Anicteric Hepatitis Research Articles

Lepromatous leprosy and australia antigen with comments on the genetics of leprosy

AUSTRALIA antigen [Au(l)] is detected in serum using an antiserum which deveIops in patients who receive large numbers of transfusions [l-3]. There is now substantial evidence that Australia antigen is associated with acute and chronic hepatitis, and with hepatitis carriers. The antigen may in fact be the virus itself or some factor very closely connected with it. This evidence has been reviewed recently [3-51 and will be summarized here. (1) Australia antigen is very rare in normal American populations, but is relatively common in acute viral hepatitis patients (in whom the antigen is transient) and in patients with persistent active hepatitis [6, 71. (2) It occurs in patients with chronic diseases characterized by an impairment of their immune mechanism, particularly of cellular hypersensitivity. Included among these are some forms of leukemia, Hodgkin’s disease, Down’s syndrome [8], chronic renal dialysis patients [9], and lepromatous leprosy. In some of these groups (i.e. Down’s syndrome, leukemia) Au(l) has been shown to be associated with chronic anicteric hepatitis. Au(l) may persist for months or years in these patients. (3) Bayer el al [IO] have shown that isolated Australia antigen has the appearance of a virus in the electron microscope. It is a particle of about 200 A dia. with what appear to be knob-like subunits on its surface and with a central core in some of the particles. This has now been confirmed in other laboratories (see, for example, ref. 11). (4) Fluorescein labeled anti-Au( 1) reacts with granules present in the nuclei of the liver cells of patients with acute and chronic hepatitis who have Australia antigen in their serum. These granules are not seen in the liver cells of patients without hepatitis [12]. (5) Patients transfused with the blood of donors containing Australia antigen may develop acute

Cytomegalovirus in children.

Cytomegalovirus (CMV) was isolated from the urine and/or blood of eight of 21 (38%) pediatric renal allograft recipients. The recovery of CMV was associated with clinical symptomatology in four of the eight patients. Three had cryptogenic fever, and one had anicteric hepatitis. In addition to fever, one patient had evidence of transplant lung. All of the eight patients had multiple positive urine cultures for as long as 14 months. However, all attempts at virus isolation during these periods were not successful. The fact that cytomegaloviruria was intermittent in all infected patients emphasizes the need for multiple, serial isolation attempts if the true incidence of CMV in renal allograft recipients is to be determined.

Australia antigen (a hepatitis-associated antigen): purification and physical properties.

Australia antigen [Au(1)], a particle associated with viral hepatitis, was isolated from the plasma of a patient with chronic anicteric hepatitis and leukemia who had received radioactive phosphorus. We have found that the immunoreactivity and appearance of Au(1) in the electron microscope were not altered by treatment with enzymes including trypsin, pronase, lipase, phospholipase C, ribonuclease, deoxyribonuclease, amylase, and neuraminidase. In contrast, other serum constituents were degraded by these enzymes. Therefore, treatment of the patient's plasma with many enzymes was exploited as an initial step for the isolation of Au(1). Subsequently, Au(1) was purified from the enzyme-treated (32)P-labeled plasma by gel filtration through Sephadex G-200 and centrifugation through sucrose and in cesium chloride gradients. There were no detectable human serum components in the purest fractions, as tested by immunoelectrophoresis and immunodiffusion. The density of the purified Au(1) was 1.21 in CsCl. The particle measured about 200 A in diameter, was predominantly spherical in shape and appeared to be composed of subunits. Nucleic acids were not detected by spectrophotometric, radiochemical, and chemical analyses. Immunoreactivity of purified Au(1) was destroyed by heating for 1 hr at 85 degrees C but was stable at 56 degrees C. Treatment with Carnoy's solution (3 parts ethanol:1 part glacial acetic acid) followed by pronase disrupted the particles as seen with the electron microscope. These findings, combined with other published information on Australia antigen and viral hepatitis, suggest that the bulk of Australia antigen in the blood of this patient is an incomplete virus or virus capsid.

Anicteric and Icteric Hepatitis after Open-Heart Surgery

Fifty patients undergoing open-heart surgery were transfused with an average of 12.9 U of whole blood. During the 6 months following surgery, they were tested every 2 weeks for total bilirubin and transaminase levels in order to detect hepatitis. Between the 5th and 9th postoperative weeks, 2 and 8 % of the patients developed icteric and anicteric hepatitis, respectively, according to the elevated serum transaminase levels. Two of the 4 patients diagnosed as having anicteric hepatitis maintained elevations in serum transaminase levels which persisted without symptoms for up to 2 years. No patient received γ-globulin, fibrinogen, or pooled plasma. Compared with other reports dealing with multiple transfusions, the case incidence of post-transfusion hepatitis that we encountered was relatively low. We believe that this is due to the use of blood from volunteers and possibly to the pooled γ-globulin content in the multiple transfusions administered to each patient.

Australia antigen and hepatitis. Studies in asymptomatic people and lepromatous leprosy patient.

Australia antigen is intimately associated with a hepatitis virus. It is found in the blood of many individuals who have acute viral hepatitis and in some patients with chronic diseases (ie, some forms of leukemia, Down's syndrome, etc) who have a form of chronic anicteric hepatitis. It is also found in relatively high frequency in apparently normal people living in the tropics, and in even higher frequency in patients with lepromatous leprosy who reside in these areas. Patients with lepromatous leprosy who have the antigen in their blood do not have acute hepatitis, but do have slightly elevated serum glutamic pyruvic transaminase levels. We could not detect any clinical or biochemical evidence of liver abnormality in the apparently normal individuals with Australia antigen.

Posttransfusion hepatitis after open-heart operations. Incidence after the administration of blood from commercial and volunteer donor populations.

The incidence of icteric and anicteric hepatitis was determined prospectively in 110 patients undergoing open-heart operations in which cardiopulmonary bypass was used. Patients were supplied with blood from two commercial blood banks (82 patients), or from local volunteer donors (28 patients). Serial determinations of serum transaminase levels were obtained for six months following operation. Hepatitis developed in 51% (42) of the recipients of commercial blood, but the disease did not occur in any patient who received blood from volunteer donors. The hepatitis carrier rate for commercial blood donors was 6.3%, but, for volunteer donors, was less than 0.6%. This difference in carrier rates probably reflects differences in the donor populations.

Posttransfusion Hepatitis After Open-Heart Operations

The incidence of icteric and anicteric hepatitis was determined prospectively in 110 patients undergoing open-heart operations in which cardiopulmonary bypass was used. Patients were supplied with blood from two commercial blood banks (82 patients), or from local volunteer donors (28 patients). Serial determinations of serum transaminase levels were obtained for six months following operation. Hepatitis developed in 51% (42) of the recipients of commercial blood, but the disease did not occur in any patient who received blood from volunteer donors. The hepatitis carrier rate for commercial blood donors was 6.3%, but, for volunteer donors, was less than 0.6%. This difference in carrier rates probably reflects differences in the donor populations.

Anicteric hepatitis induced by diphenylhydantoin

Anicteric hepatitis induced by diphenylhydantoin

Anicteric Hepatitis Induced by Diphenylhydantoin

Diphenylhydantoin has been widely used as an anticonvulsant since its introduction by Merritt and Putnam¹in 1938. While the drug is well tolerated by the majority of patients, it can produce a great variety of toxic and allergic reactions.²During the first several weeks of therapy, a skin rash occurs in about 5% of patients.³Usually this eruption is erythematous or morbilliform, is not accompanied by systemic symptoms, and does not necessitate permanent discontinuation of therapy. Occasionally, however, a more severe reaction occurs, with a pleomorphic, often exfoliative rash and high fever; hepatitis may be an associated finding. To our knowledge, the patient described here is the tenth patient reported to have had acute hepatitis accompanying the diphenylhydantoin reaction of fever and skin rash. <h3>Patient Summary</h3> A 19-year-old Negro male was admitted to Douglas County Hospital on Dec 11, 1966, after his second grand mal seizure, the

Volume expansion and flow promotion in shock.

Summary Volume replacement is the most important step in treating hypovolaemic shock. Blood is needed when the oxygen carrying capacity threatens to fall below a critical level, but has the disadvantage of transmitting virus hepatitis. Anicteric hepatitis is about four times more frequent than the icteric form. Pasteurized plasma protein solution and albumin are free from the risk of transmitting hepatitis virus, and are good volume restorers. Dextran 70 represents the best artificial colloid with additional anti-thrombotic properties. Dextran 40 is indicated in special situations to promote flow. There is no proof that large amounts of Ringer solution are superior for treating hypovolaemic shock in man compared with colloids and electrolytes.

Some Antigenic and Physical Properties of Virus-Like Particles in Sera of Hepatitis Patients

Abstract The Australia antigen was detected by Blumberg, Alter and Visnich in 1965 in human sera by formation of a precipitin line in Ouchterlony gel diffusion slides (1). Antibodies used to detect the antigen are found in sera from patients who have received multiple transfusions The antigen is rare in healthy Americans, but common in patients with either infectious or serum hepatitis, patients with Down's syndrome who have anicteric hepatitis, patients with leukemia or leprosy, and apparently healthy persons in certain tropical populations (2). Bayer, Blumberg and Werner described 19 to 21 mµ particles in antigen-containing serum fractions from sucrose gradients (3). The particles were aggregated by the same sera that precipitated the antigen. Blumberg and co-workers and Prince have suggested that the antigen is a virus or is intimately associated with a virus that is responsible for hepatitis in man (2–5).

Additional specificities of Australia antigen and the possible identification of hepatitis carriers.

IN 1964 (ref. 1), we identified an antibody which is common in the blood of transfused haemophiliacs and which reacts with an antigen (first identified in an Australian aborigine, thus “Australia antigen”) found in some human sera2. Australia antigen, Au(1), is found transiently in the sera of many patients with acute viral hepatitis3–6 (13 per cent in infectious hepatitis, 34 per cent of post transfusion hepatitis7–9). This association with hepatitis has been confirmed by other workers using reference antisera from our laboratory (refs. 10 and 11, and unpublished results of Vierucci). Okochi and Murakami10 used an anti-Australia antiserum from a transfused patient which seems to be identical with reference sera we have exchanged. The “SH antigen” recently described by Prince is identical with Australia antigen11. In addition to its presence in acute viral hepatitis, Australia antigen is found in patients with some forms of leukaemia2 and Down's syndrome (who have chronic anicteric hepatitis)2,3,12,13. It is also found in 5–20 per cent of apparently normal populations in the tropics and south-east Asia2,9,14, who may be hepatitis carriers10.

Anicteric hepatitis associated with Australia antigen. Occurrence in patients with Down's syndrome

Anicteric hepatitis associated with Australia antigen. Occurrence in patients with Down's syndrome

Syndrome of hepatitis and aplastic anemia

Nine cases of pancytopenia and aplasia of the bone marrow following icteric hepatitis are presented, seven of which terminated fatally. An additional case of pancytopenia which probably followed anicteric hepatitis is also reported. The patients were mostly male and ranged in age from two to twenty years. The hepatitis in these cases is presumably viral, and the hematologic disorder may possibly result from viral induced chromosomal damage to the bone marrow. It is suggested that some cases of idiopathic aplastic anemia in children may be a sequel to anicteric hepatitis.

Risk of anicteric hepatitis following blood transfusion.

Risk of anicteric hepatitis following blood transfusion.

Anicteric viral hepatitis. A clinicopathological follow-up study in Taiwan.

ANICTERIC viral hepatitis is a widely discussed but little studied entity. Its existence has been acknowledged for many years on the basis of epidemiologic and clinical data, mostly indirect and inferential. For example, during epidemics when the hepatitis infection rate is high, cases in which clinical evidence of hepatitis develops without jaundice are often diagnosed as anicteric hepatitis.1 2 3 In addition, clinicopathological studies have been done on patients in whom chronic liver disease developed without jaundice or with the late appearance of jaundice; the diagnosis of anicteric hepatitis was made retrospectively.4 5 6 The military population of Taiwan offers advantages to the study . . .

The problem of anicteric hepatitis.

The problem of anicteric hepatitis.

Anicteric Hepatitis in Korea: Comparative Studies of Asymptomatic and Symptomatic Series

Summary A previous survey utilizing SGOT determinations for screening detected anicteric hepatitis by liver biopsy in about 1.5% of young, healthy appearing Korean soldiers. Their most frequent sign was hepatomegaly. Therefore, another 1666 clinically healthy soldiers were screened for hepatomegaly, and in 14 with such findings, liver biopsy revealed normal liver in 3, 1 case each with chronic active hepatitis of spotty necrotic and undetermined type, 4 instances of hepatitis suggestive of the spotty necrotic type and 5 of nonspecific reactive hepatitis. Since several of the soldiers with hepatitis had normal SGOT activity and would have been missed in the first survey, an additional incidence of 0.42% raises the total incidence of anicteric hepatitis in these Korean soldiers to about 2.0%. Laboratory and clinical examinations supplement each other in the detection of anicteric hepatitis. The observations in the asymptomatic soldiers were compared with another group of soldiers who had anicteric hepatitis with clinical symptoms referable to the liver, and similar histologic and laboratory findings were encountered in both groups. The histologic findings in the symptomless soldiers in this and in the previous study and in the symptomatic cases as well as the clinical observations suggest a spectrum of anicteric hepatitis from a mild, symptomless form to a more severe symptomatic form with the possibility of persisting activity. Although histologic features considered diagnostic of viral hepatitis were seen, and icteric viral hepatitis is endemic in Korea, the etiology of the described anicteric hepatitis is not established.

Abstracts

A 35‐year‐old man developed swelling and discomfort over the left elbow. Two years before, he had experienced stiffness and edema of the fingers. Salicylate therapy had been helpful. Shortly thereafter he had a brief episode of what had been considered “mild anicteric hepatitis” which subsided within a month.

Anicteric Infectious Hepatitis: A Population Study.

s1 October 1964Anicteric Infectious Hepatitis: A Population Study.Frederick W. Sprong, Robert DeForest, James G. Harmeling, Jack T. JonesFrederick W. SprongSearch for more papers by this author, Robert DeForestSearch for more papers by this author, James G. HarmelingSearch for more papers by this author, Jack T. JonesSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-808_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe incidence of anicteric infectious hepatitis was studied in 737 military personnel from a group who had been inadvertently exposed to infectious hepatitis by the development of this disease in a food handler in their mess. Each week for 10 weeks, the men were questioned for symptomatology consistent with infectious hepatitis and a blood sample obtained for determination of serum glutamic oxaloacetic transaminase (SGOT). Of the entire group, 76% had an elevated SGOT at some time during the course of the study: 96 of these were admitted to the hospital for further study. All but a few of those admitted... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Frederick W. Sprong; Robert DeForest; James G. Harmeling; Jack T. JonesAffiliations: Newport, R. I. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 808-809KeywordsArmed forcesBloodFoodInfectious diseasesInfectious hepatitisSerum glutamic oxaloacetic transaminase ePublished: 1 December 2008 Issue Published: 1 October 1964 PDF downloadLoading ...