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V Agnello

Publications and source records attributed to V Agnello.

12 recordsLinked to original sources
PubMed1992

A role for hepatitis C virus infection in type II cryoglobulinemia.

BACKGROUND: Type II cryoglobulinemia is a vasculitis characterized by cryoglobulins consisting of complexes of polyclonal IgG and monoclonal IgM rheumatoid factors. The cause of these immune complexes is unknown, though both the hepatitis B (HBV) and C (HCV) viruses have been suspected. METHODS: We studied 19 patients with Type II cryoglobulinemia for markers of HCV and HBV infection. Quantitative HCV antibody and RNA studies were performed on whole serum, cryoprecipitates, and supernatants. RESULTS: Eight patients (42 percent) had HCV antibodies, and 16 (84 percent) had HCV RNA: Of the 19 patients, 5 (26 percent) had HBV markers, but only 1 had evidence of active HBV infection. Control serum samples from nine patients with Type I cryoglobulinemia were negative for HCV antibody and HCV RNA: There was a close, although not exclusive, association of one type of rheumatoid factor (WA) with HCV RNA: HCV antibody and HCV RNA were concentrated approximately 10-fold and 1000-fold, respectively, in the Type II cryoglobulins examined. CONCLUSIONS: Type II cryoglobulinemia is strongly associated with concomitant HCV infection and a high rate of false negative serologic tests. HCV virions and HCV antigen-antibody complexes are concentrated in the cryoprecipitates, most commonly in association with the WA type of rheumatoid factor, suggesting a role for HCV in the pathogenesis of mixed cryoglobulinemia.

Cryoglobulinemia↗
PubMed1978

Association of systemic lupus erythematosus and SLE-like syndromes with hereditary and acquired complement deficiency states.

The most prominent association of rheumatic diseases with hereditary complement deficiency is systemic lupus erythematosus (SLE) and discoid lupus erythematosus with homozygous C2 deficiency in females. The lupus disease in these patients differ from classic lupus in 1) the increased incidence of discoid lesions, 2) the low incidence of renal disease, 3) the low or absent titers of antibodies to native DNA, and 4) the infrequent finding of immunoglobulin and complement in skin lesions. The strong positive linkage disequilibrium between C2 deficiency and HLA genes raises the possibility that genes other than those determining C2 levels may have the primary role in determining predisposition to disease in these patients. However, the finding of similar diseases in certain patients with hereditary angioedema and SLE-related syndrome who have acquired deficiency of the early components of complement supports a primary role of the C2 deficiency gene in predisposing to lupus disease in these patients.

Arthritis, Rheumatoid↗
PubMed1978

Evidence for a silent or null gene in hereditary C2 deficiency.

Three generations of a family with hereditary C2 deficiency were studied, Six members heterozygous for C2 deficiency were identified by serum C2 levels that were approximately 50% of normal C2 values and the identity was supported by HLA analysis. All six members with low C2 levels had only a single electrophoretic variant. Two of four children did not have the variant found in the parent from whom they inherited the partial C2 deficiency. It is inferred that the low levels of C2 result from the inheritance of a silent or null gene, C2D allelic with the structural genes controlling the electrophoretic variants.

Antigens↗
PubMed1977

Detection of immune complexes. The use of radioimmunoassays with Clq and monoclonal rheumatoid factor.

This study describes two sensitive, rapid, relatively simple, competitive inhibition radioimmunoassays for detecting immune complex. The tests are based on the inhibition of I125-Clq or I125-monoclonal rheumatoid factor (mRF) binding to an insoluble substrate, IgG-Sepharose. The assays can be performed in 5 h utilizing 10 micronl of serum. Heating of serum is not required and polyclonal rheumatoid factors do not interefere. With the two assays, a wide range of complexes of various size and complement fixing activity can be detected. The Clq test can detect complement fixing Ig complexes larger than 19S, while the mRF tests detect complexes of IgG as small as 8S irrespective of their complement fixing activity. Mouse, rabbit, and human aggregated IgG (agg IgG) can be detected in the Clq test, and human and rabbit agg IgG in the mRF test. As low as 4 microng/ml of isolated human agg IgG can be detected in the Clq test and 0.5 microng/ml in the rheumatoid factor test. Sensitivity is greater for mouse agg IgG. For pathologic sera which must be diluted to eliminate interfering factors, the sensitivity of the assay is approximately 10 times less. The Clq test showed marked inhibition by systemic lupus erythematosus sera with close correlation with CH50 levels and disease activity. The mRF test showed better correlation with rheumatoid arthritis sera. In addition, anionic macromolecules known to react with Clq and other Clq reactants that occur in pathologic sera such as the "low molecular weight" substances in systemic lupus erythematosus are also detected. These reactants are not detectable in the mRF test and can be eliminated in the Clq test by performing the test at higher ionic strength. The tests can be applied to the study of a variety of pathologic states where immune complexes appear to play a role.

Animals↗
PubMed1975

Hereditary C2 deficiency in systemic lupus erythematosus and acquired complement abnormalities in an unusual SLE-related syndrome.

Early study of kindreds with C2 deficiency indicated that absence of C2 had no detrimental effect on affected individuals. Studies of additional kindreds, however, show a high incidence of SLE and other connective tissue diseases among homozygous C2-deficient members. A group of patients with an unusual SLE-related syndrome is described. In common with certain SLE patients they have marked depression of early complement components and presence of circulating Clq precipitins. It is suggested that early complement components are involved in specific host defense mechanisms and deficiencies of these components may predispose to such diseases.

Antibodies, Antinuclear↗
PubMedDate not supplied

Hereditary C2 deficiency: association with skin lesions resembling the discoid lesion of systemic lupus erythematosus.

Two patients with hereditary homozygous C2 deficiency are described. They showed many similar clinical features. Both had discoid-like skin rashes and serologic abnormalities consistent with SLE, but neither had evidence of involvement of any organ other than skin. Although biopsy of these lesions revealed expected changes by light microscopy, typical immunofluorescent findings were not present. The presence of the HL-A haplotype 10, W18 was seen in both families and was associated with the C2 deficiency gene. The 2 patients were mutually nonreactive in MLC tests and both were found to be homozygous for the LD7a type.

Adult↗