• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • Baseline WBC count and baseline measures


    Baseline WBC count and baseline measures of hepatic and renal function for responders and nonresponders are shown in Table 1. No relationship was evident between responders to decitabine or treatment choice and baseline WBC counts, or between responders and baseline measures of hepatic function (ALT, AST, total bilirubin, and albumin). Regarding renal function (BUN, creatinine, creatinine clearance), nonresponders had a significantly higher mean baseline creatinine level compared with responders (86.78 vs 80.23μmol/L, respectively; P=0.005), and correspondingly lower, although not significantly, creatinine clearance (68.35 vs 72.42μmol/L, respectively; P=0.067). However, no significant difference between nonresponders and responders was noted in mean baseline BUN (6.97 vs 6.48mmol/L, respectively; P=0.067) [7]. An analysis was also conducted on creatinine data for responders and nonresponders by treatment group (decitabine vs treatment choice). Mean baseline creatinine levels (± standard deviation) by treatment group were 78.81±15.78μmol/L for decitabine responders (n=68) and 83.06±23.94μmol/L for treatment choice responders (n=34). Corresponding levels for nonresponders were 85.78±26.99μmol/L for decitabine (n=171) and 87.62±27.19μmol/L for treatment choice (n=206). No significant differences were seen when treatment groups were compared within responder categories. Changes in creatinine levels over time by response to decitabine or treatment choice (Fig. 1) showed no clear trends or differences in change from baseline in creatinine levels between responders and nonresponders by treatment group.
    Discussion This post hoc analysis of data from a large phase 3 trial in older patients with AML [7] suggests that AEBSF no relationship exists between baseline WBC count or hepatic function and response to treatment with decitabine or patient′s treatment choice of either supportive care or cytarabine. In contrast, another study of older patients with AML reported that higher peripheral blood blast counts were associated with poorer response rates to decitabine [9]. Regarding renal function, although baseline BUN and creatinine clearance had no effect on response to treatment with decitabine or treatment choice, higher mean creatinine levels in nonresponders across both treatment groups suggested a possible prognostic relationship. However, the clinical relevance of this result is questionable. Other explanations might be patient-related, e.g., comorbidities or poor physical condition, and patients who have AML with a high monocytic component may have increased creatinine at diagnosis [10]. A logistic regression analysis of confounding factors and creatinine levels confirmed that patients receiving SC were less likely to respond as creatinine levels increased, as were patients with an ECOG PS ≥2.
    Role of the funding source
    Author contributions
    Conflict of interest statement
    Acknowledgments The original study and this analysis were funded by Eisai Inc, Woodcliff Lakes, NJ. Medical writing, editing, and graphics assistance was provided by Peloton Advantage, LLC, and was funded by Eisai Inc. The authors thank Yvonne E. Yarker, PhD, CMPP, of Peloton Advantage for medical writing support and Yuhan Li, MS, of Eisai Inc. for statistical analyses provided during the development of this manuscript.
    Introduction A 72 year-old man was referred to our Hematology service with a history of four months of recurrent fevers, sweats, weight loss, headache, proximal limb girdle pain and mild cough. Physical examination was normal. He had no neurological deficit, and cardiovascular, respiratory and abdominal examinations disclosed no significant abnormalities. On laboratory analysis creatinine, alanine aminotransferase, aspartate aminotransferase and immunoglobulin levels were within normal range. However, lactate dehydrogenase 901UI/L (reference range 230–480UI/L), gamma-glutamyl transferase 210UI/L (reference range 10–71UI/L), Beta-2 microglobulin 4.1mg/L (reference range 1.1–2.5) and reactive C protein 219mg/L (reference range 0–10mg/L) were raised. He also had anemia (Hb 8.4g/dL) and a leukocyte count of 10.900/μl with normal differential count; platelet count was 304,000/μl. Autoimmunity was negative. Blood, sputum, synovial fluid, bone marrow, urine and stool cultures, serological determinations and cultures for various microorganisms (Mycobacterium tuberculosis (Bone Marrow and sputum culture), Leishmania sp (bone marrow culture), Brucella sp, Syphilis, Toxoplasma gondii, human immunodeficiency virus, Hepatitis B virus, Hepatitis C virus, Epstein Barr virus and Cytomegalovirus) gave repeated negative results.