Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High risk splenectomy is often encountered in cases of hypersplenism with massive splenomegaly (10 times usual weight of 150-200 g) resulting from myelophthisic processes. Intra-operative ligation of the splenic artery through the lesser sac is a technically useful method of gaining vascular control prior to mobilizing the challenging spleen. However, a massive or inaccessible spleen imposes mechanical limitations during surgery and may be complicated by torrential intra-operative hemorrhage in the setting of severe thrombocytopenia refractile to platelet transfusions. The authors describe pre-operative intravascular proximal splenic artery control in four adult patients (3 men, 1 woman) with extreme splenomegaly (2,250-10,000 g). The massive splenomegaly in this group resulted from chronic myelogenous leukemia (n = 2), isolated splenic lymphoma (n = 1), and agnogenic myeloid metaplasia (n = 1). Chief symptom manifestations included left upper quadrant abdominal pain, early satiety, post-prandial emesis, dyspnea, petechiae, and associated easy bruising. Prior to surgery, all the patients were taken to the radiology suite where either detachable silastic balloons or stainless steel coils were placed selectively into the splenic artery under fluoroscopic guidance requiring approximately 35 minutes. Splenic artery occlusion aided normalization of thrombocytopenia (average increases 19,000/microliter to 215,000/microliter) with prolongation in survival of platelets. Successful splenectomy was subsequently performed with no additional transfusion requirements and was made technically easier by reducing splenic bulk. There were no adverse consequences of intravascular occlusion and no peri-operative morbidity or mortality. Preoperative intravascular selective splenic artery occlusion, used as an important potential adjunct to anticipated high risk splenectomy, is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preoperative splenic artery occlusion as an adjunct for high risk splenectomy. 317 46

A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin-induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (greater than or equal to 2 mM) induced minimal reversible aggregation. 14C-serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin-layer radiochromatographic analysis of the metabolites of 14C-AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet-rich plasma was added to a reaction mixture in which thromboxane A2 (TXA2) had been generated. TXA2 produced by patient's platelets showed normal platelet-aggregating activity. These results suggest that a subnormal platelet response to TXA2 is included as a mechanism for this acquired hypofunction of the platelet.
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PMID:Subnormal platelet response to thromboxane A2 in a patient with chronic myeloid leukaemia. 680 32

A 48-year-old Japanese man was admitted to our hospital because of general fatigue, nasal bleeding, and petechiae on his extremities. He was diagnosed with acute myelomonocytic leukemia with trilineage myelodysplasia (T-MDS). Chromosomal analysis of bone marrow cells revealed t(7;11)(p15;p15), which has been rarely reported but known to be characteristic of Japanese patients. Although t(7;11)(p15;p15) has been reported mainly in acute myelogenous leukemia (AML), it can be occasionally found in so-called stem cell diseases such as chronic myelogenous leukemia or chronic myeloproliferative disorders. Therefore, t(7;11)(p15;p15) might affect trilineage progenitors or stem cells as well as myeloid lineage cells, subsequently resulting in AML with T-MDS, as in our case reported here.
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PMID:t(7;11) and trilineage myelodysplasia in acute myelomonocytic leukemia. 861 92

Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor initially approved by the US Food and Drug Administration in 2001 for chronic myeloid leukemia (CML). Since then, the number of indicated uses for imatinib has substantially increased. It is increasingly important that dermatologists recognize adverse cutaneous manifestations of imatinib and are aware of their management and outcomes to avoid unnecessarily discontinuing a potentially lifesaving medication. Adverse cutaneous manifestations in response to imat-inib are not infrequent and can include dry skin, alopecia, facial edema, and photosensitivity rash. Other less common manifestations include exfoliative dermatitis, nail disorders, psoriasis, folliculitis, hypotrichosis, urticaria, petechiae, Stevens-Johnson syndrome, erythema multiforme, Sweet syndrome, and leukocytoclastic vasculitis. We report a case of imatinib-induced lichenoid drug eruption (LDE), a rare cutaneous manifestation, along with a review of the literature.
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PMID:Imatinib mesylate-induced lichenoid drug eruption. 2839 13