We have developed a model that estimates the risk of respiratory hospitalisation and death in patients with COPD.

Background: Multidrug resistance is the most common cause of treatment failure in dogs with multicentric lymphoma. 5‐(3,3‐Dimethyl‐1‐triazeno)‐imidazole‐4‐carboxamide (DTIC) is an atypical alkylator used as standard treatment in human Hodgkin's lymphoma, and has been effective in combination treatment to treat resistant lymphoma in dogs. However, no data are available on the use of DTIC as a single agent in the treatment of relapsed canine lymphoma. Hypothesis: Single‐agent DTIC is effective and safe in treating dogs with lymphoma that relapsed or failed to respond to previous chemotherapy. Animals: Forty client‐owned dogs with relapsed lymphoma. Methods: Dogs were eligible for the retrospective study if they had a histologically or cytologically confirmed diagnosis of lymphoma and had relapsed. Dogs received DTIC (800–1,000 mg/m2 every 2–3 weeks as a 4–5‐hour IV infusion) and were evaluated for response rate and duration. Hematologic and gastrointestinal toxicity was assessed. Results: The overall response rate for dogs being treated with DTIC was 35% (14 dogs) with a median progression‐free interval of 43 days. Thirteen dogs had a partial response and 1 dog had a complete response. Stable disease was achieved in 3 dogs. Mild gastrointestinal toxicity was reported in 3 dogs posttreatment. Thrombocytopenia was the principal toxicity observed 7–14 days after the treatment. Treatments were delayed because of thrombocytopenia. Conclusions: DTIC, when used alone, is effective in the treatment of dogs with relapsed lymphoma.

No abstract

56 adults with hematologic malignancies underwent blood cell allografts from A/B-DR-identical MSDs or A/B/C/DRB1/DQB1-allele-identical MUDs after 100 mg/m2 melphalan with (n=39; no prior autograft) or without (n=17; prior autograft) 50 mg/kg cyclophosphamide. GVHD prophylaxis comprised mycophenolate with cyclosporine (MSD) or tacrolimus (MUD). No growth factors were used. Supportive care was uniform. There were significant differences between groups (Table 1); most strikingly with respect to donor age. MSD (n=37) MUD (n=19) P Pt age 53 (38–66) 47 (27–62) 0.085 Pt age >55 32% 32% 0.95 Donor age 51 (31–69) 33 (24–50) <0.0001 Donor age >45 76% 16% <0.0001 Refractory disease 49% 68% 0.16 PS 2–3 22% 32% 0.42 LDH 172 (83–1298) 237 (105–1919) 0.082 Abnormal LDH 43% 63% 0.16 CD34+ cell dose 5.0 (3.0–7.6) 6.0 (1.4–11.8) 0.12 CD34+ cell dose >6 11% 47% 0.002 10 patients experienced transplant-related mortality (TRM), and 29 relapsed (23 dead). The following factors were analyzed in a Cox model for effect on outcome: chemosensitive (n=25) vs refractory disease (n=31), patient age ≤55 (n=38) vs >55 (n=18), performance status (PS) 0–1 (n=42) vs 2–3 (n=14), normal (n=28) vs abnormal (n=28) LDH, prior autograft or not, CD34+ cell dose ≤6 (n=43) vs 6 (n=13) x 106/kg, MSD vs MUD, male (n=38) vs female (n=18) donor, and donor age ≤45 (n=25) vs >45 (n=31). Donor age was also analyzed as a continuous variable. Patient age >55 and PS 2–3 resulted in higher TRM. Refractory disease and abnormal LDH resulted in higher relapse, and lower disease-free (DFS) and overall (OS) survival. PS 2–3 resulted in lower DFS and OS. Patient age >55 and MSD resulted in lower OS. OS was reanalyzed after excluding donor type as a variable (*) because of its correlation with donor age. Table 2 shows the favorable effect of donor age ≤45 on relapse, DFS and OS. Outcome RR (95% CI) P Relapse 0.28 (0.12–0.64) 0.003 DFS 0.27 (0.13–0.57) 0.001 OS* 0.42 (0.19–0.94) 0.035 When analyzed as a continuous variable, lower age resulted in lower relapse and higher OS with donor type in the model, and with higher DFS when donor type was excluded. Figures 1 and 2 show the effect of donor age on relapse and DFS in plots generated from the Cox model at the means of the covariates. Figure Figure These data appear to suggest that a young MUD may be preferable to an older MSD. However, small numbers preclude obtaining an answer to the question of the age at which a sibling donor should be considered too old. Additionally, logistic issues involved in obtaining a MUD may reduce any benefit from having a young donor. We conclude that a younger donor should be chosen whenever possible. Further work is required to address the intrguing possibility of superiority of MUD over MSD based on age.