Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 15-y-o girl who had relapsed acute lymphoblastic leukemia, followed by the two-years complete remission, was treated with a reinduction chemotherapy including methotrexate, vincristine, L-asparaginase and dexamethasone (MOAD). During the chemotherapy, a remarkable hyperlipidemia has developed. The plasma levels of triglyceride and total cholesterol reached 14,450 mg/dl and 1,750 mg/dl, respectively. The laboratory data strongly suggest that L-asparaginase could induce this hyperlipidemia of Friedrickson type V. We could successfully reduce the levels of triglyceride and total cholesterol to the normal range by LDL-apheresis, and treat the patient with the chemotherapy excluding L-asparaginase to attain the second CR.
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PMID:[L-asparaginase-induced hyperlipidemia in a case of acute lymphoblastic leukemia]. 204 Nov 67

A nine-year old girl with T cell acute lymphoblastic leukemia (ALL) had acute severe neurologic complications at the end of the remission-induction chemotherapy course. Thirty-six hours following triple intrathecal (IT) therapy and intravenous (IV) administration of L-asparaginase (L-asp), tetraplegia developed and she became unconscious. She had bouts of hypertension and persistent tachycardia unresponsive to digitalis therapy. Magnetic resonance imaging (MRI) showed multiple brain white matter hyperintensities and filling defects in the saggital sinus, suggesting thrombosis. Over the 40 days, in addition to her neurologic compromise she also had transient diabetes mellitus, severe hyperlipidemia, hypoproteinemia and edema, liver and heart failure and staphylococcus aureus sepsis with prolonged bone marrow depression. Despite, coexistence of all these chemotherapy related complications, her neurologic functions and multiple organ failure improved gradually. After a 70 days' period of interruption, chemotherapy was resumed and continued without any further complications. Although, the etiology of her extensive sensitivity to some drugs remains unclear, we believe that it is important to document these unusual events in this child.
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PMID:Coexistence of life threatening chemotherapy related leukoencephalopathy, saggital sinus thrombosis and multiple organ failure in a child with acute lymphoblastic leukemia: an unusual case with clinical recovery. 932 1

Serpins are key actors of systems involving proteolytic reactions, such as the haemostatic system, as they are irreversible suicide inhibitors of serine proteases. The structural flexibility and physical properties of serpins that are required for their efficient inhibitory mechanism also make them especially vulnerable to even minor factors that induce conformational changes in the native form of these molecules, leading to a number of inactive conformations, such as latent, cleaved or polymers. Increasing numbers of conformational mutations affecting haemostatic serpins, mainly antithrombin, the main endogenous anticoagulant, have been described. These mutations cause circulating deficiencies of the molecules, in most cases due to intracellular retention, which may be associated with a hyper-coagulable state. Indeed, conformational mutations in antithrombin have been identified in patients with severe venous thrombosis, which has led to the hypothesis that these disorders might be included in the group of conformational diseases. Moreover, we have recently demonstrated that other factors, including both drugs, such as the treatment with L-asparaginase, or environmental factors, such as high temperatures or hyperlipidemia, may also have conformational consequences on hepatic antithrombin, thus resulting in intracellular aggregation and plasma deficiency, which may increase the risk of thrombosis. In this study, we review the causes of deficiency of haemostatic serpins that may be explained by conformational mechanisms, and their association with an increased risk of venous thrombosis.
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PMID:Factors with conformational effects on haemostatic serpins: implications in thrombosis. 1784 43

A 24-year-old male patient with T-cell acute lymphoblastic leukemia was diagnosed with severe hypertriglyceridemia after the sixth administration of L-asparaginase during remission-induction therapy of the Japan Adult Leukemia Study Group (JALSG) -ALL 202-U protocol. Lipoprotein analysis revealed type IV hyperlipidemia, which is associated with a relatively low risk for pancreatitis. Hypertriglyceridemia immediately resolved after discontinuing L-asparaginase and beginning a lipid-restricted diet. The patient did not develop any severe complications of hypertriglyceridemia (e.g., pancreatitis and thrombosis) ; therefore, L-asparaginase could be readministered according to the treatment protocol. Four adult patients with L-asparaginase-induced severe hypertriglyceridemia have been reported to date; however, none of the reports indicated that L-asparaginase had been readministered. Thus, this is the first report of a patient receiving such readministeration. In order to evaluate the safety of continuing L-asparaginase, it is considered necessary to accumulate similar readministration cases.
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PMID:[Successful readministration of L-asparaginase after development of severe hypertriglyceridemia in a young adult with T-cell acute lymphoblastic leukemia]. 3062 88

Severe hyperlipidemia (>1000 mg/dL) at initial presentation of acute lymphoblastic leukemia (ALL) is rare. Cases of hyperlipidemia during therapy for childhood ALL where they were secondary to L-asparaginase or steroids have been described. This is a case report of a one-and-half-year-old boy who presented to us with fever, abdominal distension, severe pallor, and hepatosplenomegaly. Although his investigations were suggestive of ALL, the initial blood samples were found to be grossly lipemic. The lipid profile was abnormal, showing severe hypertriglyceridemia (serum triglycerides 1552 mg/dL). High-density lipoprotein and low-density lipoprotein levels were low, but there were raised very low-density lipoprotein level and serum lactate dehydrogenase (18117 U/L). The patient was started on induction of remission with careful monitoring of biochemical parameters. Abnormal lipid levels declined gradually with normalization of the levels at the end of one week of chemotherapy. No further complications were encountered during the course of induction of remission.
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PMID:Severe hyperlipidemia in a case of acute lymphoblastic leukemia. 3106 41