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)

There were 72 patients (19 with hepatic failure, 10 with fulminant hepatitis, eight with paraquat poisoning, eight with rheumatoid arthritis, five with myasthenia gravis, four with hyperlipidemia, four with systemic arteriosclerosis including brain infarction, three with pemphigus vulgaris, two with multiple myeloma, two with systemic lupus erythematosus, two cases non-specific Ig-G antibody, two cases medication with an anticancer drug, one with multiple sclerosis, one with Crohn's disease with amyloid kidney and one with chronic myeloblastic leukemia) treated by plasma exchange in the Kidney Center, Tokai University School of Medicine from Jan. 1983 to Dec. 1986. We performed plasma exchange using fresh frozen plasma in 40 cases and Lactate-Ringer's solution containing albumin (4.0-5.0%) in 20 cases as the replacement fluid. In 17 cases, we performed double filtration plasma exchange with the recycle system and no replacement fluid. Although PE therapy did not constitute a basic therapy for hyperlipidemia, pemphigus vulgaris, rheumatoid arthritis, myasthenia gravis, and systemic lupus erythematosus, it was effective in relieving severe clinical symptoms. At the present time, conventional plasma exchange does not improve the survival rate of patients with hepatic failure and fulminant hepatitis. Developments of a new artificial liver support apparatus and identity of many toxic substances in hepatic failure are necessary. No hypotension, hypovolemic shock or other significant complications were experienced.
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PMID:Clinical reports on plasma exchange in the Kidney Center, Tokai University School of Medicine. 344 83

Gingival plane xanthomas are unusual oral presentations of hyperlipidemia and they may be of minimal clinical significance to the patient because they are asymptomatic. However, the presence of gingival xanthomas should be considered as a possible precursor of an underlying life-threatening disease process. Many of these systemic conditions may severely compromise dental therapy; they include atherosclerotic coronary disease, peripheral vascular disease, diabetes mellitus, biliary cirrhosis, multiple myelomas, leukemia, and hyperthyroidism. Clinicians should be aware of this association and its important implications.
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PMID:Multiple asymptomatic yellowish-white nodules on the free gingiva. 347 Mar 59

Studies were conducted on lipemic serum obtained from a 26 month old male to determine possible mechanisms for the association of a Type V hyperlipidemic phenotype with advanced lymphoblastic leukemia (ALL). Antibodies to apolipoproteins and endogenous heparin were not detected as previously reported. Fatty acid analysis of the triglyceride esters revealed a high proportion of stearic-acid (18:0) which was associated with a slower in vitro degradation of very low density lipoproteins (VLDL) by human milk lipoprotein lipase (LPL). This suggests that a cause of the hyperlipidemia could be abnormal composition of triglycerides which render the VLDL a poor substrate for lipoprotein lipase. Hyperlipidemia in leukemia may be more prevalent than previously realized since nine other cases of newly diagnosed ALL have been studied who had moderate hypertriglyceridemia associated with elevated ApoB and low ApoA-I levels, but normal triglyceride composition. These findings suggest that the abnormal triglyceride composition is a late feature of the hyperlipidemia in leukemia, as observed in the case studied.
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PMID:Hyperlipidemia in acute lymphoblastic leukemia. 658 75

To investigate the possible role of previous medical history and previous medications as risk factors for hairy cell leukaemia (HCL) we performed a population based case-control study on 121 male HCL patients and 484 controls. The data were collected through a self-administered mailed questionnaire. Elevated odds ratios (OR) were found for a history of appendicitis [OR 1.9; 95% confidence interval (CI) 0.9-4.2] and pneumonia (OR 2.9; CI 0.9-9.6). We found a reduced risk for HCL associated with a history of myocardial infarction (OR 0.3; CI 0.4-2.5), hypertension (OR 0.6; CI 0.3-1.2) and thromboembolic disease (OR 0.6; CI 0.1-2.7). Reduced OR was also associated to a history of diabetes mellitus (OR 0.6; CI 0.1-2.9) and a diagnosis of hyperlipidemia (OR 0.8; CI 0.2-3.6). HCL is an indolent disease with a clinical course of many years and it can not be excluded that the disease leads to metabolic changes, resulting in a changed risk for these diagnoses. When the role of previous medications were investigated, increased OR was found for NSAID (OR 3.4; CI 1.1-10.2). Decreased OR was found for the anti-coagulative agent warfarin (OR 0.4; CI 0.1-1.5). A history of a previous malignancy preceeding the diagnosis of HCL as reported to the Swedish Cancer Registry yielded an increased OR of 3.2 (CI 1.2-8.5). All results must be interpreted with caution, as there is a possibility of misclassification. Medications is difficults to remember, particularly several years after consumption. As many comparisons were made, there is always a possibility of correlations occuring by chance.
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PMID:Previous medical history and medications as risk factors for hairy cell leukaemia. 1002 13

The index patient is a 23-year-old female with end-stage renal disease (ESRD) secondary to chemotherapeutic agents. Continuous cycling peritoneal dialysis (CCPD) has been the renal replacement therapy for the past 5 years since a failed cadaveric renal transplant. Past medical history was significant for diabetes mellitus, hypertension, anemia, bilateral subclavian vein thrombosis with superior vena cava syndrome, secondary hyperparathyroidism, leukemia (at age 8), and hyperlipidemia. On presentation, soft tissue nodules were noted in the anterolateral surfaces of the legs. After 3 months of continued low-calcium-dialysate CCPD, calcitriol, and oral phosphate binders, a 2 x 3 cm nodule was noted on the posterior aspect of the thorax at the scapula. The only complaint at this time was shoulder pain at the acromioclavicular joint. Radiological examination revealed a 3 x 4 cm soft tissue opacity in the superior segment of the left lower lobe laterally. Despite a prior subtotal parathyroidectomy, phosphate binders, and calcitriol, the parathyroid hormone levels continued to increase, with development of tumoral calcinosis, worsening renal osteodystrophy, and calciphylaxis. Computed tomography examination revealed extensive soft tissue calcification consistent with tumoral calcinosis. An ulcerative lesion (1 cm) developed on the lateral aspect of the upper thigh owing to warfarin necrosis versus calciphylaxis. At this time, the phosphate binder was changed from calcium acetate to sevelamer hydrochloride. Aggressive wound treatment and aggressive calcium and phosphate control added to the treatment regimen has resulted in healing of the single ulcer and a decrease in the size of the tumoral lesions. In conclusion, early recognition and aggressive treatment of calciphylaxis can result in reduced morbidity and mortality from calciphylaxis in ESRD patients.
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PMID:Spectrum of complications related to secondary hyperparathyroidism in a peritoneal dialysis patient. 1104 12

We report two patients who survived childhood acute lymphoblastic leukaemia (ALL) following treatment with chemotherapy, total body irradiation (TBI) and bone marrow transplantation (BMT). The first case presented with an acute cerebral infarction at 23 years of age and was found to have non-ketotic diabetes and gross mixed hyperlipidaemia; the second presented with non-ketotic diabetes, hypertension, proteinuria and dyslipidaemia at age 16 years. The association of glucose intolerance with other vascular risk factors in young adult survivors of BMT was recently highlighted in a follow-up study of 23 survivors of BMT [1], but none presented with such gross mixed hyperlipidaemia. The improving survival rates of childhood malignancy over the last two decades will present adult physicians with patients who have accelerated vascular risk at a young age who will require early treatment to modify it.
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PMID:Adverse metabolic and cardiovascular risk following treatment of acute lymphoblastic leukaemia in childhood; two case reports and a literature review. 1167 78

A 71-year-old man with acute myelogenous leukemia (AML, M2) developed signs of chest oppression, and was diagnosed as having acute myocardial infarction (AMI). At the same time, his leukemia relapsed in association with disseminated intravascular coagulation (DIC). The patient's risk factors for AMI were hyperlipidemia, hyperglycemia, and a history of smoking. Coronary angiography showed occlusion of the circumflex branch. Percutaneous transluminal angioplasty (PTCA) was performed successfully, followed by administration of heparin. After chemotherapy, the patient's DIC improved and a second remission was attained. When elderly patients with AML show evidence of DIC, we should be aware of AMI as a possible complication. PTCA is a safe operation for such patients.
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PMID:[Acute myelogenous leukemia associated with disseminated intravascular coagulation and acute myocardial infarction at relapse]. 1168 Sep 86

Although recent developments in initial chemotherapeutic regimens and stem cell transplantation have achieved improvements of initial remission for myeloma patients, relapse and recurrence are still major problems. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been developed for treating hyperlipidemia. Recently, there have been several reports concerning the effects of statins on cancer cells including liver, colon, leukemia, malignant B, stomach, and breast cells. In this study, the in vitro effects of pravastatin on human myeloma cells and the factors closely related to its growth inhibitory effects were examined. Although concentrations were higher than those used clinically, 4 out of 10 myeloma lines showed growth inhibition by pravastatin. The study of factors related to the inhibition indicated IL-6 is important. Indeed, rhIL-6 abolished pravastatin-induced growth inhibition in KMS-21BM cells which did not express IL-6. Statins may be useful in maintenance therapy for myeloma after the screening of IL-6 status.
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PMID:IL-6 is a key factor in growth inhibition of human myeloma cells induced by pravastatin, an HMG-CoA reductase inhibitor. 1288 15

The Philadelphia chromosome-negative chronic myeloproliferative disorders (CMPD), polycythemia vera (PV), essential thrombocythemia (ET) and chronic idiopathic myelofibrosis (IMF), have overlapping clinical features but exhibit different natural histories and different therapeutic requirements. Phenotypic mimicry amongst these disorders and between them and nonclonal hematopoietic disorders, lack of clonal diagnostic markers, lack of understanding of their molecular basis and paucity of controlled, prospective therapeutic trials have made the diagnosis and management of PV, ET and IMF difficult. In Section I, Dr. Jerry Spivak introduces current clinical controversies involving the CMPD, in particular the diagnostic challenges. Two new molecular assays may prove useful in the diagnosis and classification of CMPD. In 2000, the overexpression in PV granulocytes of the mRNA for the neutrophil antigen NBI/CD177, a member of the uPAR/Ly6/CD59 family of plasma membrane proteins, was documented. Overexpression of PRV-1 mRNA appeared to be specific for PV since it was not observed in secondary erythrocytosis. At this time, it appears that overexpression of granulocyte PRV-1 in the presence of an elevated red cell mass supports a diagnosis of PV; absence of PRV-1 expression, however, should not be grounds for excluding PV as a diagnostic possibility. Impaired expression of Mpl, the receptor for thrombopoietin, in platelets and megakaryocytes has been first described in PV, but it has also been observed in some patients with ET and IMF. The biologic basis appears to be either alternative splicing of Mpl mRNA or a single nucleotide polymorphism, both of which involve Mpl exon 2 and both of which lead to impaired posttranslational glycosylation and a dominant negative effect on normal Mpl expression. To date, no Mpl DNA structural abnormality or mutation has been identified in PV, ET or IMF. In Section II, Dr. Tiziano Barbui reviews the best clinical evidence for treatment strategy design in PV and ET. Current recommendations for cytoreductive therapy in PV are still largely similar to those at the end of the PVSG era. Phlebotomy to reduce the red cell mass and keep it at a safe level (hematocrit < 45%) remains the cornerstone of treatment. Venesection is an effective and safe therapy and previous concerns about potential side effects, including severe iron deficiency and an increased tendency to thrombosis or myelofibrosis, were erroneous. Many patients require no other therapy for many years. For others, however, poor compliance to phlebotomy or progressive myeloproliferation, as indicated by increasing splenomegaly or very high leukocyte or platelet counts, may call for the introduction of cytoreductive drugs. In ET, the therapeutic trade-off between reducing thrombotic events and increasing the risk of leukemia with the use of cytoreductive drugs should be approached by patient risk stratification. Thrombotic deaths seem very rare in low-risk ET subjects and there are no data indicating that fatalities can be prevented by starting cytoreductive drugs early. Therefore, withholding chemotherapy might be justifiable in young, asymptomatic ET patients with a platelet count below 1500000/mm(3) and with no additional risk factors for thrombosis. If cardiovascular risk factors together with ET are identified (smoking, obesity, hypertension, hyperlipidemia) it is wise to consider platelet-lowering agents on an individual basis. In Section III, Dr. Gianni Tognoni discusses the role of aspirin therapy in PV based on the recently completed European Collaboration on Low-dose Aspirin in Polycythemia Vera (ECLAP) Study, a multi-country, multicenter project aimed at describing the natural history of PV as well as the efficacy of low-dose aspirin. Aspirin treatment lowered the risk of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke (relative risk 0.41 [95% CI 0.15-1.15], P =.0912). Total and cardiovascular mortality were also reduced by 46% and 59%, respectively. Major bleedings were slightly increased nonsignificnsignificantly by aspirin (relative risk 1.62, 95% CI 0.27-9.71). In Section IV, Dr. Giovanni Barosi reviews our current understanding of the pathophysiology of IMF and, in particular, the contributions of anomalous megakaryocyte proliferation, neoangiogenesis and abnormal CD34(+) stem cell trafficking to disease pathogenesis. The role of newer therapies, such as low-conditioning stem cell transplantation and thalidomide, is discussed in the context of a general treatment strategy for IMF. The results of a Phase II trial of low-dose thalidomide as a single agent in 63 patients with myelofibrosis with meloid metaplasia (MMM) using a dose-escalation design and an overall low dose of the drug (The European Collaboration on MMM) will be presented. Considering only patients who completed 4 weeks of treatment, 31% had a response: this was mostly due to a beneficial effect of thalidomide on patients with transfusion dependent anemia, 39% of whom abolished transfusions, patients with moderate to severe thrombocytopenia, 28% of whom increased their platelet count by more than 50 x 10(9)/L, and patients with the largest splenomegalies, 42% of whom reduced spleen size of more than 2 cm.
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PMID:Chronic myeloproliferative disorders. 1463 83

Guggulsterone, derived from Commiphora mukul and used to treat obesity, diabetes, hyperlipidemia, atherosclerosis, and osteoarthritis, has been recently shown to antagonize the farnesoid X receptor and decrease the expression of bile acid-activated genes. Because activation of NF-kappaB has been closely linked with inflammatory diseases affected by guggulsterone, we postulated that it must modulate NF-kappaB activation. In the present study, we tested this hypothesis by investigating the effect of this steroid on the activation of NF-kappaB induced by inflammatory agents and carcinogens. Guggulsterone suppressed DNA binding of NF-kappaB induced by tumor necrosis factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and interleukin-1. NF-kappaB activation was not cell type-specific, because both epithelial and leukemia cells were inhibited. Guggulsterone also suppressed constitutive NF-kappaB activation expressed in most tumor cells. Through inhibition of IkappaB kinase activation, this steroid blocked IkappaBalpha phosphorylation and degradation, thus suppressing p65 phosphorylation and nuclear translocation. NF-kappaB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, NIK, and IKK was also blocked by guggulsterone but without affecting p65-mediated gene transcription. In addition, guggulsterone decreased the expression of gene products involved in anti-apoptosis (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP, and survivin), proliferation (cyclin D1 and c-Myc), and metastasis (MMP-9, COX-2, and VEGF); this correlated with enhancement of apoptosis induced by TNF and chemotherapeutic agents. Overall, our results indicate that guggulsterone suppresses NF-kappaB and NF-kappaB-regulated gene products, which may explain its anti-inflammatory activities.
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PMID:Guggulsterone inhibits NF-kappaB and IkappaBalpha kinase activation, suppresses expression of anti-apoptotic gene products, and enhances apoptosis. 1532 87


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