Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit. In idiopathic myelofibrosis (IMF) PDGF is considered to be one of the growth factors responsible for the development of bone marrow fibrosis. Recently, it has been shown that imatinib has antifibrogenic effect on bone marrow fibrosis in chronic myelogenous leukemia. Treatment with imatinib alone in IMF has been associated with significant side effects. In this study, the safety and efficacy of imatinib therapy in IMF, either administered as a single agent or in combination with hydroxyurea (HU) and/or alpha-interferon (IFN-alpha) are evaluated. Eleven patients (median age, 63 years; range, 33-82 years) with IMF (n = 8) or postpolycythemic myelofibrosis (PPMF) (n = 3) were studied All patients had been treated with HU (n = 9) and/or IFN (n = 7) before study entry. In all but one patient, treatment with these agents was discontinued when imatinib therapy was instituted. One patient continued IFN when treatment with imatinib was started. Imatinib was given at a dose of 400 mg/day. Nine patients were in an advanced disease phase. The patients have been followed for a median period of 2 months (range, 0.5-12 months). Treatment with imatinib has been stopped in six patients (55%), because of overt side effects (n = 4), recurrence of transitory dizziness and visual defects owing to a rising platelet count (n = 1), or the occurrence of an acute subdural hemorrhage that was evacuated without neurological deficits (n = 1). In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN. The combined treatment modalities were followed by a rapid decrease in cell counts and were well tolerated apart from IFN side effects. A beneficial effect of imatinib was documented in three patients. It is concluded that leukocytosis and thrombocytosis are seen in most patients with myelofibrosis during treatment with imatinib. Combination therapy with HU or IFN seems safe and well tolerated and followed by a decrease in disease activity. A subgroup of patients in an early disease phase might benefit from imatinib therapy alone.
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PMID:Imatinib mesylate in idiopathic and postpolycythemic myelofibrosis. 1463 3

A 65-year-old man is presented here with a huge mass of 13 cm in diameter in the left upper abdomen. Histopathologic assessment of endoscopic forceps biopsy revealed a c-kit positive gastrointestinal storomal tumor (GIST) of the stomach. Abdominal computed tomography (CT) showed a direct invasion to the pancreas. Imatinib mesilate was administered as neoadjuvant therapy according to the NCCN Guidelines. Imatinib mesilate therapy was stopped within 2 weeks because of adverse events such as Grade 2 of facial edema and dizziness. However, no hematological adverse event was shown. After three months of treatment (relative dose intensity was 87.5%), CT revealed a reduction in tumor diameter of 35.6% and showed no longer a direct invasion to the pancreas. The radical operation was considered feasible and partial gastrectomy was performed. The tumor was well encapsulated and radical surgery was possible without rupture. Adjuvant therapy was not performed. The patient has now been in good health without a recurrence for three months after the surgery.
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PMID:[Neoadjuvant therapy with imatinib mesilate for gastrointestinal stromal tumor of the stomach before subsequent successful surgical resection]. 1721 33

Imatinib mesylate is a selective competitive inhibitor of the bcr-abl tyrosine kinase and c-KIT. Other kinases, such as phosphatidylinositol- 3'-kinase (PI-3K) involved in insulin signaling, have also been shown to be indirectly affected by imatinib. A recent report described a lowering of blood glucose levels in Type 2 diabetic patients treated with imatinib resulting in a reduction of oral antidiabetic medication or insulin dosage. We present a female non-diabetic patient with a resected gastrointestinal stromal tumor with an increased insulin response following an oral glucose challenge and hypoglycemic episodes following imatinib therapy. In addition to a rise in insulin sensitivity, the patient showed inappropriately high insulin secretion rates in relation to the actual blood glucose concentrations during and after the completion of imatinib treatment. The symptoms suggestive of hypoglycemia such as dizziness and shivering formerly observed in patients treated with imatinib may be related to hypoglycemic glucose concentrations. Physicians treating patients with imatinib should be aware of the possible occurrence of hypoglycemic episodes in non-diabetic patients.
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PMID:Symptomatic hypoglycemia during imatinib mesylate in a non-diabetic female patient with gastrointestinal stromal tumor. 1792 2

In the present study, a case of chronic myeloid leukemia (CML) with complete situs inversus in a 68-year-old female patient was reported. The patient presented with general weakness, abdominal distension and tenderness in the right hypochondrium. A chest X-ray revealed a right-sided heart. Ultrasonography revealed situs inversus totalis. A bone marrow smear demonstrated CML in the accelerated phase. Imatinib mesylate was subsequently administered; the patient stopped taking imatinib mesylate following discharge from the hospital. The patient presented with dizziness, fatigue, and abdominal distention and pain 1 year subsequently. A bone marrow smear demonstrated CML in the blast crisis phase; CML had progressed to acute myeloid leukemia (AML) M2a. The patient was treated with imatinib mesylate and cytarabine. After 5 days, the white blood cell count had decreased compared with that measured at the time of admission, and the previous relevant symptoms had disappeared. The patient succumbed to AML 3 months after discharge from the hospital. Situs inversus totalis is an uncommon congenital anomaly that often occurs concomitantly with other disorders. The present study documented, to the best of our knowledge, the second recorded case of CML in a patient with situs inversus totalis. Previous studies on the pathogenesis of situs inversus have suggested it is caused by embryonic cells failing to rotate normally during early embryonic development. Although there are case reports of situs inversus totalis in patients with cancer, there are few reports on the association between situs inversus totalis and cancer. The present study examined a case of CML with situs inversus totalis and assessed whether the latter may be associated with cancer.
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PMID:A patient with chronic myeloid leukemia and situs inversus totalis: A case report. 2934 83