Introduction. The tyrosine kinase inhibitor imatinib mesylate (IM) specifically inhibits the kinase activity of ABL, platelet-derived growth factor receptor beta (PDGFR[]), and c-KIT tyrosine kinases and has impressive clinical efficacy in chronic myeloid leukemia (CML)[1]. IM prevented also the development of atherosclerotic lesions and diabetes-induced inflammatory cytokine overexpression [2,3].

Case report. A 36 years old male patient with a history of acute myocardial infarction and double coronarian by-pass eight years ago was admitted for the first time on December 2005 complaining of wheigt loss, intermittent discomfort in upper left abdomenum, polydipsia.and polyuria. By the examination of the peripheral blood and of the bone marrow the diagnosis of chronic phase CML-Ph(+) has been established. Simultaneously, type II diabetes mellitus and dyslipidemia (Table 1) were discovered. After a short course of Hydrea, associated with diet and oral antidiabetic therapy, IM 400 mg/d has been started on April 2006. The hematologic remission and a concomitant reduction of the serum levels of cholesterol, and of low-density lipoproteins (LDL) has been obtained (Table 1).

Table 1.

The dynamics of the peripheral blood counts and lipidic profile during IM therapy

ParametersAprilMayJuneJully
Hemoglobin (g/dl) 9,6 11,1 12 12 
Leukocyte count (×109/l) 5.2 4.6 7.5 7.8 
Platelet count (×109/l) 168 287 210 215 
Serum total cholesterol (mg/dl) 310 189 157 152 
Serum LD lipoproteins (mg/dl) 219 128 85 87 
Serum HD lipoproteins(mg/dL) 49 53 52 50 
ParametersAprilMayJuneJully
Hemoglobin (g/dl) 9,6 11,1 12 12 
Leukocyte count (×109/l) 5.2 4.6 7.5 7.8 
Platelet count (×109/l) 168 287 210 215 
Serum total cholesterol (mg/dl) 310 189 157 152 
Serum LD lipoproteins (mg/dl) 219 128 85 87 
Serum HD lipoproteins(mg/dL) 49 53 52 50 
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Comments and conclusions. The effects observed in this reported case and in other similar patients [4] indicates that the treatment with IM induces a favourable control not only on cell growth and replication but also on the homeostasis of lipoproteins and glucose. A possible mechanism of action could be the inhibition by IM of PDGFR-dependent phosphorylation of the LDL-receptor related protein. IM appears to be a novel therapeutic option to retard the development of atherosclerosis, specifically in the context of diabetes and the treatment of choice for patients suffering of CML and dyslipidemia. Further prolonged observation of this and other similar patients is necessary for more pertinent data.

Topics:
imatinib mesylate, diabetes mellitus, type 2, lipoproteins, platelet-derived growth factor receptor, dyslipidemias, low-density lipoproteins, phosphotransferases, antidiabetics, atherosclerosis, cholesterol

Disclosure: No relevant conflicts of interest to declare.

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2006, The American Society of Hematology
2006
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