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Biomedical subjects

G L Davis

Publications and source records attributed to G L Davis.

At least 163 records · Page 9Linked to original sources
PubMed1985

Decision making in pathology: what is the impact of economic and technologic change?

Diagnostic anatomic pathologists have to resolve a number of conflicts. They have been thrust into medical marketplace competition with which they have little experience. New technology and CPT-4 codes have given them an economic base at the same time that DRGs are limiting expenditures. Computerized surgical pathology reports are possible, but do they communicate useful information? So as not to be replaced by the very tools they use, the author explains why diagnostic anatomic pathologists must report useful information and select only the most cost-effective techniques.

Clinical Laboratory Techniques↗
PubMed1985

Tubuloreticular inclusions in peripheral blood mononuclear cells related to systemic therapy with alpha-interferon.

Tubuloreticular inclusions (TRI) developed within the endoplasmic reticulum of peripheral blood mononuclear cells (PBMC) sampled from eight patients with chronic type B hepatitis during cycles of therapy with DNA-recombinant human alpha-interferon (rIFN alpha A). Each cycle of therapy consisted of a series of six intramuscular injections (triweekly) of a fixed dose of rIFN alpha A (from 18 to 68 X 10(6) IU/dose). In PBMC examined by transmission electron microscopy, TRI were absent prior to therapy and developed during therapy in all cases. Peak serum levels of alpha-interferon (320 to 960 IU/ml) were achieved within 12 hours. At 24 hours. TRI were detected in 0.5 to 6.5% of PBMC sections, and they persisted in 1.4 to 6.8% of sections examined at 48 hours. After five sequential interferon doses, TRI were observed in 1.6 to 9.8% of PBMC sections. TRI could no longer be detected at 5 to 16 days after cessation of rIFN alpha A, but they reappeared during subsequent cycles of therapy. Subpopulations of the PBMC with TRI were differentiated by immunoelectron microscopy utilizing a battery of anti-Leu monoclonal antibodies: surface markers of T cells, helper/inducer or cytotoxic/suppressor T cell subsets, natural killer cells, or B-cells were identified by direct or indirect procedures utilizing avidin and biotinylated peroxidase. In cases analyzed with multiple monoclonal antisera, TRI were expressed in all of the major PBMC subpopulations. Monocytes with TRI were demonstrated by the endogenous peroxidase reaction. TRI were not found in circulating polymorphonuclear granulocytes. Lymphocytes isolated from healthy donors and exposed to rIFN alpha A (100 IU/ml), for 48 to 72 hours in vitro, developed TRI in proportions of PBMC sections (2.3 to 8.4%) comparable to those observed in the interferon-treated patients. Stimulation of lymphocytes with concanavalin A, for 72 hours before rIFN alpha A exposure, enhanced formation of TRI which could then be found in T blasts. Stimulation of donor lymphocytes with Sendai virus, a potent inducer of alpha-interferon, also resulted in formation of TRI by 48 hours. This suggested that lymphocytotrophic virus infections could exercise a primary role in the natural pathogenesis of TRI.

Antibodies, Monoclonal↗
PubMed1984

Acute type A hepatitis during chronic hepatitis B virus infection: association of depressed hepatitis B virus replication with appearance of endogenous alpha interferon.

Two patients with chronic type B hepatitis and intercurrent episodes of acute type A hepatitis are presented. Serological markers of hepatitis B virus replication decreased or became undetectable in both patients during the acute illness, while interferon activity was transiently detected in serum. The presence of serum leukocyte (alpha) interferon was confirmed by neutralization with specific antisera and tests of pH2 stability. These observations suggest a role for natural leukocyte (alpha) interferon in the modulation and control of hepatitis B virus infection and provide further evidence to support trials of exogenous leukocyte (alpha) interferon in the chronic infection.

Acute Disease↗
PubMed1984

Development and prognosis of histologic cirrhosis in corticosteroid-treated hepatitis B surface antigen-negative chronic active hepatitis.

To determine the frequency and prognosis of histologic cirrhosis developing during or after corticosteroid therapy of hepatitis B surface antigen-negative chronic active hepatitis, we followed 83 patients for 90 +/- 5 mo after administration of corticosteroids. Thirty-three patients satisfied histologic criteria for cirrhosis after 30 +/- 5 mo. In 25 patients, cirrhosis developed during treatment; in 8 patients, cirrhosis eventuated after remission and cessation of therapy. The probability of developing histologic findings of cirrhosis was 59% if remission had not been achieved after 3 yr of continuous therapy. Longer requirements for treatment and deterioration during therapy characterized these patients. Once remission was achieved, the mean annual incidence of cirrhosis was only 2.6%. Patients who manifested evidence of cirrhosis in their biopsy specimens could not be distinguished by initial clinical, biochemical, or histologic findings. Ascites, encephalopathy, and esophageal varices developed infrequently; 5-yr survival after documentation of cirrhosis was 93%. We conclude that histologic features of cirrhosis develop commonly during therapy, especially if remission is not achieved quickly. After remission, cirrhosis develops infrequently. The development of histologic cirrhosis does not influence immediate morbidity and 5-yr life expectancy.

Adult↗
PubMed1984

Spontaneous reactivation of chronic hepatitis B virus infection.

Studies on the natural history of chronic type B hepatitis have shown that loss of hepatitis B e antigen and seroconversion to antibody to hepatitis B e antigen are usually accompanied by remission of disease activity and improvement in serum aminotransferase levels. Twenty-five symptomatic patients with biopsy-documented chronic type B hepatitis were followed for 25 +/- 2 mo (mean +/- SEM) after disappearance of hepatitis B e antigen, hepatitis B virus-deoxyribonucleic acid, and deoxyribonucleic acid polymerase activity from the serum. Twenty-four patients developed the antibody to hepatitis B e antigen. All 25 patients demonstrated a decrease in serum aminotransferase levels, and most became asymptomatic. However, during subsequent follow-up, 8 of the 25 patients (32%) exhibited reactivation of chronic type B hepatitis manifested by abrupt elevation of serum aminotransferase levels and reappearance of serum hepatitis B virus-deoxyribonucleic acid, deoxyribonucleic acid polymerase activity, and, in 7 patients, hepatitis B e antigen. All 8 patients developed symptoms: 3 became icteric, 3 developed ascites, and 2 bled from esophageal varices. One of these patients died. Episodes of reactivation invariably occurred within 1 yr of loss of hepatitis B e antigen and lasted for up to 13 mo. These observations suggest that loss of hepatitis B e antigen and seroconversion to the antibody to hepatitis B e antigen do not necessarily imply permanent remission of chronic type B hepatitis, and subsequent spontaneous reactivation may be an important cause of progression of hepatic injury.

Adult↗
PubMed1983

Factor VIII complex in chronic renal failure: influence of protein C, fibrinolysis and diabetes mellitus.

Chronic renal failure causes elevations of factor VIII coagulant activity and Factor VIII-related antigen even before the patients enter chronic hemodialysis. The change from control of Factor VIII ristocetin cofactor does not reach significance. The elevations are not effected by entering onto hemodialysis. These parameters are the same for non-diabetic and diabetic patients. Protein C, plasminogen and total fibrinolytic capacity are normal in diabetic and non-diabetic patients, with or without hemodialysis for chronic renal failure. However, before entering onto hemodialysis some of these parameters had negative correlation coefficients with parts of the factor VIII complex among the diabetic and non-diabetic patients. These negative correlates turned positive after hemodialysis. Thus, there are differences in these catabolic mechanisms for factor VIII when hemodialysis is used for diabetic and non-diabetic patients with chronic renal failure.

Adult↗
PubMed1983

Autoimmune features as determinants of prognosis in steroid-treated chronic active hepatitis of uncertain etiology.

To determine if autoimmune features influence the prognosis of severe sporadic chronic active hepatitis of uncertain etiology, 126 corticosteroid-treated patients who had been screened to exclude active hepatitis B infection and possible drug effects or transfusion-related disease were categorized according to the presence of the lupus erythematosus cell, antinuclear antibody, smooth muscle antibody, and coexistent autoimmune diseases. Patients with autoimmune markers had findings similar to those without these features and responses to therapy were comparable. Remission (77% vs. 68%), treatment failure (16% vs. 14%), progression to cirrhosis (31% vs. 39%), and death from hepatic failure (4% vs. 12%) occurred with similar frequency in patients with and without the lupus erythematosus cell or antinuclear antibody. Although patients with the lupus erythematosus cell or antinuclear antibody tended to relapse less frequently than others, 5-yr survival was not increased (92% vs. 87%). Autoimmune diseases occurred as commonly in patients without the lupus erythematosus cell or antinuclear antibody as in those with these findings (16% vs. 17%), and the presence of these conditions did not identify patients with a different clinical behavior. In severe sporadic chronic active hepatitis of uncertain etiology, a clinically and prognostically distinct subgroup reflective of a possible autoimmune disorder cannot be defined.

Adolescent↗
PubMed1983

Hepatic adenoma and focal nodular hyperplasia: clinical, pathologic, and radiologic features.

Based on strict predefined histologic criteria, we identified 23 patients with hepatic adenoma and 41 patients with focal nodular hyperplasia seen at this institution between 1961 and 1980. Patients with hepatic adenoma were young and 91% were female. When a reliable history was available, 89% had used oral contraceptives; 53% presented acutely or with pain. Eleven of 11 radionuclide scans were abnormal; 15 of 15 angiograms showed a hypervascular mass with 7 of 15 showing areas of hypovascularity. Eighteen resections were performed with one operative death. Two tumors contained areas of unequivocal hepatocellular carcinoma. Fifteen of 18 patients followed for 82 +/- 11 mo were living and well and had discontinued oral contraceptives. Focal nodular hyperplasia patients were older, 88% were female, and 58% had used oral contraceptives. Their lesions were discovered accidentally. Seven of 12 radionuclide scans demonstrated voids, while 13 of 13 angiograms showed hypervascular lesions with no areas of hypovascularity. Seventeen tumors were resected. Twenty-three of 24 patients followed for 45 +/- 7 mo were living and well. One died of nonhepatic causes. Based on the findings of this review, we believe that if the clinical suspicion of hepatic adenoma or focal nodular hyperplasia is strong, elective laparotomy for diagnosis is usually the best approach. Hepatic adenoma should be resected if technically feasible. Intraoperative wedge biopsy is appropriate for focal nodular hyperplasia.

Abdomen↗
PubMed1983

Procoagulant activity associated with plasma membrane vesicles shed by cultured tumor cells.

Thirteen of 14 tumor cells or tumor cell lines of guinea pig, mouse, and human origin spontaneously shed procoagulant activity in short-term (4 or 14 to 22 hr) tissue culture under conditions of high cell viability. This released procoagulant activity was pelletable in the ultracentrifuge and was associated with plasma membrane-derived vesicles as determined by transmission electron microscopy and marker enzyme analysis. The procoagulant activity shed corresponded to a substantial fraction of that expressed by intact or sonicated tumor cells and was composed of activities interacting at more than a single step in the clotting sequence. One procoagulant activity associated with shed human tumor vesicles behaved as tissue factor, requiring Factor VII for activity and being inhibited by a specific anti-bovine tissue factor antibody. Guinea pig tumor vesicles also exhibited tissue factor-like activity in a two-stage assay using homologous first-stage Factor VII/X concentrate. None of the human vesicles tested expressed a direct Factor X cleaving activity, independent of Factor VII. Shed tumor vesicles also acted at a second step late in the clotting cascade at the level of prothrombinase generation, presumably by providing a phospholipid surface. Taken together, these data indicate that a wide variety of tumor cells release plasma membrane vesicles with procoagulant activity. Such vesicles, as well as intact tumor cells themselves, may play an important role in the biology of tumor growth by inducing the local fibrin deposits found in association with many solid tumors.

Animals↗
PubMed1982

Hepatitis non A, non B. Manifestations and implications of acute and chronic disease.

Application of sensitive radioimmunoassays for the detection of hepatitis A and B viruses has demonstrated that up to 25% of cases of acute sporadic hepatitis and up to 90% of cases of posttransfusion hepatitis cannot be classified by etiologic agent and warrant designation as non-A, non-B hepatitis. Epidemiologic studies have indicated a pattern of transmission similar to that of hepatitis B virus, with predominance of parenteral routes of spread. Spontaneous resolution of acute infection fails to occur in up to 60% of patients; a chronic asymptomatic but infectious carrier state is recognized. Although the chronic hepatitis is usually mild, a potential for progression to cirrhosis has been described. Transmission studies in chimpanzees have suggested the existence of at least two non-A, non-B agents, which produce strain-specific ultrastructural changes in the hepatocyte and confer a homologous immunity. Multiple assay systems for detecting putative viral antigens have been developed, but their specificity has not been confirmed. Elimination of blood procured by contract from commercial blood banks diminishes the risk of posttransfusion hepatitis and is recommended for prophylaxis. Although the effectiveness of immune serum globulin in the prevention of sporadic disease has not been established, its administration should be considered after exposure to incriminated blood, in spouses during the acute illness, and in neonates of infected mothers.

Acute Disease↗
PubMed1982

Prognostic and therapeutic implications of extreme serum aminotransferase elevation in chronic active hepatitis.

Extreme elevation of the serum aspartate aminotransferase level typically suggests acute hepatocellular necrosis and may militate against the diagnosis of chronic active hepatitis. However, we found that 26 of 160 patients (16%) with chronic active hepatitis had aminotransferase elevations of more than 1,000 IU/liter. These patients were younger and more often jaundiced than the others, but they exhibited signs of chronic liver disease as often. In only 2 of 26 patients with extreme aminotransferase abnormality were features of chronic disease absent. Patients with extreme enzyme elevation had histologic findings of confluent necrosis (P greater than 0.005) and features associated with acute viral infection (P greater than 0.005) more often than others, but they as often had cirrhosis on biopsy specimens. Virologic markers did not distinguish the patients or correlate with viral features in liver tissue. Corticosteroids improved immediate survival (P greater than 0.005) and the likelihood of remission (P greater than 0.005). Although chronic active hepatitis may present with extreme aminotransferase elevation and histologic features associated with acute viral infection, ancillary features of chronic disease facilitate the correct diagnosis and the initiation of appropriate therapy.

Adult↗
PubMed1981

Current concepts in the diagnosis and management of hepatitis B surface antigen-positive chronic active hepatitis.

Serologic manifestations of the hepatitis B virus are present in up to 25% of patients with chronic active hepatitis in the United States. Progression to cirrhosis and death from liver failure or malignancy are possible long-term consequences of this association. Corticosteroids have been less effective in managing B-related disease than non-B illness. Immunosuppressive treatment may actually facilitate viral replication and enhance morbidity and mortality. Virus-induced alterations of the hepatocyte probably trigger antigen-specific cytotoxic humoral and cellular immune responses that perpetuate liver injury. Treatments to interrupt these pathogenetic mechanisms include immunosuppression, antiviral therapy, immunostimulation, and antibody induction. Experiences with antiviral and immunostimulatory agents have shown some promise, but controlled observations are rare, and results have been inconsistent.

Adrenal Cortex Hormones↗
PubMed1981

Intrathoracic extension of retroperitoneal urine collections.

Five patients with retroperitoneal urine collections (urinomas) had clinical and radiographic evidence of intrathoracic disease. All five patients rapidly accumulated pleural fluid, documented chemically in three patients to be urine. Two patients developed acute mediastinal widening which rapidly cleared after surgical drainage of the retroperitoneal urinoma. Although rare, thoracic collections of urine should be considered when pleural effusions or mediastinal widening occur in patients with urinary tract obstruction or retroperitoneal urinomas.

Aged↗
PubMed1981

In vitro models of viral-induced congenital deafness.

Cytomegalovirus (CMV) infects 1 to 2 percent of liveborn infants in the United States and causes varying degrees of perceptive hearing loss. There are eight reported pathologic studies of temporal bones in CMV-infected neonates. Viral replication occurs in nonsensory endolabyrinthine epithelium, but viral antigen is also found in the organ of Corti and spiral ganglion neurons, and CMV has been cultured from perilymph. Further clinicopathologic correlation is frustrated, since the inner ear cannot be biopsied during life, and the number of temporal bones available for study is limited, owing to the decrease in the number of autopsies being performed. Inoculation of CMV into newborn mice, and extracorporeal preparations of mouse and guinea pig fetal inner ears, either in organ culture or as grafts on chick chorioallantoic membranes, yields viral perilabyrinthitis. The different ultrastructural appearances of CMV replicating in epithelial and mesenchymal cells show that animal CMV replicates in mesenchymal cells and human CMV replicates in epithelial cells of the inner ear. These different ultrastructural patterns indicate that the chromophobe (transitional) cells of the stria vascularis of the guinea pig are of mesenchymal origin.

Animals↗
PubMed1981

Case study: complications associated with anticoagulant therapy.

A 42 year old male with gram negative pneumonia complicated by deep venous thrombosis was followed throughout his hospital stay and for two weeks following discharge. The treatment course is divided into five treatment periods, each with accompanying commentary. Drug interactions and neutralizations as well as dietary factors contributed to a complicated course. Laboratory determinations were used to directly evaluate therapeutic anticoagulant effects, and dosage regimens were adjusted to achieve desired anticoagulant levels.

Adult↗