[Investigation and Measurement of Hypophosphatemia Induced by Tyrosine Kinase Inhibitors in Patients with Chronic Myeloid Leukemia].

We retrospectively investigated hypophosphatemia induced byty rosine kinase inhibitors(TKIs), in patients with chronic myeloid leukemia. Subjects evaluated were 14, 11, and 8 patients who received TKIs(imatinib, dasatinib and nilotinib), respectively, at the Department of Hematology in Ichinomiya Municipal Hospital, between 1st January 2006 and 31st Decem- ber 2016. The incidence of hypophosphatemia was 85.7%(12/14)for imatinib, 18.2%(2/11)for dasatinib, and 37.5%(3/ 8)for nilotinib, and hypophosphatemiaBgrade 3 occurred in 57.1%(8/14)of imatinib- and 9.1%(1/11)of dasatinibtreated patients. Instances of hypophosphatemiaBgrade 3 were not confirmed for nilotinib. Six patients received oral phosphate for hypophosphatemia, and all of these were patients who had been administered imatinib. We confirmed a significant improvement(p<0.05, 95%CI: 0.111-0.989)in serum phosphate levels after administration of oral phosphate, suggesting that it constitutes an effective measure against this situation.

[A Case of Hypophosphatemia Induced by Administration of Amrubicin in a Patient with Small Cell Lung Cancer].

A man in his 50s with small cell lung cancer received amrubicin as the fourth-line therapy from August 201X-1. Serum phosphorus levels before treatment were normal at 2.9mg/dL, but grade 2 hypophosphatemia(2.1mg/dL)was observed at the beginning of the 2nd course. He underwent laryngoplasty after the 4th course. Retreatment was initiated in June 201X due to disease progression. After reinitiating treatment, the disease developed to grade 3 hypophosphatemia. As we identi- fied lower levels(1.1mg/dL)at the start of the 10th course, a pharmacist proposed oral phosphate therapy to the attending physician, which we administered. After then, the levels improved to 2.2mg/dL; thus, oral phosphate therapy was interrupted. However, because of a decline in serum phosphorus levels to grade 3, we administered the therapy again, and observed favorable improvement. For hypophosphatemia in this case, general reasons in clinical practice were not applicable; thus, amrubicin is considered to be a most possible cause.

Renoprotective Effect of Dipeptidyl Peptidase-4 Inhibitors in Patients with Type 2 Diabetes Mellitus.

Diabetic nephropathy is one of three major complications of diabetes mellitus, often leading to chronic renal failure requiring dialysis. Recently developed dipeptidyl peptidase-4 (DPP-4) inhibitors may exhibit renoprotective effects in addition to antihyperglycemic effects. In this study, we retrospectively investigated temporal changes in the renal function index of patients with type 2 diabetes mellitus (DM) and examined the influence of DPP-4 inhibitors on renal function. Patients with type 2 DM (>18 years old) prescribed hypoglycemic agents at Gifu Municipal Hospital for ≥3 months between March 2010 and April 2014 were included in the study. Renal function was evaluated as estimated the decline in 12-month glomerular filtration rate from the baseline in patients receiving and not receiving DPP-4 inhibitors. Patient data from the DPP-4 inhibitor-treated (501 patients, 58.6%) and untreated (354, 41.4%) groups were analyzed using multiple logistic regression analysis, as well as Cox proportional-hazards regression analysis (616, 55.6% and 491, 44.4%, for DPP-4 inhibitors-treated and untreated groups). Multiple logistic regression analysis indicated that DPP-4 inhibitors significantly lowered the estimated glomerular filtration rate (eGFR) decline [20% over 12 months; odds ratio (OR), 0.626; 95% confidence interval [CI], 0.409-0.958; P = 0.031]. Similar results were obtained using Cox proportional-hazards regression analysis (hazard ratio [HR], 0.707; 95% CI, 0.572-0.874; P = 0.001). These findings suggest that DPP-4 inhibitors suppress the decrease of estimated glomerular filtration rate in patients with type 2 DM and show a renoprotective effect.

[A Case of a Multidisciplinary Team Approach to Serious Hand-Foot Syndrome Induced by High-Dose Cytarabine Therapy].

A 40's year-old female patient with acute myeloblastic leukemia received high-dose cytarabine(HD-Ara-C)as her third induction therapy. Because the pharmacist in charge noticed on a prior interview that she had experienced a mild skin eruption similar to hand-foot syndrome(HFS)in the previous round oftherapy(idarubicin and cytarabine), heparinoid lotion and hypoallergenic soap were used to prevent HFS. However, HFS occurred on day 3, and further developed on day 6 to grade 3 with painful erythema, swelling, and paresthesia affecting the entire surface of both hands. We cared for her with moisturization, lifestyle guidance, rotation of steroid ointment, and occlusive dressing techniques according to a multidisciplinary team approach composed ofa hematologist, dermatologist, pharmacist, and nurse. Her symptoms resolved on day 40.