Background: Chronic Myeloid Leukemia (CML) is largely treated with BCR-ABL protein targeted drugs called tyrosine kinase inhibitors (TKIs) , imatinib, which have led to dramatical improvement in 2001.Nilotinib and dasatinib were approved as the second new TK inhibitor in 2010, and Radotinib in 2012.However, the only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant.Case: A 42-year-old man was diagnosed CML in June 2011.He had achieved complete cytogenetic response in 5 months later by nilotinib treatment.It did not lead to major molecular response in the 18 th month, and blastic phase of acute promyelocytic leukemia (M3) occurred in the 19 th months.Leukemia cells had both promyelocytic leukemia gene/retinoic acid receptor alpha (PML/RARα) and BCR/ABL translocations.A retinoic acid was administered for M3.The dasatinib was administered for the blast crisis, and remission was obtained.Transplantation: Hematopoietic stem cell transplantation (HSCT) from umbilical cord blood was performed at remission, but it was rejected twice.The third HSCT was succeeded from a sister who had hyperthyroidism.Conclusion: After 2 times of graft failures, HSCT was succeeded.Long plan of treatment is necessary for middle aged CML patients.
The concurrence of autoimmune hemolytic anemia (AIHA), thrombocytopenic purpura (Evans syndrome) and solid cancer is rare.In this study, we report a diabetic patient with gastric cancer who developed AIHA and idiopathic thrombocytopenic purpura.Steroid therapy for Evans syndrome restored platelet count; however, no improvement in AIHA was observed.Rituximab administration as a second-line therapy resulted in gradual improvement of anemia.Our observation suggested rituximab as an effective therapy for steroid-resistant AIHA.
We have previously reported that decrease in level of serum thyroxine T4 by Kanechor 500 (KC500) in rats would occur through the increase in hepatic T4 accumulation rather than the increase in hepatic T4-glucuronyl transferase activity. In the present study, to understand the mechanism underlying the KC500-mediated increase in hepatic T4 accumulation, we examined the relationship between the KC500-mediated changes in hepatic T4 accumulation and the expression levels of mRNAs of hepatic transporters including T4 transporters. [125I]T4 was intravenously injected into KC500-pretreated and control (KC500-untreated) Wistar rats, and [125I]T4 uptake levels of liver parenchymal cells were comparatively examined. The amount of [125I]T4 uptake by hepatic cells increased in a time-dependent manner up to 96 hr after KC500 treatment. Following KC500 treatment, a time-dependent increase in the mRNA level of hepatic T4 influx transporter LAT1 was observed up to 96 hr later, while a significant increase in hepatic T4 influx transporter Oatp2 mRNA occurred only at 96 hr later. No KC500-mediated increases in the mRNAs of other hepatic transporters (Oatp1, Oatp3, Oatp4, Ntcp, LAT2, and Mrp2) were observed at any timepoints, although the mRNA expression of the T4 conjugate(s) efflux transporter Mrp3 significantly increased in a time-dependent manner 24-96 hr following KC500 treatment. The present findings suggest that KC500-mediated increase in hepatic T4 accumulation occurs, at least in part, through the increase in the expression of hepatic T4-transporters, such as LAT1 and Oatp2.
CyBorD is one of the most effective triplet regimens for both transplant-eligible and ineligible patients with multiple myeloma. In comparison, once-weekly bortezomib induction therapy with a reduced dosage of dexamethasone (modified-CyBorD) showed less toxicity but an equally high response rate. However, this modification still resulted in bortezomib-induced PN in more than half of patients. We therefore introduced a once-weekly schedule of bortezomib combined with continuous low-dose oral cyclophosphamide and reduced dosage of dexamethasone (reduced-CyBorD) in transplantineligible patients with multiple myeloma in our hospital. A total of 32 patients, including 20 who were newly diagnosed and 12 who were refractory/resistant, were treated with reduced-CyBorD, and the regimen’s efficacy and safety were evaluated. The median age was 72 years; 17 patients were male and 15 were female. The overall response rate was 90.6% with 43.8% complete response/near complete response. The median progression-free and overall survival was 14.9 months and 43 months, respectively. Three patients (9.4%) developed grade 1 peripheral neuropathy, and no patients had to reduce or discontinue bortezomib. In conclusion, our results suggested that this reduced combination therapy might be a safe and effective approach in transplant-ineligible patients with multiple myeloma.
