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)

Intravascular coagulation of the intraosseous microcirculation (capillaries and venous sinusoids) progressing to generalized venous thrombosis, and less commonly retrograde arterial occlusion, now appears to be the cause of nontraumatic osteonecrosis. However, this coagulopathy is only an intermediary event, which is always activated by some underlying etiologic risk factor(s). Conditions capable of triggering intravascular coagulation include familial thrombophilia (resistance to activated protein C, decreased protein C, protein S, or antithrombin III), hyperlipemia and embolic lipid (alcoholism and hypercortisonism), hypersensitivity reactions (allograft organ rejection, immune complexes, and antiphospholipid antibodies), bacterial endotoxic (Shwartzman) reactions and various viral infections, proteolytic enzymes (pancreatitis), tissue factor release (inflammatory bowel disease, malignancies, neurotrauma, and pregnancy), and other prothrombotic and hypofibrinolytic conditions.
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PMID:Coagulopathies and osteonecrosis. 1008 10

Certain fractures and/or dislocations of the femoral head are known to cause arterial injury and result in post-traumatic osteonecrosis. However, the more complex etiology of non-traumatic osteonecrosis is multifactorial and includes chemotherapy, radiotherapy, thermal injuries, and especially coagulopathies, which are now commonly observed in these patients. Intravascular coagulation with fibrin thrombosis begins in the capillaries and sinusoids of the intraosseous microcirculation, and residual venous thrombosis is more likely to occur if there is coexistent hypofibrinolysis. Coagulopathies are intermediary events, which are always activated by some underlying etiologic risk factor(s). Conditions capable of triggering intravascular coagulation include familial thrombophilia (resistance to activated protein C, decreased protein C, protein S, or antithrombin III, and hyperhomocystinemia), hyperlipemia and embolic lipid (alcoholism and hypercortisonism), hypersensitivity reactions (allograft organ rejection, immune complexes, and antiphospholipid antibodies), bacterial endotoxic (Shwartzman) reactions and various viral infections, proteolytic enzymes (pancreatitis), tissue factor release (inflammatory bowel disease, malignancies, neurotrauma, and pregnancy), and other thrombophilic and hypofibrinolytic disorders. Currently known risk factors for non-traumatic osteonecrosis of the femoral head are described briefly in this review article.
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PMID:[Epidemiological risk factors for non-traumatic osteonecrosis]. 1087 31

Several genomewide screens have been performed to identify novel loci predisposing to unfavorable serum lipid levels and coronary heart disease (CHD). We hypothesized that the accumulating data of these screens in different study populations could be combined to verify which of the identified loci truly harbor susceptibility genes. The power of this strategy has recently been demonstrated with other complex diseases, such as inflammatory bowel disease and asthma. We assessed the largely unknown genetic background of CHD by investigating the most common dyslipidemia predisposing to CHD, familial combined hyperlipidemia (FCHL), affecting 1%-2% of Western populations and 10%-20% of families with premature CHD. To be able to perform a combined data analysis, we unified the diagnostic criteria for FCHL and its component traits and combined the data from two genomewide scans performed in two populations, the Finns and the Dutch. As a result of our pooled data analysis, we identified three chromosomal regions, on chromosomes 2p25.1, 9p23, and 16q24.1, exceeding the statistical significance level of a LOD score >2.0. The 2p25.1 region was detected for the FCHL trait, and the 9p23 and 16q24.1 regions were detected for the low high-density lipoprotein cholesterol (HDL-C) trait. In addition, the previously recognized 1q21 region also obtained additional support in the other study sample, when the triglyceride trait was used. Analysis of the 16q24.1 region resulted in a statistically significant LOD score of 3.6 when the data from Finnish families with low HDL-C were included in the analysis. To search for the underlying gene in the 16q24.1 region, we investigated a novel functional and positional candidate gene, helix/forkhead transcription factor (FOXC2), by sequencing and by genotyping of two single-nucleotide polymorphisms in the families.
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PMID:Combined analysis of genome scans of dutch and finnish families reveals a susceptibility locus for high-density lipoprotein cholesterol on chromosome 16q. 1263 83

Liver steatosis is a common human disease, most often caused by long-term alcohol consumption. Non-alcoholic steatohepatitis (NASH) is characterized by similar histopathological features to those observed in alcoholic liver disease, but occurs in the absence of significant alcohol consumption. Several aetiological factors contribute to NASH: obesity, type 2 diabetes mellitus, hyperlipidaemia, pregnancy, different chemical intoxications, parenteral nutrition, jejeuno-ileal bypass, chronic inflammatory bowel disease, nutritional protein deficiency and congenital metabolic disorders. Biochemically, oxidative stress and lipid peroxidation and their ensuing damage are implicated in the pathogenesis of NASH and alcoholic steatohepatitis (probably resulting from free fatty acids in the mitochondria, and induction of the cytochrome P450 isoform CYP2E1 in hepatocytes and Kupffer's cells). This paper deals with the pathomechanisms, clinical findings and currently available therapies for NASH. The potential use of metadoxine in the treatment of NASH is also discussed.
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PMID:A new approach to drug therapy in non-alcoholic steatohepatitis (NASH). 1470 19

Progress in the development of antisense drugs over the last decade has led to the approval of the first such drug--Vitravene for AIDS-related CMV retinitis--and the development of a large number of antisense drugs in clinical trials. Antisense drugs are now being studied in Phase 3 trials for patients with cancer and inflammatory bowel disease. Other antisense drugs are in development for rheumatoid arthritis, other inflammatory conditions, and hepatitis C. Still other antisense drugs are entering clinical trials for treatment of metabolic conditions such as diabetes and hyperlipidemia. These latter applications provide the potential for target effects to be more directly measured in the clinic. Improved antisense chemistry, which will enhance the feasibility of subcutaneous and oral administration of antisense drugs and offer the potential of less frequent dosing, is expected to further expand the opportunities for antisense drug development.
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PMID:Applying antisense technology: Affinitak and other antisense oligonucleotides in clinical development. 1475 39

Probiotics have been defined by The Food Agricultural Organization/World Health Organization (FAO/WHO) as "live microorganisms which when administered in adequate amounts confer a health benefit to the host." They have been used for centuries in the form of dairy-based fermented products, but the potential use of probiotics as a form of medical nutrition therapy has not received formal recognition. A detailed literature review (from 1950 through February 2004) of English-language articles was undertaken to find articles showing a relationship between probiotic use and medical conditions. Medical conditions that have been reportedly treated or have the potential to be treated with probiotics include diarrhea, gastroenteritis, irritable bowel syndrome, and inflammatory bowel disease (Crohn's disease and ulcerative colitis), cancer, depressed immune function, inadequate lactase digestion, infant allergies, failure-to-thrive, hyperlipidemia, hepatic diseases, Helicobacter pylori infections, genitourinary tract infections, and others. The use of probiotics should be further investigated for possible benefits and side-effects in patients affected by these medical conditions.
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PMID:Probiotics and medical nutrition therapy. 1548 39

Curcumin has long been expected to be a therapeutic or preventive agent for several major human diseases because of its antioxidative, anti-inflammatory, and anticancerous effects. In phase I clinical studies, curcumin with doses up to 3600-8000 mg daily for 4 months did not result in discernible toxicities except mild nausea and diarrhea. The pharmacokinetic studies of curcumin indicated in general a low bioavailability of curcumin following oral application. Nevertheless, the pharmacologically active concentration of curcumin could be achieved in colorectal tissue in patients taking curcumin orally and might also be achievable in tissues such as skin and oral mucosa, which are directly exposed to the drugs applied locally or topically. The effect of curcumin was studied in patients with rheumatoid arthritis, inflammatory eye diseases, inflammatory bowel disease, chronic pancreatitis, psoriasis, hyperlipidemia, and cancers. Although the preliminary results did support the efficacy of curcumin in these diseases, the data to date are all preliminary and not conclusive. It is imperative that well-designed clinical trials, supported by better formulations of curcumin or novel routes of administration, be conducted in the near future.
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PMID:Clinical studies with curcumin. 1756 25

Chronic inflammation with the presence of excess serum acute-phase proteins, cytokines and cell adhesion molecules is increasingly being implicated in atherosclerosis. The association between inflammatory bowel disease (IBD) and coronary artery disease (CAD) is unstudied. This is a preliminary, thesis-generating cross-sectional study aimed at evaluating the presence of traditional atherosclerotic risk factors in patients with IBD and CAD compared with the control population. The medical records of 42 consecutive IBD patients with CAD from 1999 to 2005 (27 men) were reviewed for the Framingham risk factors. The Framingham risk score (FRS) is calculated based on age, sex, hypertension, diabetes and hyperlipidemia. FRS of patients with IBD and CAD was compared with the FRS of 137 age- and sex-matched (102 men) consecutive patients with CAD (controls). When the Framingham risk score adjusted for group and gender with age as a covariate, the adjusted total FRS score was higher in patients with CAD alone (10.0 [3.75]) as compared to those with; IBD and CAD: (8.1 [3.47]; p = 0.001). FRS is lower in cases (patients with IBD and CAD) when compared with the controls (CAD alone).
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PMID:Inflammatory bowel disease and coronary artery disease. 1952 99

Acute pancreatitis and chronic pancreatitis are complex inflammatory disorders of the pancreas with unpredictable severity, complications, and clinical courses. Growing evidence for genetic risk and modifying factors, plus strong evidence that only a minority of patients with these disorders are heavy alcohol drinkers, has revolutionized our concept of these diseases. Once considered a self-inflicted injury, pancreatitis is now recognized as a complex inflammatory condition like inflammatory bowel disease. Genetic linkage and candidate gene studies have identified six pancreas-targeting factors that are associated with changes in susceptibility to acute and/or chronic pancreatitis, including cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), serine protease inhibitor Kazal 1 (SPINK1), cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsinogen C (CTRC) and calcium-sensing receptor (CASR). Patients with mutations in these genes are at increased risk of pancreatitis caused by a variety of stresses including hyperlipidemia and hypercalcemia. Multiple studies are reporting new polymorphisms, as well as complex gene x gene and gene x environmental interactions.
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PMID:Genetic aspects of pancreatitis. 2005 46

It has been estimated that up to 10% of hypercoagulable state manifestations in patients with inflammatory bowel disease (IBD) are ischemic strokes. The literature search through MEDLINE and EMBASE highlighted 33 case reports of IBD patients complicated with cerebral arterial infarction during the course of their disease. Most of these patients presented with either left or right sided hemiparesis on admission, while the most common site of arterial infarction was either the right or the left middle cerebral artery. Thrombocytosis and anemia were the most commonly observed potential risk factors for stroke in the laboratory analysis. Other coagulation abnormalities, hereditary thrombotic mutations, hyperhomocysteinemia, hyperlipidemia, structural cardiac abnormalities, endocarditis and cerebral artery vasculitis have also been reported in some of the cases that were reviewed. Even though many of these findings are commonly observed in IBD patients, literature data is still controversial about their causal relationship to ischemic stroke. Similarly, there is also lack of steady evidence and official guidelines for stroke management in both children and adults with IBD comorbidity. Finally, an algorithm based on both the American Heart Association and European Stroke Organization guidelines for stroke management and prevention in the general population, is presented as a reference point for the treatment of IBD patients who are complicated by an ischemic cerebral event.
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PMID:Cerebral arterial infarction in inflammatory bowel diseases. 2402 31


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