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F V Chisari

Publications and source records attributed to F V Chisari.

197 records · Page 11Linked to original sources
PubMed1975

Laboratory tests for diagnosis of autoimmune diseases.

1. Antimitochondrial antibody titers of 1:160 are practically diagnostic of primary biliary cirrhosis [71]. Serum antimitochondrial antibody titers of less than 1:16 are seen in 10% of cases of primary biliary cirrhosis. The antimitochondrial antibodies are usually absent in jaundiced patients with extrahepatic obstruction, drug sensitivity, and viral hepatitis. 2. Anti-smooth-muscle antibodies are noted in the various autoimmune liver disorders, viral hepatitis, infectious mononucleosis, malignancy, and intrinsic bronchial asthma. The smooth muscle antibody test helps in the differential diagnosis of lupoid hepatitis vs. systemic lupus erythematosus. The anti-smooth-muscle antibodies are usually absent in systemic lupus erythematosus. 3. The antinuclear antibody is frequently positive in the autoimmune liver diseases. In cases of chronic aggressive hepatitis associated with a high titer of antinuclear antibody the prognosis is usually grave. 4. The presence of antimicrosomal liver and kidney antibody is indicative of chronic aggressive liver disease, which is different from the classic lupoid hepatitis [95, 97]. 5. Hepatitis-B-antigen assay should be performed routinely to exclude viral hepatitis, type B. Heterophile antibody tests should done when the possibility of infectious mononucleosis must be considered. 6. Serum immunoglobulin determinations are of secondary importance in the laboratory diagnosis of autoimmune liver disorders. There is usually a polyclonal elevation of the major immunoglobulin in most chronic parenchymal liver diseases[48].

Age Factors↗
PubMed1974

Human T lymphocyte "E" rosette function. I. A process modulated by intracellular cyclic AMP.

The capacity of normal human T lymphocytes to form rosettes with sheep red blood cells can be inhibited by drugs or agents which induce elevations in intracellular levels of cyclic AMP. The effect is early in the presence of agents which elicit rapid elevations in intracellular cyclic AMP (isoproterenol, aminophylline) and occurs later in the presence of cholera toxin which induces a dalayed increase in endogenous cyclic AMP. Dibutyryl cyclic AMP is inhibitory, and the effects of dibutyryl cyclic AMP and the adenyl cyclase stimulators are potentiated by inhibition of phosphodiesterase. These data provide substantial evidence that elevation of intracellular cyclic AMP diminishes E rosette function of lymphocytes.

Aminophylline↗
PubMed1972

Parathyroid necrosis and hypocalcemic tetany induced in rabbits by L-asparaginase.

Fifty percent of New Zealand white rabbits became profoundly weak, had generalized seizures and died between 22 and 47 hours after an intravenous injection of 1000 IU/kg of L-asparaginase. The biochemical correlate of this syndrome is severe hypocalcemia associated with marked, single cell, oxyphilic necrosis in the parathyroid glands. Although survivors remained clinically well, they also developed hypocalcemia and parathyroid necrosis but to a lesser degree. Rabbits given an equivolumetric amount of saline did not develop alterations in any of these parameters. L-Asparaginase, therefore, exerts a direct toxic effect on the parathyroid glands of rabbits. The implications of this finding for man are briefly discussed.

Animals↗
PubMedDate not supplied

Suppression of lymphocyte activation by a protein released from isolated perfused rat liver.

Isolated rat liver perfusates contain a substance which inhibits 3H-thymidine uptake by phytohemagglutinin-stimulated human peripheral blood lymphocytes in a dose-dependent, noncytotoxic fashion. Suppression is not due to interference of lymphocyte-phytohemagglutinin interaction or dilution of the thymidine pool. Complete inhibition of thymidine uptake is achieved with less than 1.0 microgram of material per ml (which is a potentially achievable concentration in vivo). The release of this material is directly and quantitatively associated with hepatocellular injury as measured by release of glutamic pyruvate transaminase. The material is a highly basic protein with a molecular weight of approximately 65,000 to 80,000 daltons. It is a product of the hepatocyte rather than of nonparenchymal liver cells. Liver-derived materials, such as the presently described molecule, may play a role in in situ regulation of lymphocyte function during immunologically mediated liver disease.

Alanine Transaminase↗
PubMedDate not supplied

Production of two distinct and independent hepatic immunoregulatory molecules by the perfused rat liver.

By manipulating dietary sugar intake and perfusate glucose concentration, we have identified two independent hepatic immunoregulatory molecules produced by the perfused rat liver. The first is released by injured hepatocytes, appears in perfusates together with hepatocellular glutamic pyruvic transaminase, is quantitatively inhibited by exogenous L-arginine and coelutes with arginase on high-pressure liquid chromatography. Based on these findings, we conclude that this activity is due to the release of cytoplasmic arginase from injured hepatocytes. Since supplementation studies reveal that lymphocyte proliferation is exquisitely arginine-dependent, it is conceivable that arginase released by injured hepatocytes might influence lymphocyte function in vivo by local arginine depletion. The second immunoregulatory molecule is released by noninjured hepatocytes following induction by sugar, particularly glucose, both in vivo or in vitro. This inducible activity is arginase-independent, triglyceride-rich and floats at a density less than 1.006 gm per ml upon ultracentrifugation. Based on these characteristics, we tentatively ascribe this activity to hepatic very low density lipoprotein, the serum counterpart of which is known to express many immunoregulatory properties. These results directly illustrate for the first time the pathophysiological conditions required for the secretion and release of these distinct and independent hepatic immunoregulatory molecules, and they suggest possible routes by which they may influence immunological homeostasis and immunologically mediated liver disease.

Alanine Transaminase↗
PubMedDate not supplied

Behçet's disease.

Behçet's disease is characterized by three primary components: iridocyclitis (historically with hypopyon), aphthous lesions in the mouth, and ulceration of the genitalia. Erythema nodosum, arthropathy and thrombophlebitis often accompany these manifestations, but the ocular symptoms may be the most important and serious manifestations of the disease. Central nervous system involvement, most often due to necrotizing vasculitis, may be the most protean manifestation of the disease, leading to death. The frequency of ocular manifestations is 70-85% in patients with the disease; the underlying disease mechanism in all organ systems is an occlusive vasculitis. Although the most common ocular symptom is that of anterior uveitis, often with hypopyon as a very late sign, the presence of necrotizing retinal vascular lesions is well known and often obscured by the severity of the anterior reaction. Definitions, incidence, clinical characteristics, differential diagnosis, and management of Behçet's ocular disease are discussed, as are the interrelationships of the different organ manifestations. The ophthalmologist should be familiar with the full spectrum of disease presentation since he or she may be the first physician to encounter the Behçet's patient.

Adolescent↗
PubMedDate not supplied

Foodborne outbreak of hepatitis A: clinical and laboratory features of acute and protracted illness.

During a 1974 foodborne outbreak of viral hepatitis type A among Navy recruits, we evaluated clinical and laboratory features prospectively in 130 affected persons. The ratio of anicteric to icteric persons identified during the outbreak was 1:3.5 but illness was relatively mild in this population of young adults. Infrequently reported in association with type A hepatitis, rash and arthralgias (but not arthritis) were reported by 14 and 10% of affected persons, respectively. Fourteen weeks after onset of acute illness, 8.5% of patients had persistently elevated aminotransferase activities and underwent percutaneous liver biopsy. Morphologic features included piecemeal necrosis, but clinical, biochemical, and histological evidence of disease resolved within five months to one year after the outbreak. Fecal shedding of hepatitis A virus began during the preicteric stage, did not persist beyond the second day of jaundice (even in patients with protracted illness), and was not detected in anicteric patients. Feces and serum obtained during the late incubation period, but not urine, were infectious in chimpanzees. Antibody to hepatitis A virus developed during convalescence, and serum anticomplementary activity was noted during acute illness. Failure of T-lymphocytes to bind sheep erythrocytes and form rosettes was observed, was found to be modulated in several cases by an intrinsic lymphocyte defect and in others by the presence in serum of an extrinsic immunoregulatory serum lipoprotein, "rosette inhibitory factor," which persisted in patients with slow resolution.

Adult↗
PubMedDate not supplied

Immunological aspects of hepatitis B virus infection.

Infection of man and chimpanzees with the hepatitis B virus (HBV) is associated with diffuse hepatocellular infection and variable manifestations of disease which may not only reflect the character of the host immune response, but also depend upon differences in the cellular biology of this minimally cytopathic or noncytopathic agent. The presence of hepatocellular injury and the course of disease do not appear to be related to the presence of viral antigens in hepatocytes or to the specific pattern of genome expression. HBV infection is typically associated with both humoral and cellular immune responses to viral and hepatocellular antigens. Whereas cellular effector systems may be responsible for immunologically mediated hepatocellular injury, the patterns of viral antigen synthesis and expression may be modulated by the humoral immune response. Aberration of lymphocyte function occurs during acute hepatitis type B. Thymus-derived lymphocyte function is abnormal and is associated with persistent humoral suppression of T lymphocyte function during the development of the chronic carrier state. Extrahepatic disease appears attributable to the formation and deposition of HBS Ag-antibody complexes. Current information of the biology and immunology of HBV and other viruses has been integrated into a hypothesis to explain the pathogenesis of injury and events associated with persistent infection. Hepatocellular injury and persistence of viral synthesis may be determined by the regulation of synthesis and hepatocyte surface expression of viral and cellular antigens as well as by the specificity and character of the host immune response. Termination of HBV infection is viewed as suppression of viral genome rather than eradication of infected cells.

Animals↗