Thalidomide plus oral melphalan for advanced multiple myeloma: a phase II study.
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Biomedical subjects
Publications and source records attributed to Pietro Leoni.
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CONTEXT: Celiac disease is one of the most common lifelong disorders. Non-Hodgkin lymphoma is a possible complication of celiac disease and may lead to a large portion of lymphoma cases. OBJECTIVE: To quantify the risk for developing non-Hodgkin lymphoma of any primary site associated with celiac disease. DESIGN AND SETTING: Multicenter, case-control study conducted between January 1996 and December 1999 throughout Italy. PATIENTS: Cases were older than 20 years (median, 57; range, 20-92 years) with non-Hodgkin lymphoma of any primary site and histological type and were recruited at the time of the diagnosis. Controls were healthy adults (2739 men and 2981 women) from the general population. MAIN OUTCOME MEASURE: Positive test result for class A serum antiendomysial antibody. RESULTS: Celiac disease was diagnosed in 6 (0.92%) of 653 patients with lymphoma. Of the 6 cases, 3 were of B-cell and 3 were of T-cell origin. Four of 6 cases had lymphoma primarily located in the gut. In the control group, 24 (0.42%) had celiac disease. The odds ratio (adjusted for age and sex) for non-Hodgkin lymphoma of any primary site associated with celiac disease was 3.1 (95% confidence interval [CI], 1.3-7.6), 16.9 (95% CI, 7.4-38.7) for gut lymphoma, and 19.2 (95% CI, 7.9-46.6) for T-cell lymphoma, respectively. The risk for non-Hodgkin lymphoma for the overall population, which was adjusted for age and sex, was 0.63% (95% CI, - 0.12% to 1.37%). CONCLUSION: Celiac disease is associated with an increased risk for non-Hodgkin lymphoma, especially of T-cell type and primarily localized in the gut. However, the association does not represent a great enough risk to justify early mass screening for celiac disease.
The GIMEMA ALL 0288 trial was designed to evaluate the impact of a 7-day prednisone (PDN) pretreatment on complete remission (CR) achievement and length, the influence of the addition of cyclophosphamide (random I) to a conventional 4-drug induction on CR rate and duration, and whether an early post-CR intensification (random II) by an 8-drug consolidation could improve CR duration. Median follow-up of this study was 7.3 years. From January 1988 to April 1994, among 794 adult (> 12 but < 60 years) patients registered, 778 were eligible. Their median age was 27.5 years; 73% had B-lineage acute lymphoblastic leukemia (ALL) and 22% had T-lineage disease; 18% showed associated myeloid markers; 47 of 216 analyzed patients (22%) had Philadelphia chromosome-positive ALL. Response to PDN pretreatment was observed in 65% of cases. CR was achieved in 627 patients (82%). Resistant patients and induction death rates were 11% and 7%, respectively. Random II was applied to 388 patients with CR; 201 had maintenance alone and 187 had consolidation followed by maintenance. The relapse rate was 60%; isolated central nervous system relapses were 8% of all CRs and 13% of all relapses. Median survival (overall survival [OS]), continuous complete remission (CCR), and disease-free survival (DFS) were 2.2, 2.4, and 2 years, respectively. PDN pretreatment response resulted the main independent factor influencing CR achievement, OS, CCR, and DFS; the addition of cyclophosphamide in induction significantly influenced CR achievement in a multivariate analysis. Neither induction intensification nor early consolidation appeared to influence CCR and DFS duration. For the first time PDN pretreatment response proved to be a powerful factor predicting disease outcome in adult ALL patients.
We describe the peculiar histopathology of the bone marrow in a case of IgG/lambda MGUS. Striking eosinophilic crystals with a rectangular, rhomboid or square shape lay in the interstitium, sometimes in optically empty spaces, but failed to elicit a foreign body giant cell reaction. Their histochemical properties, immunoreactivity for anti-lambda light chain antiserum, and ultrastructural features strongly supported their relationship with the paraprotein synthesized by the monoclonal plasma cells. The crystals were not observed on bone marrow aspirate smear, suggesting that they had formed during trephine biopsy processing or, alternatively, that they had been removed during the smear preparation. We feel that pathologists should be aware of the existence of this type of crystals, which differ from both the amyloid deposits and the proteinaceous material sometimes observed in plasma cell proliferations. Their presence in the bone marrow should alert the clinician to investigate the involvement of other organs with immunoglobulin deposits.