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Titlebook: Diagnostic Molecular Pathology in Practice; A Case-Based Approac Iris Schrijver Book 2011 Springer-Verlag Berlin Heidelberg 2011 Hematopath

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Pharmacogeneticsicant for a mildly elevated white blood cell count, creatine kinase of 541 U/L (normal 70–185 U/L), CK-MB of 78.4 ng/mL (normal <6.0 ng/mL), and troponin I of 4.53 ng/mL (normal <0.034 ng/mL), consistent with myocardial infarction.
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Alpha ThalassemiaIron studies were normal, and the normal HbA. results effectively ruled out beta thalassemia trait. DNA testing for alpha thalassemia was therefore performed, but both parents were negative for six common deletional mutations that cause most cases of alpha thalassemia.
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Malignant Hyperthermiading bolus of 2.5 mg/kg intravenous dantrolene, an antidote to MH-triggering agents. Subsequent bolus doses of 1 mg/kg were administered intravenously until the signs of acute MH abated and the ETCO. normalized. The patient had an unconfirmed family history of a similar episode in a maternal uncle.
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Chronic Myelogenous Leukemiaof presentation are shown in Table 15.1. The patient underwent a bone marrow biopsy which also showed increased granulocytic precursors with maturation (Fig. 15.1a). The patient’s family history was negative for any hematologic disorders.
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Posttransplant Lymphoproliferative Disordernce the time of transplantation, the patient has been on immunosuppressive therapy (azathioprine and cyclosporine) to prevent graft rejection. Then the patient presented with a fever unresponsive to anti­biotics. Physical examination revealed abdominal lym­phadenopathy.
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Josef Ehmer,Ursula Ferdinand,Jürgen ReuleckeIron studies were normal, and the normal HbA. results effectively ruled out beta thalassemia trait. DNA testing for alpha thalassemia was therefore performed, but both parents were negative for six common deletional mutations that cause most cases of alpha thalassemia.
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https://doi.org/10.1007/978-3-662-56627-5of presentation are shown in Table 15.1. The patient underwent a bone marrow biopsy which also showed increased granulocytic precursors with maturation (Fig. 15.1a). The patient’s family history was negative for any hematologic disorders.
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