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)

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
 ...
PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59

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.
 ...
PMID:A patient with chronic myeloid leukemia and situs inversus totalis: A case report. 2934 83

Lineage switch is very rare in blastic crisis of chronic myeloid leukemia (CML-BC). Here, we report a case of CML-BC in which the blast lineage switched from myeloid to B-lymphoid. A 35-year-old male was initially admitted to our hospital because of abdominal distention for over a year and dizziness for one week. Prior to presentation at our hospital, he visited a local hospital because of abdominal distention where his white blood cell count and bone marrow (BM) smear indicated CML. Results from peripheral blood (PB) counts, bone marrow analysis, immunophenotyping by flow cytometry, and the detection of the Philadelphia chromosome were consistent with a diagnosis of myeloid blast crisis from CML. The patient received chemotherapy with imatinib for induction, which diminished the number of blasts. However, after three months, the blasts were increased in the PB and BM. The BM study and immunophenotyping by flow cytometry revealed B-lymphoblastic leukemia. In accordance with his first admission, a chromosome study revealed a karyotype of 46, XY, t(9; 22)(q34; q11) in all 20 cells analyzed, and B-lymphoblastic transformation from CML was diagnosed. Despite three months of treatment with DVCP (daunorubicin, vincristine, cyclophosphamide and prednisone) chemotherapy in combination with dasatinib, the patient did not achieve complete remission. The patient decided to stop treatment and was discharged from the hospital for financial reasons. This case implicates the Philadelphia chromosome with p210 BCR-ABL1 fusion proteins as a key molecule in CML-BC. Further research is needed to assess the frequency, treatment, and prognosis of CML-BC patients with lineage switch.
 ...
PMID:Myeloid Blast Crisis of Chronic Myeloid Leukemia Followed by Lineage Switch to B-Lymphoblastic Leukemia: A Case Report. 3236 84