Stuart S. Kassan

Increased Risk of Lymphoma in Sicca Syndrome

The risk of cancer was ascertained in 136 women with sicca syndrome followed at the National Institutes of Health (NIH). Seven patients developed non-Hodgkins lymphoma from 6 months to 13 years after their first admission to NIH. This was 43.8 times (P less than 0.01) the incidence expected from the rates of cancer prevailing among women of the same age range in the general population during this time. In addition, three cases of Waldenströms macroglobulinemia occurred in this study group. Eight patients developed cancers other than lymphoma, similar to the number expected based on the rates prevailing in the general population. Patients with a history of parotid enlargement, splenomegaly, and lymphadenopahy had an increased risk of lymphoma. These clinical conditions did not appear to be early manifestations of undiagnosed lymphoma but rather seemed to identify a subgroup of patients with sicca syndrome with marked lymphoid reactivity, who had a particularly high risk of subsequently developing lymphoma.

Sjögren's Syndrome Associated with HLA-Dw3

Abstract Sjogrens syndrome is associated with a serologically defined histocompatibility antigen of the HLA-B locus, HLA-B8. Another closely linked locus, HLA-D, determines lymphocyte-defined cell...

Antibody to a soluble acidic nuclear antigen in Sjögren's syndrome.

Abstract The presence of a precipitating antibody to an extractable nuclear antigen, termed Ha, was examined by immunodiffusion in gel in three subpopulations of patients with Sjogrens syndrome (SS): (1) those with sicca complex alone, (2) those with SS and rheumatoid arthritis (SS-RA) and (3) those with SS and systemic lupus erythematosus (SS-SLE). Control populations included patients with rheumatoid arthritis (RA) alone and systemic lupus erythematosus (SLE) alone, and normal age-matched blood donors without a history of SS or other connective tissue disease. The results demonstrate the high incidence of anti-Ha antibody in sicca complex (68 per cent) versus the low incidence of the antibody in SS-RA (5 per cent) (p No correlations were found between anti-Ha antibody positivity and clinical parameters, such as serum immunoglobulin concentration, degree of abnormality of parotid scan, titer of rheumatoid factor or focal score of labial biopsy in the patients with SS. However, a correlation between anti-Ha antibody titer and clinical disease activity was noted in two patients examined. The appearance of the anti-Ha antibody was correlated with the development of pseudolymphoma in a third patient. The presence of the anti-Ha antibody may identify a subpopulation of patients with SS at greater risk of rapid progression of the disease and/or the development of pseudolymphoma.

Impairment of primary in vitro response of New Zealand mouse spleen cells to a thymic-dependent antigen

Abstract New Zealand Black (NZB) and NZB by New Zealand White (NZW) F 1 hybrid ( B W ) mice develop clinical signs of autoimmune disease between 6 and 10 months of age but spleen cells from these strains have a greatly reduced in vitro response to sheep erythrocytes (SRBC) as early as 5–6 weeks of age. This hyporesponsiveness can be only partially restored with 2-mercaptoethanol, allogeneic macrophages or spleen cells, or allogeneic factor. The response of NZB and B W spleen cells to the thymic independent antigen DNP-Ficoll is nearly normal. The reduced in vitro SRBC response was found to be attributable to splenic T and B cells rather than macrophages. Macrophages from NZB mice were found to function normally. The in vitro behavior of NZB lymphocytes is very similar to non-autoimmune mice infected with common murine viral pathogens. NZB and B W mice may be making an active immune response as early as 5 weeks of age.