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Biomedical subjects

R S Koff

Publications and source records attributed to R S Koff.

At least 91 records · Page 5Linked to original sources
PubMed1987

Fulminant hepatitis due to HBV/HDV coinfection.

The diagnosis of acute viral hepatitis is based on a thorough history (with a detailed review of possible modes of transmission), consistent physical findings (in which stigmata of chronic liver disease are absent), and laboratory tests confirming the presence of acute hepatocyte damage. Specific etiologic entities can be identified by serologic testing. In some cases, infection by more than one hepatitis virus may be revealed. The occurrence of HBV/HDV coinfection may lead to typical, uncomplicated acute hepatitis. In some patients, however, the development of a prolonged prothrombin time and encephalopathy indicates the presence of fulminant disease. The management of patients with such disease usually requires admission to an intensive care unit in order to increase the likelihood that complications will be recognized at an early stage, when intervention might make a difference. Standard interventions include vigorous treatment of hypoglycemia, attention to electrolyte and acid-base disturbances, and antibiotic therapy for bacterial sepsis. Despite aggressive management by experienced teams, fatality rates remain exceedingly high: As many as 75% to 100% of patients with severe encephalopathy die. Liver transplantation has been attempted in a number of cases. Its role remains ambiguous. Survival rates of 50% to 60% have been reported, but selection bias may turn out to have contributed to this apparently favorable outcome. In the patient under discussion, results of a follow-up physical two months after discharge were entirely normal. Liver chemistries were within normal limits, but a test for HBsAg was still positive. During the course of the examination, the patient admitted to having accidentally pricked his skin nearly two months before the onset of his illness while holding a needle that a friend had used for the intravenous injection of heroin. One year later, HBsAg was no longer detectable, but tests for anti-HBc and anti-HBs were both positive. The anti-HBc positivity was attributable to IgG rather than IgG anti-HBc. A test for anti-HDV was negative.

Acute Disease↗
PubMed1987

A serologic follow-up of the 1942 epidemic of post-vaccination hepatitis in the United States Army.

An epidemic of icteric hepatitis in 1942 affected approximately 50,000 U.S. Army personnel. This outbreak was linked to specific lots of yellow-fever vaccine stabilized with human serum. To identify the responsible virus and the consequences of the epidemic, during 1985 we interviewed and serologically screened 597 veterans who had been in the army in 1942. These subjects were selected from three groups. Group I consisted of patients who had received the implicated vaccine and had jaundice; Group II had received the implicated vaccine but remained well; Group III had received a new, serum-free vaccine, with no subsequent jaundice. Ninety-seven percent of Group I, 76 percent of Group II, and 13 percent of Group III were positive for antibodies to hepatitis B virus. Only one subject had hepatitis B surface antigen, for a carrier rate of 0.26 percent among recipients of the implicated vaccine. The prevalence of hepatitis A antibody was similar in all three groups, and no subject had antibody to hepatitis delta virus. We conclude that hepatitis B caused the outbreak, that about 330,000 persons may have been infected, that the hepatitis B virus carrier state was a rare consequence, and that the outbreak induced hepatitis B antibodies that appear to persist for life.

Aged↗
PubMed1986

Evolving concepts of the clinical and serologic consequences of hepatitis B virus infection.

Measurement of conventional markers has provided a general understanding of HBV infection, and conceptual advances in knowledge of the clinical and serologic events associated with persistent HBV infection have resulted from the development and application of new methodologies. These studies suggest that persistent HBV infection is a dynamic process, with replicative and nonreplicative phases, that nonreplicative infection may be the precursor of PHC, and that the natural history of persistent infection can be modified by a variety of factors, including viral reactivation and viral superinfections. Further understanding of these phenomena may lead to the development of new therapeutic approaches.

Carcinoma, Hepatocellular↗
PubMed1984

Hepatic amyloidosis. A histopathologic analysis of primary (AL) and secondary (AA) forms.

The liver is a major site of amyloid deposition. The spectrum of histopathologic changes in the liver was studied in 38 patients with systemic amyloidosis (25 with primary or myeloma-associated amyloidosis [AL] and 13 with secondary, reactive [AA] amyloidosis). Overall architectural distortion, alterations of portal triads, as well as predilection for topographic deposition in the parenchyma and/or blood vessel walls were noted. Significant histopathologic differences in AL or AA amyloid liver involvement included 1) portal fibrosis, seen in 7 of 25 (28%) AL patients and 8 of 13 (62%) AA patients (P = 0.05), 2) parenchymal amyloid deposition in 25 of 25 (100%) AL amyloid and 10 of 13 (77%) AA amyloid patients (P = 0.04), and 3) vascular amyloid deposition found in 17 of 25 (68%) with AL amyloid and 13 of 13 (100%) patients with AA amyloid (P = 0.02). These data vary from the widely held concept that deposition of amyloid is predominantly vascular in the AL form and parenchymal in amyloid AA. Clearly, however, in individual cases significant overlap occurred, and characterization of amyloid types based on morphologic distribution of amyloid deposits may be possible in only a minority of cases. In most cases, differentiation of amyloid AL and amyloid AA forms requires clinical, histochemical, immunochemical, and sometimes more elaborate laboratory amino acid sequence studies for accurate identification.

Amyloid↗
PubMed1984

Therapy for chronic active hepatitis.

As is apparent from the foregoing, there is only one etiologic variant of CAH for which specific therapy is available, namely, that associated with Wilson's disease. However, Wilson's disease is responsible for only a minute portion of the total cases of CAH. Drug-induced CAH also seems highly responsive to appropriate management--in this instance, removal of an offending agent rather than administration of a therapeutic drug. However, as stated, it too is an infrequent contributor to the CAH pool. Among the remaining forms of CAH, a reasonably consistent response to treatment can be expected only from patients with autoimmune CAH. This entity is a serious disorder with unequivocally high morbidity and mortality and thus clearly warrants treatment. Despite the considerable side effects that invariably result from the long-term use of corticosteroids--the only available, although nonspecific, form of treatment--corticosteroid use is justified and indeed recommended. Current evidence, derived from the Mayo Clinic data, suggests that the best therapeutic approach is to use both corticosteroids and azathioprine, a combination that offers the highest therapeutic index with the lowest rate of side effects. Using this regimen, complete remission is reported to result in 65% of cases within 2-3 years, although a considerable proportion of these individuals relapse and require retreatment. Much publicity has surrounded the Mayo Clinic and Royal Free Hospital treatment trials; however, it is probable that autoimmune CAH represents far less than 20% of all cases, and that severe disease requiring corticosteroid therapy comprises but a minor fraction of these. Thus, the bulk of cases of CAH in the United States occur in patients with either established or inferred viral-related disease, the group for which clearly effective therapy is not yet available. Most of these persons are asymptomatic, their disease having been detected through routine screening programs or at the time of evaluation of other disorders. Much interest is evoked, at present, by the new experimental forms of treatment, but none has proved to be consistently effective, and for some, toxicity is high. All appear to reduce levels of replicating virus, but none clearly affects HBsAg or disease activity. Research in this area continues, with highest expectations of success for the use of combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adjuvants, Immunologic↗
PubMed1983

Predicting clinical recovery from alcoholic liver disease.

We postulated that three tests could be used to advantage in the prognosis of patients with alcoholic liver disease. Ninety-eight patients who entered the hospital in hepatic failure, and who survived that illness, were observed for an average of 3.5 years after discharge. At the time of entry, most had jaundice, ascites, edema, and hepatosplenomegaly. Biopsy of the liver disclosed both cirrhosis and hepatitis in 75-80%. Neither clinical features nor laboratory tests could differentiate these patients at the time of entry. However, as early as 3 months after hospitalization, the clinical course and laboratory tests served to distinguish two groups: group 1 comprised 46 patients in whom the serum bilirubin was less than 2 mg/dl; the aspartate aminotransferase less than 55 mU/ml; and the alkaline phosphatase less than 125 mU/ml. In 40 (87%) of these 46 patients, clinical findings improved concomitantly with laboratory tests. Group 2 comprised 52 patients in whom one or more of these three tests showed persistent abnormality; only 12 (23%) of the 52 patients in this group improved clinically and three subsequently died. Although the majority of patients (76%) in group 1 reported abstinence on follow-up, 44% of group 2 patients also claimed abstinence. Complications of liver disease, shunt surgery, and continuing alcoholism contributed to liver failure. Early identification of such patients should aid in the management of alcoholic liver disease.

Alkaline Phosphatase↗
PubMed1982

Circulating CEA levels in patients with fulminant hepatitis.

CEA levels were determined in blood specimens from 14 persons suffering from fulminant hepatitis. Values ranged from 1.9 to 21 ng/ml with a mean of 7.0 ng/ml. All except one patient had a CEA level greater than 2.5 ng/ml, but only three exceeded 10 ng/ml. There was no correlation between single CEA levels and prognosis, routine liver chemistries, or histopathologic characterization of hepatic tissue obtained at postmortem examination. These data show that patients with fulminant hepatitis commonly had increased circulating levels of CEA, but these elevations were far less than may be found in patients with hepatic metastases. In severe hepatic dysfunction reduced hepatic clearance of CEA may be responsible for the increased levels.

Adolescent↗
PubMed1981

Serodiagnosis of viral hepatitis A by a solid-phase radioimmunoassay specific for IgM antibodies.

A solid-phase radioimmunoassay for detecting specific IgM antibodies to hepatitis A virus (HAV) was developed and characterized. The test utilized microtiter plates coated with anti-IgM to specifically absorb the IgM antibodies from the test serum. The anti-hepatitis A IgM antibodies are measured by the specific consecutive binding of hepatitis A antigen and radiolabelled anti-hepatitis A antibodies (anti-HA). In 6 chimpanzees infected with HAV, IgM anti-HA was detected from about the first date of elevated transaminases and was positive for about 3 months. The usefulness of the test was confirmed by testing acute phase sera of 30 patients from a common source outbreak of epidemic hepatitis, and negative sera from 2 control groups. A collection of serum specimens from 190 patients with sporadic HBsAg-negative hepatitis in Brazil was also tested and an etiologic association with HAV was confirmed in the majority of these cases.

Alanine Transaminase↗
PubMed1981

In vitro studies of enhanced IgG synthesis in severe alcoholic liver disease.

Elevated serum immunoglobulin levels are a frequent finding in patients with severe alcoholic liver disease. We measured in vitro peripheral blood lymphocyte IgA synthesis by radioimmunoassay in 13 patients with severe alcoholic liver disease and hypergammaglobulinaemia and in normal control subjects. We found an increase in spontaneous IgA synthesis compared to controls (P greater than 0.001). On the other hand, there was no difference between groups in percentage stimulation of IgG production by B cells exposed to pokeweed mitogen. We also searched for defects in concanavalin A (Con A) induced suppressor T cell activity. There was no difference between patients with alcoholic liver disease and controls in the capability of such suppressor T cells to inhibit the response of allogeneic cells to a T cell mitogen. Similarly, we examined the capability of Con A-induced suppressor T cells to inhibit pokeweed mitogen-stimulated IgG synthesis by both autologous and allogeneic responder cells and observed no difference between alcoholic patients and controls. Thus these measured suppressor T-T and T-B cell interactions appeared no different from those in control subjects. Our studies suggest, therefore, that B cell IgG synthesis in vitro is enhanced in alcoholic liver disease. Furthermore, the capability to induce suppressor T cells which affects both T and B cell function appears intact; a finding in contrast to our previous observation in chronic active hepatitis. The investigations suggest that enhanced spontaneous IgG synthesis in vitro may result from intense antigenic stimulation in vivo.

Concanavalin A↗