Academic literature on the topic '362.82/092 b'

9612 Background: Aprepitant (A) is a NK1-antagonist approved for prevention of chemotherapy-induced nausea and vomiting (CINV). Though melphalan (M) is regarded only moderately emetogenic, CINV after high-dose M conditioning in autologous TPX can severely interfere with patients’ (pts) quality of life. Here we present the results of our monocentric, randomized (1:1), placebo-controlled, double-blind phase IIIb trial of A, granisetrone (G) and dexamethasone (D) in this setting. Methods: Pts were treated with A 125 mg po day 1, A 80 mg po days 2-4, G 2 mg po days 1-4 and D 4 mg po day 1, D 2 mg po days 2-3 (arm A) or placebo (P) days 1-4, G 2 mg po days 1-4 and D 8 mg day 1, D 4 mg days 2-3 (arm B). Melphalan 100 mg/m² iv was administered days 1-2. Episodes of emesis, modified functional living index – emesis questionnaire (FLIE) and intensity of nausea by visual analogue scale (VAS) were recorded between days 1-6. Primary endpoint was defined as no episode of vomiting and no additional antiemetic therapy within 120h of M administration. Results: Between 07/05 and 01/12 a total of 362 pts were randomized. 361 subjects (arm A=180; arm B=181; male n=229; female n=132; median age arm A=59.5 years; median age arm B=58 years) were available for the efficacy analysis. There were no significant differences in gender distribution and previous experience of CINV. Significantly less pts receiving A failed the primary endpoint (42% vs. 59%, OR=0.53 [0.34; 0.82], p=.0046). This effect was stressed in women (57% vs. 82%, OR=0.30) and patients with previous CINV (48% vs. 71%, OR=0.38). Emesis within 120h occurred in 22% of pts receiving A and 35% receiving P (OR=0.5 [0.31; 0.80], p=.0036). Though differences in overall nausea (16% vs. 22%, OR=0.65 [0.83; 1.10], p=.11) did not reach statistical significance, major nausea (VAS >25mm) was reduced (6% vs. 12%, OR=0.42 [0.19; 0.92], p=.026). Difference in FLIE score was -8.2 (p=.0007). Study medication was well tolerated. PK analyses showed no interaction between M and A. Conclusions: The combination therapy with A resulted in significantly less CINV compared to placebo. This effect was pronounced in women and pts with previous CINV. Clinical trial information: NCT00571168.

BackgroundSarcoidosis is a multi-system disease with unknown etiology characterized by the formation of granulomas in various organs. It affects people of all ethnic backgrounds and occurs at any time of life. This disease can affect any organ with a frequency varying according to ethnicity, sex and age most of the time affecting the pulmonary system with symmetrical bilateral hilar adenopathy. Extrapulmonary manifestations in skin, eyes, liver or lymphatic system can take a great morbimortality in patients.ObjectivesToa) indicate the phenotypes with similar characteristics with a cluster analysis andb) describe the principal features of those phenotypes.MethodsA model-based clustering was performed in a cohort of 342 sarcoidosis patients, diagnosed and follow-up from 1999 to 2019 at northern Spain hospital. Four homogeneous phenotypes were proposed in our study (C1: parenchymal lung involvement with dyspnea; C2: erythema nodosum and articular involvement with asthenia; C3: isolated hilar adenopathy; C4: miscellaneous extrapulmonary sarcoidosis). Chi-square test and ANOVA were used to compare, respectively, categorical, and continuous variables among groups. Two-sample t-tests and the partition of Pearson’s chi-square statistic for were used in pairwise comparisons.ResultsCluster analysis identified four groups: C1 (n=128; 37.4%), C2 (n=75; 21.9%), C3 (n=82; 24.0%), and C4 (n=57; 16.7%)(Table 1).Lung involvement was predominant in all clusters, ranged from 93.3% (C2) to 100% (C3). Extrapulmonary involvement was significantly higher in C2 (97.3%) and C4 (98.2%). Systemic steroids were significantly more used in cluster 1 (75.8%) compared to the rest (C2: 57.3%; C3: 48.8%; C4: 47.4%)(Figure 1).ConclusionSarcoidosis has a heterogenous disease, and a cluster analysis can be a useful tool to identify the clinical patterns and can be useful for the management.Reference[1]Sève P, Pacheco et al. Cells 2021;10. PMDI: 1739240.Table 1.Demographic and clinical characteristics of the study population. Data presented: n (%) or mean±SDCharacteristicsWhole cohort n=342C1 n=128C2 n=75C3 n=82C4 n=57p-valueq-valueGender (female)177 (51,8)45 (35.2)A,B,C47 (62.7)A46 (56.1)B39 (68.4)C<0.001<0.001Age at diagnosis (years)47.7±15.146.4±14.0A43.4±13.1B, C51.7±16.8A, B50.5±15.5C0.002<0.004Ethnicity0.80.8Caucasian322 (94.2)121 (94.5)70 (93.0)76 (92.7)56 (98.2)Hispanic15 (4.4)5 (3.9)4 (5.3)5 (6.1)1 (1.8)Black4 (1.2)2 (1.6)1 (1.3)1 (1.2)0Pulmonary involvement302 (88.3)120 (93.8)A70 (93.3)B82 (100)A,B30 (52.6)A,B<0.001<0.001Extrapulmonary involvement234 (68.6)68 (53.1)A,B73 (97.3)A,C37 (45.1)C,D56 (98.2)B,D<0.001<0.001Skin117 (34.2)26 (20.3)A56 (74.7)A3 (3.7)A32 (56.1)A<0.001<0.001Eye61 (17.8)22 (17.2)A15 (20.0)B21 (25.6)C3 (5.3)A,B,C0.020.04Liver33 (9.6)12 (9.4)5 (6.7)10 (12.2)6 (10.5)0.70.8Spleen7 (2.0)5 (3.9)1 (1.3)1 (1.2)00.30.4Bone4 (1.2)1 (0.8)2 (2.7)01 (1.8)0.40.5Joint95 (27.8)23 (18.0)A49 (65.3)A0A25 (43.9)A<0.001<0.001Parotid4 (2.3)2 (1.6)3 (4.0)2 (2.4)1 (1.8)0.70.8Kidney13 (3.8)2 (1.6)A0B0C11 (19.3)A,B,C<0.001<0.001Nervous system29 (8.5)6 (4.7)A16 (21.3)A,B,C6 (7.3)B1 (1.8)C<0.001<0.001Heart5 (1.5)3 (2.3)002 (3.5)0.20.3CIS: conventional synthetic immunosuppressants; SD: standard deviation.Groups sharing the same letter (A, B, C, D) have statistically significative differences (q>0.005) in the pairwise comparison.Abbreviation in alphabetical order: n=number; SD: standard deviation.Figure 1.Dendrogram of the hierarchical clustering leading to four clusters.C1: parenchymal lung involvement with dyspnea;C2: erythema nodosum and articular involvement with asthenia;C3: isolated hilar adenopathy;C4: miscellaneous extrapulmonary sarcoidosis.Acknowledgements:NIL.Disclosure of InterestsFabricio Benavides-Villanueva: None declared, Raúl Fernández-Ramón: None declared, Jorge Javier Gaitán-Valdizán: None declared, Iñigo Gonzalez-Mazon: None declared, Lara Sanchez-Bilbao: None declared, José Luis Martín-Varillas: None declared, David Martínez-López: None declared, Rosalía Demetrio-Pablo: None declared, Ricardo Blanco Speakers bureau: Speakers bureau: Abbvie, Pfizer, Roche, lilly, Bristol-Myers, Janssen, Galapagos and MSD, Consultant of: Consultant of: Abbvie, Pfizer, Roche, lilly, Bristol-Myers, Janssen and MSD, Grant/research support from: Grant/research support from: Abbvie, MSD, novartis and Roche.

Objective: To compare extra-abdominal repair of uterine incision, in caesarean section with in situ repair, in terms of duration of surgery.Study Design: Comparative study. Place and Duration of Study: The study was conducted in Gynae and Obstetrics Department of CMH Abbottabad from May 2016 to Nov 2017.Materials and Methods: A total of 362 patients were randomized by creating permuted blocks of 6. In Group A (n=181), uterus was exteriorized, following delivery of baby and in Group B (n=181) in-situ repair of uterus was performed. Lower segment cesarean section (LSCS) with Pfannenstiel incision was made, with uterine repair in two layers. Data was collected by the trainee herself on the annexed pro forma. SPSS version 20 was used for data analysis.Results: The mean age of participants was 29.57 ± 5.79 years while mean age in group-A was 29.09 ± 5.52 years and in group-B was 30.04 ± 6.02 years. The mean gestational age in group-A and group-B was 37.26 ± 3.05 weeks and 37.24 ± 2.98 weeks respectively. The mean operative time in group-A was significantly lower (34.90 ± 5.84 minutes) then group-B (36.25 ± 6.36 minutes), p-value = 0.036 (< 0.05)Conclusion: The surgical time in extra abdominal uterine repair in caesarean sections was significantly short as compared to intra-abdominal repair, so exteriorization of uterus is more advantageous than in situ repair in terms of postoperative recovery. How to cite this: Kashif S, Hanif A. Comparison of Primary Outcomes in Extra-Abdominal Versus Intra-Abdominal Uterine Repair at Caesarean Section: A Randomized Controlled Trial. Life and Science. 2022; 3(2): 79-82. doi: http://doi.org/10.37185/LnS.1.1.185 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

In October, 1999, severe yellowing symptoms were observed in a melon (Cucumis melo L.) crop grown under plastic tunnels in the region of Agadir, Morocco. Large populations of whiteflies (Bemisia tabaci) were noticed during the early stages of the crop. At harvest, leaf samples were collected from two symptomatic plants and one symptomless plant. A mature yellow leaf was assayed from each symptomatic plant and for one of these two plants a younger leaf exhibiting only yellow spots. Cucurbit aphid-borne yellows virus, which causes similar symptoms in melons, was not detected by double-antibody sandwich enzyme-linked immunosorbent assay tests. Total RNA was extracted from fresh leaf tissues and submitted to reverse transcription and polymerase chain reaction with primers specific to two whitefly-transmissible viruses: Beet pseudo-yellows virus (BPYV) and Cucurbit yellow stunting disorder virus (CYSDV) (2). No amplification was obtained with BPYV-specific primers. In contrast, an expected 465-bp product was amplified in all samples from symptomatic plants with CYSDV-specific primers. No amplification was detected in samples from the symptomless plant nor from healthy control plants. B. tabaci-transmitted CYSDV has been reported in the Middle East, southwestern Europe, and North America (1,4). This is the first report of CYSDV in Morocco, and it follows the first report of another B. tabaci-transmitted virus, Tomato yellow leaf curl virus, in tomato (3), suggesting an important change in the viral pathosystem affecting vegetable crops in Morocco. References: (1) Kao et al. Plant Dis. 84:101, 2000. (2) Livieratos et al. Plant Pathol. 47:362, 1998. (3) Peterschmitt et al. Plant Dis. 83:1074, 1999. (4) Wisler et al. Plant Dis. 82:270, 1998.

Staphylococcus aureus (S. aureus) destaca-se como um dos agentes etiológicos mais frequentes da mastite bovina, que causa os maiores prejuízos econômicos à pecuária leiteira brasileira. Visando avaliar o perfil de sensibilidade deste agente aos antimicrobianos, 352 isolados provenientes de 35 rebanhos leiteiros localizados em Minas Gerais foram submetidos a testes de antibiograma, utilizando-se a técnica de difusão em disco. Nitrofurantoína, bem como as associações de neomicina, bacitracina e tetraciclina (NBT) e penicilina, nafcilina e dihidroestreptomicina (PND), apresentaram 100% de eficiência in vitro. Foram verificados baixos índices de resistência no grupo das cefalosporinas, com valores de 0, 0,28 e 0,40% para cefquimona, cefalotina e ceftiofur, respectivamente. Entre os aminoglicosídeos, observou-se 1,69% de resistência para gentamicina e 3,35% para a neomicina. O maior índice de resistência foi observado para polimixina B (82%), seguido pelos betalactâmicos, ampicilina e penicilina, com índices de resistência de 80,92 e 80,45%, respectivamente. Níveis intermediários de resistência foram observados para tetraciclina, lincomicina, cefoperazona e sulfazotrim. Entre os isolados testados, 65 (18,15%), oriundos de 24 dentre os 35 rebanhos estudados, apresentaram multirresistência (índice MAR ≥ 0,2). Os resultados apontaram grande variação nos perfis de resistência aos antimicrobianos, assim como a ocorrência de múltipla resistência entre algumas cepas estudadas, salientando a necessidade de testes de antibiograma para a escolha dos antimicrobianos mais adequados para o tratamento ou prevenção de mastite causada por S. aureus.

Abstract Introduction: Traditional prognostic factors for adult acute lymphocytic leukemia (ALL) include age, white blood count at diagnosis, and cytogenetic (CG) risk. We sought to identify a more detailed prognostic risk score for newly diagnosed adult patients (pts) based on these and other pre-treatment characteristics. Methods: 82 newly diagnosed ALL pts given induction chemotherapy (IC) at our institution between the years 2003-2011 were included, and data were obtained by chart review. Institutional review board approval was obtained. Variables examined included: gender, age, immunophenotype, CG risk, pre-IC body mass index (BMI), pre-IC and day 28 serum albumin, absolute lymphocyte (ALC) and neutrophil (ANC) counts, positive culture (blood or other) during IC, positive imaging suggestive of infection (during IC), and allogeneic hematopoietic cell transplant (AHCT). CG risk was ascribed by CALGB criteria (Blood 1999; 93: 3983). BMI was defined by: underweight (≤ 18.5), normal (> 18.5-25.0), overweight (> 25.0-30.0), moderately obese (> 30.0-35.0), severely obese (> 35.0-40.0), and very severely obese (> 40.0). The primary endpoint was overall survival (OS) which was measured from IC to death or last follow-up. Proportional hazards models were used for univariable and multivariable analyses. In the multivariable analysis stepwise variable selection was used to identify independent predictors. Results were internally validated using a bootstrap algorithm. For convenience measured factors were discretized using a recursive partitioning algorithm. Prognostic groups were formed by assigning “points” to each factor that were based on the magnitude of the estimated regression coefficients of the final model, and then summing the total number of points present. Results: Median age at diagnosis was 43 yrs (range 18-78); 58% male. 71% of pts (58/82) had a B-cell immunophenotype. CG risk included: normal: 15 pts (18%), high: 41 pts (50%), miscellaneous: 9 pts (11%), and unknown: 17 pts (21%). Twenty-four pts (29%) were Ph+. The majority of pts (70%: 57/82) received the CALGB 19802 regimen (Cancer 2013; 119: 90) for IC +/- a tyrosine kinase inhibitor (if they were Ph+). 27% of pts (22/ 82) received AHCT in CR1. Estimated median OS is 41.5 months (95% CI: 15.5-N/A). In univariable analysis age, pre-induction BMI, Day 28 ALC, pre- and Day 28 albumin, Day 28 ANC, Day 28 platelet count, evidence of infection, and CG risk were all seen to impact outcome. In multivariable analysis pre-IC BMI and albumin, age, and Day 28 ALC were identified as independent predictors. Assigning 1 “points” each for age >50, albumin prior to IC ≤ 3.2 g/dL, or Day 28 ALC ≤ 50 /uL and 2 points for BMI ≥ 35, 3 prognostic groups were defined: favorable (0 points) 32% of pts (26/80): estimated 5-yr OS of 68% +/-11%; intermediate (1 points) (29% of pts, 23/80): estimated 5 yr OS of 39% +/-11%, and unfavorable (≥ 2 points) (39% of pts, 31/80) with estimated 5 yr OS of 17% +/- 7% (Figure 1). Conclusion: We have constructed a simple prognostic model for newly diagnosed adults with ALL. This model will need to be validated in a larger group of uniformly treated patients. Table 1 Prognostic Factors for OS in Univariable and Multivariable Analysis Factor Univariable (HR (95% C.I.)) Multivariable (HR (95% C.I.)) Age at dx (≤50 vs. >50) 3.29 (1.80-5.99), p=.0001 2.83 (1.45-5.53), p=.002 Pre-IC BMI (<35 vs. >35) 2.95 (1.57-5.52), p=0.0008 3.88 (1.84-8.17), p=.0004 Pre-IC albumin (≥ 3.2 vs. < 3.2 g/dl) 2.61 (1.43-4.77), p=0.002 2.66 (1.33-5.30), p=.0006 Day 28 ALC (> 50/uL vs. ≤50/uL) 3.57 (1.61-7.91), p=0.002 3.11 (1.33-7.28), p=.009 CG risk 2.03 (0.98-4.22); p=0.06 ------ Day 28 albumin (>2.3 vs. ≤2.3 g/dl) 3.37 (1.66-6.83), p=0.0008 ------ Day 28 ANC (>200/uL vs. ≤200/uL) 4.51 (1.94-10.51), p=.0005 ------ Day 28 platelets (>75K/uL vs. ≤75K/uL) 2.44 (1.26-4.72), p=.008 ------ Any positive culture (no vs. yes) 2.19 (1.19-4.04), p=0.01 ------ Blood culture positive for bacteria (no vs. yes) 2.34 (1.28-4.30), p=0.006 ------ Positive imaging suggestive of infection (no vs. yes) 2.44 (1.34-4.46), p=0.004 ------ Positive blood culture and image (no vs. yes) 1.96 (1.07-3.57), p=0.03 ------ Figure 1 Prognostic Groups Figure 1. Prognostic Groups Disclosures No relevant conflicts of interest to declare.

In autumn 2001, severe yellowing symptoms were observed on greenhouse-grown cucumbers near Perpignan (southern France). Leaf samples were collected from two sites where plants displayed symptoms ranging from limited yellowing of the older leaves to severe, complete yellowing of the whole plant. Cucurbit aphid-borne yellows virus, a polerovirus that causes similar symptoms was not detected in doubleantibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) using a specific antiserum. Total RNA was extracted from fresh leaf tissues and used in reverse transcription-polymerase chain reaction (1) with primers specific for two whitefly-borne viruses also inducing yellows and occurring in the Mediterranean basin (1): Beet pseudo yellows virus (BPYV, genus Closterovirus) transmitted by Trialeurodes vaporariorum (West.) and Cucurbit yellow stunting disorder virus (CYSDV, genus Crinivirus) transmitted by Bemisia tabaci (Genn.). No BPYV was detected in this survey, but CYSDV was present in all samples. In subsequent surveys conducted in the spring and summer of 2002, BPYV and CYSDV were detected, sometimes in mixed infections, in samples collected from the same region. The complete CYSDV coat protein gene was amplified by PCR using specific primers (2), yielding the expected-size fragment of 756 bp. The French isolate (GenBank Accession No. AY204220) shared 99.6 to 100% nucleotide sequence identity in the sequenced CP fragments (700 nt) with isolates of the most common, highly homogenous subgroup of CYSDV that has emerged recently in the Middle East, southwestern Europe (Spain and Portugal), United States, and Morocco (2). To our knowledge, this is the first report of CYSDV in France and it shows the threat represented by the current emergence of B. tabaci-transmitted viruses. References: (1) I. C. Livieratos et al. Plant Pathol. 47:362, 1998. (2) L. Rubio et al. J. Gen. Virol. 82:929, 2001.

The objective of this study was to determine the wildlife hosts of Mycobacterium avium subsp. paratuberculosis (MAP) in the Czech Republic. A total of 8 796 wildlife animals were examined by culture of faecal or tissue samples during the years 2002–2007. MAP was isolated from 12 (0.5%) out of 2 296 red deer (Cervus elaphus), two (0.2%) out of 835 roe deer (Capreolus capreolus), 78 (5.7%) out of 1 381 fallow deer (Dama dama), 28 (3.2%)out of 866 mouflons (Ovis musimon), four (2.5%) out of 162 chamois (Rupicapra rupicapra) and from one (0.1%) out of 805 wild boar (Sus scrofa). MAP was not cultured from 82 badgers (Meles meles), 55 martens (Martes foina), one pine marten (Martes martes), 25 brown hares (Lepus europaeus), five rabbits (Oryctolagus cuniculus), nine European polecats (Mustela putorius), two steppe polecats (Mustela eversmannii), two American minks (Mustela vison), four raccoon dogs (Nyctereutes procyonoides) and four Eurasian otters (Lutra lutra). MAP was isolated from three (2.0%) out of 149 small terrestrial mammals: one (5.9%) out of 17 brown rats (Rattus norvegicus), one (1.7%) out of 59 common voles (Microtus arvalis) and one (2.6%) out of 39 lesser white-toothed shrews (Crocidura suaveolens). Culture examinations of 34 house mice (Mus musculus) and 2 113 pigeons (Columba livia f. domestica) were negative. All 123 in vitro growing MAP isolates from wild ruminants were of IS900 RFLP type B-C1. One mouflon infected with a MAP strain which did not grow on the tested media was after IS1311-PRA-PCR assessed as being infected with a “sheep” strain. The RFLP type of the MAP isolate from the wild boar was of the RFLP type A-C10. Although the detection of MAP in wildlife in the Czech Republic was not very high, their role as a potential risk factor for cattle should be considered.

Abstract Background: Pomalidomide-dexamethasone results in an overall response rate of 33% and median PFS of 4.2 months in patients with prior lenalidomide and bortezomib (Richardson et al. Blood 2014). In this randomized phase II trial, we compared pomalidomide-dexamethasone (arm B) versus the addition of oral weekly cyclophosphamide to pomalidomide-dexamethasone (arm C) in patients with lenalidomide-refractory multiple myeloma (MM). We have previously reported that the recommended phase II dose of cyclophosphamide with standard-dose pomalidomide + dexamethasone was 400 mg PO D1, 8, 15. Patients and Methods: Eligible patients had relapsed and refractory MM after at least 2 prior therapies and were lenalidomide refractory. Patients had a platelet count ≥ 50,000/mm3 and ANC ≥ 1,000/mm3 (patients with ≥50% bone marrow plasmacytosis were allowed if platelet count was ≥ 30,000/mm3and ANC could be supported with GCSF during screening and therapy). Patients were randomized (1:1) to receive pomalidomide 4 mg PO D1-21 and dexamethasone 40 mg PO D1, 8, 15, 22 (20 mg if older than 75 years) (arm B) with or without oral cyclophosphamide 400 mg PO D1, 8, 15 of a 28-day cycle (arm C). Patients randomized to arm B were allowed to cross over to arm C in the event of disease progression. Thromboprophylaxis was mandated with aspirin, warfarin, or LMWH. The primary endpoint was overall response rate using IMWG criteria. Secondary endpoints included an evaluation of PFS, OS and safety of the two arms. Results: Between 7/2012 and 3/2014, 36 patients were randomized to arm B and 34 to arm C. Patients characteristics were not different between the 2 arms (table below). The median number of prior therapies was 4 (2-12). All patients were lenalidomide refractory and none received prior pomalidomide. After a median follow up of 15 months, the overall response rate (partial response or better) was 39% and 65% (p=0.03) for arm B and C, respectively. The clinical benefit rate (minimal response or better) was 64% and 79% (p=0.2) for arm B and C, respectively. The median PFS was 4.4 months (95% CI 2.3-5.9) for arm B and 9.2 months (95% CI 4.6-16) for arm C (log rank p=0.04). As of July 2014, 28 patients had died (16 arm B, 12 arm C) with median overall survival of 10.5 versus 16.4 months (p=0.08) for arm B and C, respectively. Hematologic grade 3/4 adverse events were more frequent in arm C, although this was not statistically significant (see table). Thirteen patients crossed over and oral weekly cyclophosphamide was added to their tolerated dose of pomalidomide dexamethasone. For those patients, the best response was as follows: 2 PR, 2 MR, and 6 SD, 3 PD. Conclusions: Pomalidomide-dexamethasone in combination with oral weekly cyclophosphamide resulted in a superior response rate and PFS compared to pomalidomide-dexamethasone alone in patients with relapsed and refractory MM. The increased hematologic toxicities, as a result of the addition of oral cyclophosphamide, were manageable. Table Arm B (N=36) Arm C (N=34) P value Age, years, median (range) 63 (50-78) 64 (47-80) 0.7 Male, n (%) 23 (64) 18 (53) 0.3 Number of prior therapies, median (range) 4 (2-12) 4 (2-9) 0.5 Bortezomib refractory, n (%) 28 (78) 24 (71) 0.3 Carfilzomib refractory, n (%) 16 (44) 13 (38) 0.5 Prior high-dose therapy, n (%) 27 (75) 28 (82) 0.6 Prior alkylating agent, n (%) 32 (89) 32 (94) 1 B2-microglobulin, median (range) 3.2 (1.6-10) 3.6 (1.5-13.9) 0.5 Serum creatinine, median (range) 1 (0.5-2.3) 0.9 (0.6-2.1) 0.6 High-risk cytogenetics, n (%) 5 (24) 6 (28) 0.8 Deletion 17p, n (%) 3 (14) 4 (20) 0.8 t(4;14), n (%) 3 (14) 3 (14) 0.9 Trisomy or tetrasomy 1q, n (%) 11 (55) 6 (33) 0.4 Best response (partial response or better), n (%) 14 (39) 22 (65) 0.03 Clinical benefit rate (MR or better), n (%) 23 (64) 27 (79) 0.2 Grade 3/4 neutropenia, n (%) 12 (33) 17 (50) 0.2 Grade 3/4 febrile neutropenia, n (%) 4 (11) 6 (18) 0.5 Grade 3/4 thrombocytopenia, n (%) 2 (5) 5 (15) 0.2 Grade 3/4 anemia, n (%) 3 (8) 7 (20) 0.2 Grade 3/4 pneumonia, n (%) 4 (11) 3 (9) 1 Grade 3/4 fatigue, n (%) 2 (5) 4 (12) 0.4 Number of serious adverse events 17 20 Disclosures Baz: Celgene: Research Funding; Millenium: Research Funding; Bristol-Myers Squibb: Research Funding; Karypharm: Research Funding; Sanofi: Research Funding. Off Label Use: Pomalidomide cyclophosphamide dexamethasone in relapsed refractory myeloma. Martin:Sanofi: Research Funding; Novartis: Speakers Bureau. Alsina:Triphase: Research Funding; Millenium: Research Funding. Shain:Onyx / Amgen: Research Funding; Treshold: Research Funding. Chari:Celgene: Membership on an entity's Board of Directors or advisory committees; Millenium: Membership on an entity's Board of Directors or advisory committees; Array Biopharma: Membership on an entity's Board of Directors or advisory committees. Jagannath:Celgene: Honoraria; Millennium: Honoraria; Sanofi: Honoraria.

BackgroundPrimary Sjögren Syndrome (pSS) patients have an increased risk of Non-Hodgkin lymphoma (NHL). There is no consensus on the therapeutic management of low-grade NHL. Two strategies can be proposed; either a ‘‘wait and see’’ strategy or an active therapeutic strategy.ObjectivesTo describe characteristics of NHL in pSS, therapeutic strategies and impact of these strategies on prognosis of lymphoma and of pSS.MethodsThis multicentric retrospective study included all lymphoma patients of the ASSESS cohort, enriched with patients recruited in Rheumatology and Internal Medicine departments. For each patient, we collected biological and clinical manifestations of pSS, lymphoma’s characteristics, and treatment strategy. Progression free survival (PFS) (lymphoma-PFS and pSS relapse free survival) and overall survival (OS) were analyzed.ResultsA total of 106 pSS patients who presented a B cell lymphoma between 1985 and 2019 were included. Among them 14 (13%) had diffuse large B cell lymphoma (DLBCL) and 82 pSS patients presented a low-grade B cell-NHL, mucosa-associated lymphoid tissue (MALT) lymphomas being the most frequent histologic subtype occurring in 68/82 (83%) patients.Among these 82 patients, a “wait and watch strategy” was chosen in 19 (23%) patients; 63 patients received a specific treatment for lymphoma at lymphoma diagnosis including systemic treatment (chemotherapy and/or immunotherapy) in 49 (60%) patients and local therapy (surgery or radiotherapy) in 14 (17%) patients; 10 patients further received rituximab (RTX) maintenance therapy.Comparison of treated versus not treated patients is presented in the Table 1. Untreated patients were older and had less pulmonary lymphoma location.We then analyzed the prognosis after a mean follow up of 6.5 years. Nine patients (11%) died during the follow-up. In multivariate analysis, age (HR= 1.16 [1.06-1.27], p = 0.001) and pulmonary location (HR= 8.15 [1.57-42.3], p = 0.013) were associated with death.Last, we compared OS, lymphoma PFS and pSS relapse PFS in treated versus not treated patients after propensity score weighting We observed that starting an active treatment for NHL at lymphoma diagnosis did not impact OS and lymphoma PFS (HR= 4.81 [0.48-47.9], p=0.2 and HR=1.12 |0.50- 2.48], p=0.8, respectively). Conversely, treating lymphoma had a protective effect on the risk of pSS relapse (HR 0.4 [0.17-0.95], p = 0.038). Last, among patients treated for lymphoma, we observed that no lymphoma relapse occurred in patients who received maintenance therapy with RTX (0/10 events vs 18/53, p = 0.04).ConclusionThis study based on a large number of pSS patients with lymphoma shows that age and pulmonary location are independently associated with the risk of death. The choice of treating lymphoma at its diagnosis or not does not affect OS and PFS for lymphoma. However treatment of lymphoma reduced the risk of pSS relapse. This should be taken into account when deciding therapeutic strategy in our pSS patients with lymphoma.Table 1.VariableWait and watch N=19Active treatment N=63p-val.F18/ 19 (95%)54/ 63 (86%)Age64.0 (54.0, 75.5)56.0 (47.0, 65.5)0.041Time between pSS and lymphoma diagnosis1.0 (0.0, 8.5)3.2 (0.1, 9.0)0.6ESSDAI6.0 (4.0, 8.0)8.0 (5.0, 14.0)0.2clinESSDAI4.0 (3.0, 7.0)6.5 (4.0, 12.8)0.091BiologySSA antibodies14/ 19 (74%)44/ 61 (72%)0.9SSB antibodies8/ 19 (42%)23/ 58 (40%)0.9Positive rheumatoid factor14/ 18 (78%)39/ 54 (78%)0.8Low C42/ 11 (18%)15/ 35 (43%)0.2Hypergammaglobulinemia9/ 16 (56%)30/ 45 (67%)0.5Lymphoma type0.7MALT lymphoma15/ 19 (79%)53/ 63 (84%)Nodal marginal zone lymphoma4/ 19 (21%)10/ 63 (16%)Lymphoma disseminationSalivary and/or ganglionar limited7/ 19 (37%)35/ 63 (56%)0.2Lymphoma spread ≥ 2 locations9/ 19 (47%)28/ 63 (44%)0.8Lymphoma localizationSalivary gland limited lymphoma4/ 19 (21%)20/ 63 (56%)0.4Pulmonary lymphoma involvement0/ 19 (0%)13/ 63 (21%)0.032Salivary gland lymphoma involvement11/ 19 (58%)36/ 63 (57%)>0.9OutcomeMedian follow-up7.0 (4.5, 8.5)6.0 (4.0, 13.5)0.7Death1/ 19 (5.3%)8/ 63 (13%)-REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.