Studies within studies.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R L Koretz.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
It was recently recommended that all pregnant women undergo prenatal hepatitis B screening. This change from previous policy (which advocated screening of only those individuals with recognized epidemiologic risk factors) is a very costly strategy to use in an effort to prevent the perinatal spread of hepatitis B in the "no-risk-factor" population. Inherent problems already exist in screening, related to the following: 1) the failure for disease transmission to occur in the majority of hepatitis B e antigen-negative pregnancies, 2) the lack of established efficacy of prophylaxis in the hepatitis B e antigen-negative pregnancy, 3) the preponderance of hepatitis B e antigen negativity in pregnant hepatitis B surface antigen carriers, and 4) the compliance of the mother to ensure that the prophylaxis program is accomplished. These are further magnified by the lower rates of hepatitis B surface antigen and hepatitis B e antigen positivity in the population without risk factors. The major expense of a screening program is the hepatitis B surface antigen testing of the mother. The cost to prevent a clinically important case of hepatitis B in the neonates of mothers with no risk factors is $180,000, which is 15 times the cost of preventing a case in neonates of mothers with risk factors. This price appears not to be cost-effective.
Emergency endoscopy was performed on two patients subsequently found to be hepatitis B surface antigen carriers. Before their carrier state was determined, nine other patients underwent endoscopy using the same instruments, which had been routinely cleaned between procedures. These patients were all notified within five days of the incident, given standard gamma globulin, and prospectively followed for the development of hepatitis. After one of the endoscopes was gas sterilized, the next three patients undergoing endoscopy were also followed. One of the hepatitis B surface antigen carriers was positive for antibody to e antigen; the other carrier had neither e antigen nor antibody. None of these individuals developed signs or symptoms of hepatitis, abnormal serum glutamic pyruvate transaminase elevations, or serologic evidence of hepatitis B exposure. From these data, and other recorded experiences, it appears that routine cleansing of endoscopy equipment is sufficient in preventing the transmission of hepatitis B.
A 68-year-old male underwent cholecystectomy with a normal operative wedge liver biopsy. Five months later he presented with secondary biliary cirrhosis and signs of portal hypertension and hepatocellular failure. At autopsy, a squamous cell carcinoma of the bile duct was found. This case represents an unusually rapid development of cirrhosis secondary to extrahepatic biliary obstruction with documentation of normal liver histology five months prior to his last admission.
In a randomized double blind multicenter trial, patients treated with cimetidine (800 or 1200 mg daily) or an intensive regimen of Al-Mg antacid (210 ml daily) had similar rates of duodenal ulcer healing and pain relief. After 4 weeks of treatment, the proportion of patients with ulcer healing by endoscopy were: cimetidine (1200 mg), 21 of 33 (64 percent); cimetidine (800 mg), 19 of 32 (59 percent); and antacids, 15 of 29 (52 percent). These proportions did not differ significantly. Eighty per cent of cimetidine-treated patients became asymptomatic by week 4, as did 63 percent of antacid-treated patients (P greater than 0.1). No untoward effects were observed during cimetidine treatment. Twenty-seven per cent of antacid-treated patients reported diarrhea.
In order to assess the frequency of significant liver disease in hepatitis B surface antigen carriers with normal liver tests, 54 such individuals were identified and prospectively followed for 4 to 48 months with monthly liver tests. Upon testing, 4 were found to carry e antigen and 14 carried e antibody (anti-e). During follow-up, only 4 patients, none of whom were e antigen-positive, developed persisting abnormalities in liver tests. Of the 23 patients who underwent percutaneous liver biopsies, normal histologies were found in 2, nonspecific changes (ground glass hepatocytes, focal necrosis, fatty changes, etc.) in 18, and chronic persistent hepatitis (with or without other nonspecific changes) in 3. Chronic active hepatitis and/or cirrhosis, lesions which may carry more serious prognostic implications, were not seen in any biopsies. Two of the 4 e antigen-positive patients consented to biopsy, both of whom had chronic persistent hepatitis. All 6 patients with anti-e who underwent biopsy had ground glass hepatocytes, which were found in only about 50% of the remaining patients. It is concluded that hepatitis B surface antigen carriers should be followed with serial liver tests, and those whom tests remain normal should not be considered for liver biopsy.
Aliquots from units of blood previously transfused as part of a prospective post-transfusion hepatitis (PTH) study were rescreened for the presence of hepatitis B antibody (anti-HBS) to determine the effect of transfusion of such material. Anti-HBS was more commin in commercial blood. Infusion of anti-HBS was not associated with an increased or decreased risk of PTH, hepatitis B, or hepatitis B (HB) exposure. Receipt of anti-HBS did not modify the hepatitis which occurred. Receipt of large amounts of anti-HBS may be associated with an increased incidence of HB events. Preexisting anti-HBS was not only not protective against PTH, but more PTH (67% versus 40%) and hepatitis B (47% versus 12%) were seen in those patients with it.
To document the sequelae of acute hepatitis among recipients of commercial and volunteer blood and to assess factors influencing the development of chronic hepatitis (CH), 47 patients with post-transfusion hepatitis were followed prospectively from the time they received their transfusions. Twenty-nine had prolongation of at least 2-fold serum glutamic pyruvic transaminase (T) elevations for more than 20 weeks, and were classified as CH. When the patients with CH were compared to those with only acute hepatitis (abnormal T for less that 20 weeks), no difference was found with respect to age, sex, number of units transfused, incubation period, presence or absence of symptoms, occurrence of jaundice, maximum T, receipt or development of hepatitis B surface antigen or antibody, underlying illness, or area of the hospital where the patient was treated. Liver biopsies in 15 of the 29 revealed chronic-active hepatitis in 9, chronic persistent hepatitis in 2, unresolved hepatitis in 4. Five of the 9 patients with chronic active hepatitis were without symptoms. None of these died or have developed cirrhosis. Because chronic liver disease frequently developed after acute post-transfusion hepatitis among multiply transfused hepatitis B surface antigen negative blood recipients, close follow-up, including liver biopsy, is warranted in such patients with prolonged transaminase elevations.
Aliquots from units of blood were screened by radioimmunoassay (RIA) and reverse passive hemagglutination (RPHA) shortly after transfusion. Recipients of positive units, as well as control subjects, were followed prospectively for evidence of either post-transfusion hepatitis (PTH) or exposure to hepatitis B (HB). There was a significant correlation between receipt of either an RPHA-positive or RIA-confirmed positive unit and the subsequent development of PTH or HB exposure. Recipients of all volunteer units had a lower incidence of PTH than did recipients of all commercial units. The frequency of PTH and HB exposure was not statistically different in groups receiving 1 to 5, 6 to 10, 11 to 20 and greater or less than 21 units of blood. The PTH seen in the study presented over a wide clinical spectrum, but it was usually anicteric and frequently asymptomatic.