BackgroundHepatitis B surface antigen (HBsAg) reverse seroconversion (RS) can happen in patients with rheumatoid arthritis (RA) with resolved hepatitis B (RHB) undergoing biological disease-modifying antirheumatic drugs (bDMARDs). But the incidence and risk factors need to be delineated.MethodsFrom 2003 to 2019, 1937 patients with RA with available HBsAg and antibody to hepatitis B virus (HBV) core antigen data were retrospectively reviewed, and 489 patients with RHB undergoing bDMARDs treatment were identified. Factors associated with HBsAg RS were analysed.ResultsDuring 67 828 person-months of follow-up, 27 (5.5%) patients developed HBsAg RS after bDMARD treatment. As compared with those without HBsAg RS, patients with HBsAg RS were older, had lower frequency of antibody to HBsAg (anti-HBs), and lower baseline anti-HBs levels. In multivariate analysis, rituximab, abatacept and baseline negative for anti-HBs were the independent risk factors for HBsAg RS (adjusted HR: 87.76, 95% CI: 11.50 to 669.73, p<0.001; adjusted HR: 60.57, 95% CI: 6.99 to 525.15, p<0.001; adjusted HR: 5.15, 95% CI: 2.21 to 12.02, p<0.001, respectively). The risk of HBsAg RS was inversely related to the level of anti-HBs. Both rituximab and abatacept might result in anti-HBs loss, and abatacept had a cumulative incidence of HBsAg RS of 35.4%–62.5% in patients with low titers or negative of anti-HBs.ConclusionsNot only rituximab, but also abatacept has a high risk of HBV reactivation in patient with RA with RHB. Anti-HBs positivity cannot confer HBV reactivation-free status if the anti-HBs levels are not high enough for patients with RHB on rituximab and abatacept treatment.

Patients with Philadelphia chromosomepositive acute lymphoblastic leukemia (Ph ؉ ALL) have poor prognosis despite intensive therapeutic intervention. Recently, imatinib, a BCR-ABL tyrosine kinase inhibitor, has been proven to be an effective treatment for Ph ؉ ALL, but nearly all patients rapidly acquire resistance. High-dose imatinib administration might overcome this resistance; however, systemic toxicities would likely limit this approach. Therefore, a new delivery system allowing for the specific targeting of imatinib is urgently needed. Because almost all Ph ؉ ALL cells express CD19 on their surface, we have developed an immunoliposome carrying anti-CD19 antibody (CD19-liposomes). The internalization efficiency of the CD19-liposomes approached 100% in all Ph ؉ ALL cells but was very low in CD19 ؊ cells. The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph ؉ ALL cell lines and primary leukemia cells from patients with Ph ؉ ALL was much greater than that of imatinib with or without control liposomes. Importantly, the imatinib-CD19-liposomes did not affect the colony formation of CD34 ؉ hematopoietic cells, even at inhibitory concentration of free imatinib. Taken together, these data clearly demonstrate that the imatinib-CD19-liposomes induced specific and efficient death of Ph ؉ ALL cells. This new therapeutic approach might be a useful treatment for Ph ؉ ALL with fewer side effects than free imatinib. IntroductionDespite the successes of high-dose chemotherapy followed by hematopoietic stem cell transplantation for the treatment of leukemia, Philadelphia chromosome-positive (Ph ϩ ) acute lymphoblastic leukemia (ALL) remains refractory to most therapeutic modalities currently available. The Philadelphia chromosome includes one of several forms of fusion genes between bcr and c-abl, and these fusions play a substantial role in the pathogenesis of chronic myelogenous leukemia (CML) and ALL. 1 The p190 bcr-abl fusion gene is detected in 20% to 35% of patients with ALL, and the prognosis of these patients is particularly poor. [2][3][4] Allogenic stem cell transplantation is the only curative therapeutic option today. Long-term survival rates are between 35% and 65% in cases of first complete remissions, but survival rates quickly decline in cases of second and third remissions. [4][5][6][7][8][9] Additionally, the relapse rate for Ph ϩ ALL remains quite high even with transplantation. [4][5][6][7][8][9] Recently, targeted molecular therapy has been introduced to treat such refractory cases, and a BCR-ABL tyrosine kinase inhibitor, imatinib (Glivec, STI571), proved to be a useful agent for Ph ϩ ALL as well as CML. 10 However, in contrast to patients with CML, most of the patients with Ph ϩ ALL quickly become resistant to imatinib. 10,11 In a phase 2 clinical trial examining cases of relapsed or refractory Ph ϩ ALL, only 6% of patients maintained a complete response for more than 4 weeks, in contrast to an overall response rate of 29%. 12 Moreover, the median estimated time...

The clinical outcome of pSS patients with lung involvement in Taiwan is not very favorable. Although HRCT score was poorly correlated with PFT, high HRCT score was significantly associated with higher mortality.

No abstract

Our study showed that infection was one of the major triggers for the flare-up of SLE disease activity and occurrence of TMA in SLE. Infection is also a strong risk factor for outcome in SLE patients with TMA. Plasma exchange can be considered as an adjuvant treatment modality.

The predominant tumor component in primary tumors was a prognostic factor and could predict tumor emboli and liver metastases pathology in high-grade malignant MANECs.

GREM1 expression was correlated with tumor-associated angiogenesis and was found to be a novel prognostic marker in pancreatic NETS. Our data support a tumor suppressor role of GREM1 in pancreatic NETs.

In OA patients experiencing inadequate relief from a wide variety of analgesics, pain, function, quality of life, and treatment satisfaction significantly improved when switched to etoricoxib.