Sjogren's syndrome (SS) is characterized by an increased risk of developing non-Hodgkin's lymphoma (NHL). Optimal treatment for NHL-complicating SS is not clearly established. NHL, which expresses the CD20 antigen on tumor cell surfaces, is a disease entity candidate to treatment with anti-CD20 monoclonal antibodies. We report clinical and immunological data of a patient with SS and NHL who was treated with a regimen consisting of cyclophosphamide/vincristine/prednisone (CVP) plus rituximab. A 68-year-old women had a 26-year history of SS and autoimmune thyroiditis. The clinical course of SS was complicated with severe splenomegaly. An increased percentage of CD19+ B cells (up to 30%) was detected in peripheral blood during follow-up. Clonal rearrangement of immunoglobulin heavy chain was detected. Low-grade B marginal zone lymphoma was diagnosed (peripheral blood immunophenotype: CD19+CD20+CD23+sIg+Kappa; bone marrow immunophenotype: 25% lymphocytes; CD19+CD20+CD79A/BCL2+). She received a total of six cycles of CVP plus rituximab (375 mg/m2). Therapy was well tolerated, and B lymphocytes were depleted from the peripheral blood. Splenomegaly normalized. No evidence of neoplastic infiltration was detected in bone marrow after completion of therapy, while certain symptoms of SS (sicca and arthralgia) improved with treatment. CVP plus rituximab proved effective in a patient with SS with NHL.
myxo-fibroblastic proliferation. There was focal chorangiosis with intervening normal placental mesenchyme. The fetal chorionic plate vessels were massively dilated, tortuous and congested. There was a 3-vessel umbilical cord with furcated marginal cord insertion. Immunohistochemical studies of the abnormal myxoid villi showed minimal staining for smooth muscle actin and positive p57 KIP2 protein staining. This is only the third case of PMD with normal fetus where the p57 KIP2 protein staining was used in the diagnosis. The p57 KIP2 gene is paternally imprinted and maternally expressed. The presence of this protein indicates a functional maternal allele. This case supports the utility of p57 KIP2 protein staining in distinguishing this disorder from molar pregnancy. In our case elevated free beta-hCG level was detected in the first trimester before placental abnormalities were visualized on ultrasound. P39.05 A study to determine the veracity of the ultrasonographic measurements of the thymus during fetal development
Oral communication abstracts a prevalence of less than 15%, between 15 and 30% and above 30%. To ascertain statistically significant differences in performance between the types of centers, the AUCs were compared using bootstrapping. The optimal cutoff level per center and type was chosen corresponding to a sensitivity level as high as possible (preferable above 90%) while still keeping a good specificity (80%) as this was considered to be very important in correctly identifying malignant cases. Results: Both LR1 and LR2 performed better, although not statistically significant, in centers with a lower prevalence of malignant cases. The AUC of centers with less than 15% of malignancy was 0.956 and 0.941, for LR1 and LR2 respectively; centers with prevalence between 15 and 30% had an AUC of 0.948 and 0.925, respectively and centers with more than 30% malignancies had an AUC of 0.933 and 0.914, respectively. The optimal cutoff per center varied between 0.05 and 0.20, but the performance in the centers with a higher percentage of malignant cases did not improve by choosing a different cutoff level. Conclusions: The performance of the logistic regression models increases with decreasing prevalence of malignancy. Because new cutoff levels per center would be based on 8 to 253 patients and the cutoff of 0.10 is optimal for all three types of center, it seems reasonable to use this cutoff in all centres.
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