Improving physicians' relationships with patients.
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Biomedical subjects
Publications and source records attributed to J Shorey.
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OBJECTIVE: To determine the reliability and validity of "standardized patients" to assess clinical performance of internal medicine residents. DESIGN: Each resident spent 2 half-days interacting with 19 standardized patients (nonphysicians taught to portray patients in a reproducible fashion). Each resident was asked to obtain focused histories, perform relevant physical examinations, and provide patient education or counseling. At the end of each 10- to 15-minute encounter, the resident was asked to identify positive findings on physical examination and to prioritize a differential diagnosis. Other, more traditional indicators of clinical skills were also obtained. PARTICIPANTS: Three hundred ten residents from nineteen internal medicine training programs in the New England region of the United States. RESULTS: Reproducible estimates of data gathering and interviewing skills were achieved with 1 day of testing. Validity analyses were difficult to interpret because of the lack of an external "gold standard." However, faculty judgments of performance from reviewing videotapes corresponded with standardized-patient-based scores. Differences in group performance were also demonstrated across years of training and between U.S. or Canadian and foreign medical graduates. CONCLUSIONS: Systematic and effective procedures for developing standardized-patient-based test materials and for training standardized patients have been developed. This technique is best used for measuring data gathering and interviewing skills. Correlations with commonly used evaluation methods were generally low; this may be because standardized patients measure different skills. Local use of this technique by residency programs and the development of regional consortia sharing resources, costs, and expertise are advocated.
Personnel in the VA dental facilities were screened for the detection of viral hepatitis and identification of factors implicating infectivity. A total of 963 personnel from 126 dental facilities throughout the United States voluntarily participated in the study. The rate of seroconversion for any hepatitis B markers was approximately 1% per year. Serial positive tests for antibody to hepatitis B core antigen or antibody to hepatitis B surface antigen (or both) were present in 16.2% of dentists and 13.0% of dental auxiliary personnel. Oral and maxillofacial surgeons composed the highest prevalence occupation (24.0%), and clinical personnel composed the lowest prevalence occupation (8.9%). There was a significant association between years in dental environment and serological positivity for viral B infection. The dentists and dental auxiliary personnel had significant linear trends of increasing serological positivity with years in the dental environment. Although a majority of personnel reported wearing gloves while treating high-risk patients or performing invasive procedures, inadequate prophylactic measures were exercised for most patients undergoing a variety of less invasive procedures. The results of the study show the need for an active immunization program against type B viral infection for dental and dental auxiliary personnel, preferably before the initial exposure to the professional environment.
It is probable that two or more different viruses account for non-A, non-B hepatitis throughout the world, with a third agent causing epidemic hepatitis in India and neighboring countries. NANB virus(es) is the major cause of transfusion-associated hepatitis, and is responsible for roughly 20% of sporadic hepatitis cases. NANB postransfusion hepatitis progresses to chronic hepatitis in half or more of cases. This form of chronic hepatitis, while usually minimally symptomatic, causes progressive liver destruction and eventual cirrhosis in a significant proportion of cases. To date, the NANB virus(es) has not been specifically identified, either serologically or by electron microscopy. When developed, serologic assays will find their most immediate application in the identification of NANB virus carriers among blood donors, thereby being applied to the prevention of post-transfusion hepatitis. No specific therapy is available for NANB virus infection. Gamma globulin is of uncertain prophylactic efficacy.
An approach has been developed for the analysis of hepatitis B viral (HBV) antigenic structure that creates numerical "signatures" of HBV strains. This technique employs high-affinity IgM and IgG monoclonal antibodies (anti-HBsAg) directed toward distinct and separate determinants on hepatitis B surface antigen (HBsAg). Such antibodies have been used to develop sensitive and specific radioimmuno-assays for measurement of HBsAg-associated determinants in serum. In performing "signature" analysis separate binding curves for each monoclonal anti-HBsAg are generated by measuring immunoreactivity in serial dilutions of HBsAg-positive serum. Since the HBsAg concentration in serum is unknown, the binding profiles of groups of samples from the same "classic" HBV subtype are aligned by an iterative maximum likelihood procedure to give the numerical signature of that HBV subtype. By using this approach, HBsAg shows far more antigenic heterogeneity than previously recognized by polyvalent anti-HBsAg antibodies. Indeed, there are subgroups within the classic HBsAg subtypes. In addition, the a domain (common to all known subtypes or strains of HBV) has been shown to be multideterminant. Thus, these studies have demonstrated heretofore unrecognized differences in HBV subtypes. This approach also has broader significance for the study of subtle or major antigenic changes among other viral agents since it is not necessary to know the concentration of virus or viral protein in complex protein mixtures.
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Radioimmunoassay methods were used to determine both the hepatitis B virus (HBV) subtype and hepatitis B e antigen (HBeAg) and antibody (anti-HBe) status of a group of hepatitis B surface antigen (HBsAg)-positive blood donors. The study involved sera containing HBV of the three major occidental subtypes, adw2, ayw3, and ayw2. The previously reported association of the y-type virus with HBeAg and the d types with anti-HBe was again observed. However, when the two y subgroups, ayw2 and ayw3, were considered individually, it was evident that the ayw3 specimens alone accounted for the association with HBeAg while the ayw2 sera were strongly associated with anti-HBe. The study also indicated that the prevalence of HBeAg declined and that of anti-HBe increased progressively with advancing age. On the average, ayw2 donors were significantly older than the adw2 donors, and donors from both of these groups were older than the ayw3 donors. It is postulated that the observed age differences account, at least in part, for the differing prevalence of e markers in the three HBV subtype groups, and that these age differences, in turn, may reflect a tendency for infections with the ayw2 viral strain to persist longer than adw2 infections, and both of these longer than ayw3 infections. Alternately, the three subtypes may represent epidemiologic shifts from remote ayw2 and adw2 infections to more recent ayw3 infections.
An outbreak of hepatitis B in a residential institution for the mentally retarded was studied. Initially one overt case of hepatitis was noted. A serologic screen of students and employees revealed a total of 12 individuals positive for hepatitis B surface antigen (HBsAg). Subtyping by radioimmunoassay subsequently demonstrated that the population of HBsAg-positive individuals could be subdivided into two groups, based on the HBsAg subtype: adw2 or ayw3. The five individuals with subtype adw2 all were carriers. The ayw3 group, in contrast, were acutely infected except for one carrier with persistent hepatitis B e antigen. Both the ayw3 carrier and several of the acutely infected individuals were aggressive biters. Human biting, a frequent occurrence in the classroom studied, was one probable mode of transmission in this outbreak. The resolution of the outbreak was achieved by rapid screening for HBsAg with subtyping of positive patients and careful observation of the setting for putative modes of transmission.
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A prospective, double-blinded, randomized trial of corticosteroid therapy in patients with severe acute viral hepatitis has been conducted. At the same time, we have examined the prognostic significance of the presence of bridging necrosis in liver biopsies obtained from such patients as well as the predictive value of certain serologic markers. Forty-two of the 77 patients admitted to the trial were shown to have bridging necrosis on their initial biopsies. Two patients progressed to death with massive hepatic necrosis, while 5 patients developed chronic liver disease. A complicated course could not be predicted by the initial biopsy findings nor by any of the serologic markers assessed. We could not identify any clinical or epidemiologic features with prognostic impact. No advantage was demonstrated to be associated with the use of corticosteroids early in the course of severe viral hepatitis.
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Nodular regenerative hyperplasia of the liver was identified at autopsy in a patient with myelofibrosis with extramedulary hematopoiesis, an association not previously reported. Portal venous hypertension, documented during the patient's terminal hospitalization, was ascribed, in part, to a high rate of blood flow through the enlarged spleen. Possible mechanisms accounting for the development of nodular regenerative hyperplasia of the liver, and evidence provided by this case pertinent to these mechanisms, are discussed.
The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.
The maternal and fetal outcomes of 50 pregnancies complicated by acute viral hepatitis were examined. Twenty (40%) cases were due to type B hepatitis virus. The clinical course of the maternal hepatitis was unaffected by the pregnant state. Maternal hepatitis (type B or nontype B) had no effect on the incidence of congenital malformations, stillbirths, abortions, or intrauterine malnutrition; it did increase the incidence of prematurity (type B 31.6%; nontype B 25%; overall 27.6%) over that seen in the general delivery population (10 to 11%). Eight mothers acquired acute type B hepatitis during the third trimester; two of their infants (25%) were found to be chronic asymptomatic carriers of hepatitis B surface antigen and to have mild, persistent elevations of SGOT for up to 45 months.
A new determinant of hepatitis B surface antigen (HBs Ag), g, which is distinct from the previously identified determinants a, d, y, w, and r, was studied. This new antigen tended to be associated with the d antigen; it was found in 97% of ad specimens and in 15% of ay specimens. With few exceptions, the atypical subtypes, adg- and ayg+, were identified in sera from blood donors, but not in sera from patients with acute viral hepatitis; this finding possibly reflects a reduced tendency of these viral strains to evoke a host immune response. The ability to identify g represents a refinement of HBs Ag serotyping that may be of value in the study of the epidemiology of hepatitis B virus.
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