Dipeptidyl‐peptidase 4 inhibitor increased and maintained platelet count in a patient with primary myelofibrosis

Abstract

Myeloproliferative neoplasms (MPNs), characterized by disorders of the hematopoietic stem cell, arises from kinase 2 (JAK2) V617F, calreticulin (CALR), myeloproliferative leukemia (MPL) mutations and a smaller number of other 'triple negative' forms where the driver mutation is not identified [1]. Mutations in these genes are almost entirely mutually exclusive. The accumulation of point mutations is also rare. Initiation and progression of these diseases by cytokine production are explained in 'A Human Inflammation Model of Cancer Development' [2]. JAK2V617F leads to the activation of genes involved in inflammatory signaling pathways including the activation of transforming growth factor β (TGF-β) [3-5]. We report the dipeptidyl-peptidase 4 (DPP4)-inhibitor rapidly increased and maintained the platelet count (PLC) in a patient with primary myelofibrosis (PMF) resulting from JAK2V617F abnormality.A 68-year-old man (BMI 19.4 kg/m2) diagnosed at 62 years with type 2 diabetes mellitus (T2DM) with accompanying overt nephropathy, receiving glimepiride therapy, was admitted to our hospital complaining of fatigue. Laboratory tests revealed pancytopenia (white blood cell (WBC) 2,200/μl, red blood cell (RBC) 1.25x10 6 /μl, hemoglobin 4.3 g/dL and platelet (PLT) 60x10 9 /L). Laboratory test results from 6 months prior to admission were normal except for blood glucose level (WBC 4,000/μl, RBC 3.52x10 6 /μl, hemoglobin 12.3 g/dL, PLT 161 x10 9 /L, postprandial blood glucose 362 mg/dL and hemoglobin A1c 7.9%). Chest radiographs, fecal occult blood tests andThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.