28 research outputs found

    Hepatocellular carcinoma recurrence after direct-acting antiviral therapy: an individual patient data meta-analysis

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    Objective: The benefit of direct-acting antivirals (DAAs) against HCV following successful treatment of hepatocellular carcinoma (HCC) remains controversial. This meta-analysis of individual patient data assessed HCC recurrence risk following DAA administration. Design: We pooled the data of 977 consecutive patients from 21 studies of HCV-related cirrhosis and HCC, who achieved complete radiological response after surgical/locoregional treatments and received DAAs (DAA group). Recurrence or death risk was expressed as HCC recurrence or death per 100 person-years (100PY). Propensity score-matched patients from the ITA.LI.CA. cohort (n=328) served as DAA-unexposed controls (no-DAA group). Risk factors for HCC recurrence were identified using random-effects Poisson. Results: Recurrence rate and death risk per 100PY in DAA-treated patients were 20 (95% CI 13.9 to 29.8, I2=74.6%) and 5.7 (2.5 to 15.3, I2=54.3), respectively. Predictive factors for recurrence were alpha-fetoprotein logarithm (relative risk (RR)=1.11, 95% CI 1.03 to 1.19; p=0.01, per 1 log of ng/mL), HCC recurrence history pre-DAA initiation (RR=1.11, 95% CI 1.07 to 1.16; p<0.001), performance status (2 vs 0, RR=4.35, 95% CI 1.54 to 11.11; 2 vs 1, RR=3.7, 95% CI 1.3 to 11.11; p=0.01) and tumour burden pre-HCC treatment (multifocal vs solitary nodule, RR=1.75, 95% CI 1.25 to 2.43; p<0.001). No significant difference was observed in RR between the DAA-exposed and DAA-unexposed groups in propensity score-matched patients (RR=0.64, 95% CI 0.37 to 1.1; p=0.1). Conclusion: Effects of DAA exposure on HCC recurrence risk remain inconclusive. Active clinical and radiological follow-up of patients with HCC after HCV eradication with DAA is justified

    The ticks of Panama (Acarina: Ixodoidea)

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    A new recombinant factor VIII: from genetics to&nbsp;clinical use

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    Christoph Kannicht,1 Guido Kohla,1 Maya Tiemeyer,2 Olaf Walter,3 Helena Sandberg4 1Octapharma Biopharmaceuticals GmbH, Molecular Biochemistry, Berlin, Germany; 2Octapharma Biopharmaceuticals GmbH, Heidelberg, Germany; 3Octapharma AG, Lachen, Switzerland; 4CoaBio AB, Bromma, SwedenThe December 2014 issue of Drug Design, Development and Therapy included a review article by Santagostino entitled &ldquo;A new recombinant factor VIII: from genetics to clinical use&rdquo;.1 The article provided a timely review of recent advances and developments in the treatment of hemophilia A with recombinant factor VIII (rFVIII).1 However, when reviewing licensed rFVIII products, Santagostino1 did not include Human-cl rhFVIII (simoctocog alfa, Nuwiq&reg;).2&ndash;4 Nuwiq&reg; is a new-generation rFVIII protein produced in HEK 293 F cells that was approved by the European Medicines Agency in July 2014 for the prevention and treatment of bleeds in hemophilia A patients of all ages.5&nbsp;Read the original article&nbsp

    Dasatinib Induced Avascular Necrosis of Femoral Head in Adult Patient with Chronic Myeloid Leukemia

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    Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of the Philadelphia (Ph) chromosome resulting from the reciprocal translocation t(9;22)(q34;q11). The molecular consequence of this translocation is the generation of the BCR-ABL fusion gene, which encodes a constitutively active protein tyrosine kinase. The oncogenic protein tyrosine kinase, which is located in the cytoplasm, is responsible for the leukemia phenotype through the constitutive activation of multiple signaling pathways involved in the cell cycle and in adhesion and apoptosis. Avascular necrosis of the femoral head (AVNFH) is not a specific disease. It occurs as a complication or secondary to various causes. These conditions probably lead to impaired blood supply to the femoral head. The diagnosis of AVNFH is based on clinical findings and is supported by specific radiological manifestations. We reported a case of a 34-year-old Sudanese female with CML who developed AVNFH after receiving dasatinib as a second-line therapy. Though the mechanism by which dasatinib can cause avascular necrosis (AVN) is not clear, it can be postulated because of microcirculatory obstruction of the femoral head. To the best of our knowledge and after extensive literature search, this is the first reported case of AVNFH induced by dasatinib in a patient with CML
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