes the method economical and adaptable to hospital laboratories.

DNA, Viral↗
PubMed1982

Results of long-term prospective study of the hepatitis B surface antigen (HBsAg) carrier state.

In a prospective study of 180 HBsAg carriers, excluding patients from renal units or active drug users, excluding were followed by up to 8 years (mean 4 years). Four became HGsAg negative. SGPT was normal throughout in 70.6%. The rest had either intermittent, persistent or occasional elevations. The commonest pattern of SGPT abnormally was the intermittent one lasting weeks or months. Serial liver biopsies in carriers with normal SGPT showed mainly lobular infiltrates which reverted to normal. In carriers with elevated SGPT, portal infiltrates were found which persisted, compatible with a clinico-pathologic diagnosis of chronic persisting hepatitis (CPH). One patient progressed to liver cirrhosis and one developed CAH and cirrhosis. No patient developed hepatocellular carcinoma. HBsAg carriers can be divided into 2 groups: a) healthy, b) with asymptomatic chronic hepatitis B. Liver biopsy is recommended in group b, but not in group a.

Adult↗
PubMed1981

Inability to detect hepatitis B surface antigen (HBsAg) in the duodenum of HBsAg-positive persons.

Incubation of hepatitis B surface antigen (HBsAg)-positive serum with duodenal fluid (DF) of normal persons results in marked reduction of immunoreactivity. This was shown to be caused by: (1) interference with radioimmunoassay (RIA) system and (2) actual destruction of HBsAg. The interference in the RIA system could be counteracted by addition of bovine serum and a reproducible detection system of HBsAg in DF was established. DF of HBsAg-positive persons was negative for HBsAg. One HBsAg carrier who had a partial pancreatectomy for an insulinoma had separate cannulae in his bile and pancreatic ducts. Whereas HBsAg could be detected in bile, it was undetectable in pancreatic juice. Incubation of his pancreatic juice with his bile resulted in disappearance of HBsAg. It appears that a factor present in pancreatic juice, or resulting from the interaction of pancreatic juice and bile, results in disappearance of HBsAg immunoreactivity.

Bile↗
PubMed1981

Removal of hepatitis B surface antigen from a contaminated applanation tonometer.

Hepatitis B surface antigen was found in the conjunctival fluid of 43% of hepatitis B surface antigen carriers and could be detected on the tonometer tip after tonometry in one of four hepatitis B surface antigen carriers whose conjunctival fluid was positive for hepatitis B surface antigen. The Goldmann applanation tonometer tip was contaminated by immersion into solutions containing high concentrations of hepatitis B surface antigen (average 15,000 cpm). Prompt rinsing of the contaminated tonometer in running tap water for ten seconds proved sufficient to remove all detectable hepatitis B surface antigen from the tonometer.

Conjunctiva↗
PubMed1980

Hepatitis non-A, non-B.

Evidence for the existence of hepatitis non-A, non-B includes epidemiologic data and results of transmission studies indicating the presence of hepatitis that could not be explained by known causative agents. The diagnosis is suggested in patients who have multiple episodes of acute hepatitis or who contract hepatitis after transfusion, hemodialysis or drug abuse. Sporadic cases are common. Three such cases are described to illustrate that the disease is clinically indistinguishable from hepatitis A or B. The diagnosis is based on the absence of serologic markers of hepatitis A and B and of infection by Epstein-Barr virus and cytomegalovirus, or on serologic evidence of previous infection with hepatitis A and B.

Adult↗