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Biomedical subjects

V Agnello

Publications and source records attributed to V Agnello.

At least 55 records · Page 3Linked to original sources
PubMed1983

Characterization of complement-fixing activity and cross-idiotypes of rheumatoid factors in idiopathic mixed cryoglobulinemia.

The complement-fixing activity, specificity for IgG, and cross-idiotypes of rheumatoid factors (RF) isolated from the mixed cryoglobulins of nine patients with idiopathic mixed cryoglobulinemia were determined. All were IgM kappa and fixed complement. The RF complement-fixing activity did not correlate with hypocomplementemia or disease manifestations. The majority of RF belonged to the same cross-idiotype group. The RF from two of three patients with predominantly neurologic manifestations did not have any of the known cross-idiotypes and reacted better with rabbit IgG than with human IgG. The patients with neurologic manifestations also differed in that their serum complement was normal.

Adult↗
PubMed1983

Immune complex assays in rheumatic diseases.

A wide variety of antigen-nonspecific immune complex assays have been developed in recent years for the detection and quantitation of immune complexes in pathologic fluids. These assays detect complexed antibody regardless of the antigen involved. Almost all of these assays use biologic reagents that may react with substances other than complexed antibody. In addition, the assays do not differentiate nonspecifically aggregated antibody from antigen-complexed antibody. Hence, these assays are not absolute tests for immune complexes. On the basis of studies using these assays, "immune complexes" have been detected in a large number of rheumatic diseases. While these findings have been of considerable investigative interest, thus far they have been of little practical clinical utility. The detection of immune complexes has not been shown to be essential in any clinical conditions but may be helpful in monitoring disease activity in systemic lupus erythematosus (SLE) and may provide useful diagnostic information in two rare syndromes, Lyme arthritis and SLE-related syndrome.

Antigen-Antibody Complex↗
PubMed1983

Partial genetic deficiency of the C4 component of complement in discoid lupus erythematosus and urticaria/angioedema.

A high incidence of discoid lupus erythematosus (DLE) and urticaria/angioedema was found among patients with selective low levels of the C4 component of complement. Although evidence for activation of C4 was present in patients' sera, studies to determine the presence of known activation mechanisms were negative. Genetic C4 typing in four pedigrees showed that all propositi carried the null allele B*QO. It is postulated that the low C4 levels in these patients are related to the skin lesions and this partial genetic deficiency.

Adult↗
PubMed1983

Selective depression of the C4 component of complement: evidence for an association with genetic deficiency of C4 and dermatologic diseases.

Thirty-four patients with selective low serum C4 levels were found among 1,731 patients studied in a hospital-based routine clinical immunology laboratory. A high incidence of dermatologic diseases, particularly discoid lupus erythematosus and angioedema/urticaria, was present among patients with selective low C4. Although evidence for activation of C4 was present in patients' sera, studies to determine the presence of known activation mechanisms of complement were negative. Genetic C4 typing in four pedigrees showed that all propositi carried the null allele B*QO. It is postulated that the selective C4 depression in these patients is related to the skin lesions and this partial genetic deficiency.

Aged↗
PubMed1983

Preliminary observations on danazol therapy of systemic lupus erythematosus: effects on DNA antibodies, thrombocytopenia and complement.

Seven patients with systemic lupus erythematosus (SLE) were treated with Danazol in a controlled study. Phenomena observed in some patients treated with Danazol were: 1) decrease in immunoglobulins and antibodies to native DNA; 2) increases in serum complement and platelets; and 3) clinical improvement. Ineffective drug trials were associated with increasing disease activity. Drug side effects were minimal. It appears that the drug may have an ameliorative effect on mildly active SLE patients and sometimes a marked effect on thrombocytopenia. Further evaluation of Danazol appears to be warranted for these types of patients but not for treatment of acute or severe forms of the disease.

Adult↗
PubMed1980

Evidence for a subset of rheumatoid factors that cross-react with DNA-histone and have a distinct cross-idiotype.

Cross-reactivity of a monoclonal rheumatoid factor with an antigen present on IgG and DNA-nucleoprotein was demonstrated, and evidence presented that the combining site of the antibody was involved in the reaction. The antigen on the DNA-nucleoprotein was shown to involve both DNA and histone fraction H2A + H2B and was trypsin sensitive. The relative binding affinity of the antibody appeared to be greater for IgG than the DNA-histone antigen. Similar polyclonal cross-reactive rheumatoid factors were found in a variety of diseases. A high incidence was found among patients with rheumatoid arthritis and mixed connective tissue disease. None were detected in patients with systemic lupus erythematosus and idiopathic cryoglobulinemia. Studies on one representative isolated polyclonal rheumatoid factor demonstrated the same reactivity with DNA-histone H2A + H2B as the monoclonal antibody. Cross-idiotype studies using antigen-binding inhibition methods demonstrated the same cross-idiotype on the polyclonal and the monoclonal rheumatoid factor which reacted with DNA-histone. This cross-idiotype was shown to be distinct from the cross-idiotypes previously demonstrated on monoclonal IgM proteins with anti-gamma-globulin activity.

Binding Sites, Antibody↗
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↗