Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical observations revealed an increased prevalence of iron deficiency anemia without chronic bleeding in patients treated with serial low-density lipoprotein (LDL) apheresis. Since several different proteins are adsorbed by LDL apheresis beside pro-atherogenic lipoproteins, we examined the modification of the full blood count, plasma iron, vitamin B12, folic acid, and hemolysis by LDL apheresis. Nineteen patients (55 (50-59) years, 4 female, 15 male) undergoing chronic LDL apheresis due to mixed dyslipidemia (N = 17), homozygous familiar hypercholesterolemia (N = 1) or isolated elevated lipoprotein(a) (N = 1) were included in this study. They were treated with direct adsorption of lipoproteins (DALI; N = 6), heparin-induced LDL-precipitation (HELP; N = 7) or double filtration plasmapheresis (DFPP; N = 6). The patients' full blood count, iron metabolism (plasma iron, ferritin, transferrin, transferrin saturation), vitamins involved in erythropoiesis (vitamin B12 and folic acid), and markers of hemolysis (haptoglobin and free hemoglobin) were analyzed directly before and after LDL apheresis. A single LDL apheresis session significantly decreased the levels (reduction in the median [25(th)-75(th) percentiles] of: ferritin 9.8 [1.3-18] %; P = 0.004), transferrin (12.1 [10.0-15.96] %; P = 0.0005), and vitamin B12 (17.8 [16.2-20.8] %; P = 0.0005). Thereby, transferrin and vitamin B12 were decreased in all (N = 19) and ferritin in 74% (N = 14) of the patients. Twelve out of 19 patients (63.2%) had mild anemia despite iron administration in 14 out of 19 patients (73.7%). LDL apheresis had no significant influence on full blood count, plasma iron, transferrin saturation, folic acid, or hemolysis. Similar changes were observed in all LDL apheresis methods used. LDL apheresis significantly decreases ferritin, transferrin, and vitamin B12, suggesting an influence of serial LDL apheresis on erythropoiesis.
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PMID:Low-density lipoprotein apheresis decreases ferritin, transferrin and vitamin B12, which may cause anemia in serially treated patients. 2043 34

Helicobacter pylori (H. pylori) is a known pathogen implicated in genesis of gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Beyond the stomach, the organism has also been implicated in the causation of immune thrombocytopenia and iron deficiency anemia. Although an area of active clinical research, the role of this gram negative organism in causation of atherosclerosis and coronary artery disease (CAD) remains enigmatic. CAD is a multifactorial disease which results from the atherosclerosis involving coronary arteries. The major risk factors include age, diabetes mellitus, smoking, hypertension and dyslipidemia. The risk of CAD is believed to increase with chronic inflammation. Various organisms like Chlamydia and Helicobacter have been suspected to have a role in genesis of atherosclerosis via causation of chronic inflammation. This paper focuses on available evidence to ascertain if the role of H. pylori in CAD causation has been proven beyond doubt and if eradication may reduce the risk of CAD or improve outcomes in these patients.
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PMID:Helicobacter pylori: Does it add to risk of coronary artery disease. 2563 15

Dyslipidemia is a common feature in immunosuppressed patients, such as kidney and bone marrow transplantation recipients and patients with breast, prostate or gynecological carcinoma or acute lymphoblastic leukemia. In addition, high levels of oxidatively modified low-density lipoproteins (oxLDLs) are closely associated with carcinogenesis. There are, however, no reports on the association between the serum oxLDL levels and the expression of important immunomodulatory molecules in patients with hematological disorders. In the present study, 39 patients with hematological disorders were stratified into four groups: Two groups with malignancies [chronic myeloid leukemia (CML) and acute myeloblastic leukemia (AML)] and two groups without malignancies [myelodysplastic syndrome (MDS) and iron deficiency anemia (IDA)]. Immunomodulatory molecules were monitored in these groups. The enzyme-linked immunosorbent assay results indicated that the plasma oxLDL levels were significantly higher in patients with AML or CML than those in patients with MDS or IDA. The quantitative polymerase chain reaction results revealed that the expression of numerous important immunomodulatory elements, including tumor-related genes, immunological and inflammatory cytokines, defense-responsive genes, genes regulating cell proliferation, adhesion and migration molecules and leukocyte chemotaxis genes, showed considerable variation in patients with hematological disorders, particularly in those with MDS or IDA, as compared with the expression in the healthy volunteers. The present study demonstrated that, in patients with a hematological malignancy (either AML or CML), the activation of numerous immune response-related molecules was inhibited. Thus, an association between hematological malignancies and dyslipidemia, i.e. high levels of oxLDL, is suggested. Further research is necessary to investigate how oxLDL influences cancer progression.
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PMID:High plasma levels of oxidatively modified low-density lipoproteins are associated with the suppressed expression of immunomodulatory molecules in patients with hematological malignancies. 2613 94