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)

Acute pancreatitis in a patient on oral contraceptive therapy is reported, and the relationship of estrogen administration to hyperlipemia and pancreatitis is discussed. A 23-year-old white woman was admitted to a hospital with epigastric pain, nausea, and vomiting. Three previous episodes of abdominal pain had been diagnosed as acute pancreatitis. On the present and previous admissions, she had just completed a cycle on her combination norethindrone 1 mg, mestranol 8 micrograms contraceptive. Laboratory results showed mild leukocytosis and elevated concentrations of blood glucose, alkaline phosphatase, serum amylase, and urine amylase. Serum cholesterol and triglycerides were elevated, and lipoprotein electrophoresis showed a type IV pattern. Abdominal sonogram revealed a normal pancreas, and all other test results were normal. The patient was treated with i.v. fluid replacement, dimenhydrinate, and meperidine hydrochloride. Within 72 hours she was asymptomatic, and serum amylase, triglyceride, and cholesterol concentrations had decreased. She was discharged with a diagnosis of acute pancreatitis secondary to oral-contraceptive-induced hyperlipidemia. Oral contraceptive therapy was not resumed. Predisposing factors, symptoms, and laboratory findings associated with estrogen-induced acute pancreatitis are presented, and the mechanisms through which serum lipid elevations and subsequent pancreatitis occur are discussed. Monitoring serum lipid concentrations before and during estrogen therapy is recommended. Research suggests that patients who are over 40 years old or have family histories of hyperlipemia are at particular risk, and that estrogen therapy should be discontinued if pancreatitis occurs.
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PMID:Estrogen-induced pancreatitis. 688 34

The chemical measurements on our Technicon SMAC of lipemic sera before and after clearing lipemia by ultracentrifugation showed that uric acid, creatinine, carbon dioxide, calcium, phosphorus, potassium, and alkaline phosphatase were not affected significantly by lipemia, whereas sodium, urea, glucose, chloride and total protein showed small but significant increases with averages of less than 1.9 percent. Albumin showed a significant decrease of 1.2 percent. In contrast, the results for the enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) showed striking differences between pre- and post-centrifuged sera in a number of specimens. With lactate dehydrogenase, thirty-two of fifty specimens registered an increase in activity while with the aminotransferases, thirty-five and forty-one out of fifty specimens showed a decrease in aspartate aminotransferase and alanine aminotransferase activities, respectively. Although much of the lipemic interference can be explained by the volume displacement of serum by lipids or by interference by lipemia with colorimetry, the anomalous effects observed with the enzymes indicate the possibility of other, as yet, undetermined factor(s).
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PMID:The effect of hyperlipidemia on Technicon SMAC measurements. 712 23

A 35-years old female with Jordans' anomaly was reported. She had been treated for diabetes mellitus and hypertension at another hospital. She was admitted to our hospital for operation for diabetic retinopathy on July 9, 1992. Wright-Giemsa stained peripheral blood smear revealed multiple vacuoles in the cytoplasm of the granulocytes and monocytes. Histochemical studies of these vacuoles showed positive for Sudan III but negative for peroxidase, alkaline phosphatase and PAS staining. Electron microscopic examination revealed that lipid containing vacuoles had no clear membrane and were not associated with cell organelles. Laboratory findings of the serum showed hyperglycemia (FBS 188mg/dl), high HbA1c level (9.4%) and mild type IIa hyperlipidemia. Abdominal sonogram and abdominal CT showed no remarkable abnormalities except for mild fatty liver. Her elder sister and daughter had similar morphological findings in granulocytes, monocytes and lymphocytes.
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PMID:[A case of Jordans' anomaly]. 786 17

Disorders in lipoprotein metabolism (dyslipidemia) can result in premature atherosclerosis or pancreatitis. Dyslipidemias can be classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low density lipoprotein cholesterol and decreased levels of HDL cholesterol predispose to premature atherosclerosis. Triglyceride levels greater than 1,000 mg/dL increase the risk for pancreatitis. In the appraisal of the dyslipidemias, measurement of serum cholesterol, triglycerides, HDL-cholesterol and obtaining the LDL cholesterol by Friedewald equation is usually sufficient in the majority of patients. However, in some cases, such as the diagnosis of the Type III dyslipidemia and when triglycerides are > or = 400 mg/dL, ultracentrifugation is required to determine the VLDL or LDL cholesterol. Lipoprotein electrophoresis can be useful in the diagnosis of Type III dyslipidemia (broad beta band) and also to detect chylomicrons. In young subjects with coronary artery disease with a normal LDL cholesterol an apolipoprotein B-100 level may be a useful test. In children and young adults with severe hypertriglyceridemia, measurement of lipoprotein lipase activity or assaying apolipoprotein C-II levels can be useful in elucidating the cause. Also, laboratory tests are useful in excluding a secondary cause of dyslipidemia (urinalysis, plasma creatinine, TSH, glucose, protein electrophoresis, alkaline phosphatase and transaminases). Thus, laboratory investigations play an important role in the management of dyslipidemia.
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PMID:A practical approach to the laboratory diagnosis of dyslipidemia. 870 23

Out of 12 patients with primary hyperlipidemia (HL) included in the study ischemic heart disease was diagnosed in 4 and hypertension stage I-II in 6 patients. HL stage II B, III, IV and V was registered in 7, 2, 2 and 1 patients, respectively. Hypolipidemic therapy included hypolipidemic diet and Lipanor (Sanofi-Chinoin-Winthrop, France) in a dose 100 mg once a day after evening meal. The course lasted 3 months. Blood serum was examined for concentrations of total cholesterol (CS), triglycerides (TG), CS of HDLP, glucose, uric acid, prothrombin, fibrinogen, alanine and asparagine transaminase, alkaline phosphatase, creatinine, total bilirubin. After 1 month of lipanol treatment mean total CS concentration in the serum fell by 21.9% and remained such for 2-3 months of treatment. 1 month after the drug discontinuation mean concentration of total CS was under the initial one by 4.65%. Mean serum concentrations of TG 1 month after treatment decreased by 41.7%, after 2 months by 48.8%. Mean concentration of HDLP CS after 1 month of treatment rose by 19.2% and by 33.1% after one more month. 1 month after Lipanor discontinuation mean HDLP CS concentration exceeded the baseline level by 16%. Fibrinogen and prothrombin index declined. Hypolipidemic effect of Lipanor varied from case to case.
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PMID:[A trial of the use of the hypolipidemic preparation Lipanor (ciprofibrate) in patients with primary hyperlipidemia]. 877 89

We administered 400 mg of bezafibrate daily to 27 patients with hyperlipidemia for seven moths. Most biochemical parameters remained unchanged, whereas levels of alkaline phosphatase (Al-P)and gamma-glutamyl transpeptidase (gamma-GTP), which are the hepatobiliary enzymes, were significantly decreased. Blood lipid levels were improved. Al-P levels decreased significantly from the baseline level of 174.5 IU/l to 116.7 IU/l (-26.5%) and gamma-GTP levels also decreased from 64.4 IU/l to 34.4 IU/l (-29.5%) (p < 0.001). When we compared the changes in serum lipid levels with those in Al-P and gamma-GTP levels following bezafibrate therapy, we found a slight degree of correlation between changes in gamma-GTP and triglyceride (T-G) levels, but no correlation at all between the changes of Al-P and total-cholesterol (T-cho), T-G or high density lipoprotein cholesterol (HDL-C). A close correlation was observed between both Al-P and gamma-GTP (r = 0.81, p < 0.001). From these results it was suggested that bezafibrate has not only a lipid lowering effect but has a favorable efficacy on the hepatobiliary enzymes.
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PMID:A lipid lowering drug (bezafibrate) has a favorable effect on liver enzymes (Al-P and gamma-GTP). 893 34

We found previously that human bone alkaline phosphatase (AP) was glycated by aseptic incubation with glucose, and partially broken down by reactive oxygen species. In this study, we examined whether selective in vivo glycation of AP molecules occurred in bone tissue, using experimental diabetic rats induced by streptozotocin and spontaneously diabetic rats. Additionally, the effects of hyperlipidemia on bone AP activity were examined. Serum AP activity was significantly elevated after incipient onset of diabetes, and the increased activity originated from the intestinal isozyme. High levels of intestinal AP activity were also observed in rats with hyperlipidemia induced by feeding high-fat or high-fructose chow, but the AP activity in bone tissues was maintained at a constant level. AP activity in bone was reduced after the onset of diabetes. The resulting bone AP molecule bound to an aminophenylboronic acid column, which had affinity for glycated proteins, and contained smaller molecular sizes than the native bone AP. These results suggest that elevated levels of serum AP activity originated from the intestinal isozyme accompanied with hyperlipidemia induced by diabetes. In contrast, the reduced serum levels of AP activity in diabetic rats might be dependent on inactivation of bone AP, which was glycated, followed by partial breakdown of bone AP molecules, possibly due to reactive oxygen species.
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PMID:Reduced alkaline phosphatase activity in diabetic rat bone: a re-evaluation. 997 13

Renal dysfunction is one of the most common and threatening complications in heart transplant recipients. Even if ciclosporin seems to play a central role in inducing renal damage, other factors may concur or predispose to renal injury. In order to identify factors responsible for renal dysfunction, we retrospectively studied a cohort of 114 cardiac transplant recipients during a follow-up period of at least 3 years. The patients had a normal renal function before and 0.5 months after heart transplantation. Doubling of baseline serum creatinine or attainment of serum creatinine steadily above 176.8 micromol/l (2.0 mg/dl) was used as criterion to define the end-point renal dysfunction. A series of clinical and laboratory variables were obtained from the patients' charts at different time intervals, and their prognostic value for the occurrence of renal dysfunction was calculated by Cox proportional hazards models. 23 out of 114 patients reached the end point after a median time period of 21 months. High serum triglyceride, alanine aminotransferase, alkaline phosphatase, ciclosporin, urea, glucose, and hemoglobin levels were shown to be associated with the development of renal dysfunction. Four variables, i.e., triglyceride, ciclosporin, urea, and alkaline phosphatase, had an independent prognostic value. Our results confirm a role for ciclosporin in inducing renal dysfunction and identify hyperlipidemia and an increased plasma urea level as risk factors for renal dysfunction in heart transplant recipients.
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PMID:Risk factors for chronic renal dysfunction in cardiac allograft recipients. 1064 4

Liver transplant recipients have an increased risk for cardiovascular disease because of a high incidence of obesity, arterial hypertension, diabetes mellitus, and hyperlipidemia. Hyperhomocysteinemia has been found to be an important risk factor for cardiovascular disease in large studies. Fasting serum levels of homocysteine were measured in 105 liver transplant recipients, and hyperhomocysteinemia was defined as a fasting serum homocysteine level greater than 13 micromol/L. Patients with versus without hyperhomocysteinemia were compared. The possible association of hyperhomocysteinemia with age, sex, cause of liver disease, time elapsed since liver transplantation, immunosuppressive therapy, folic acid level, liver function test results, renal function, and other cardiovascular risk factors was investigated. Patients with serum homocysteine levels greater than 15 micromol/L were treated with folic acid, 10 mg/d, and serum homocysteine levels were measured again 1 to 3 months later in 10 patients. Hyperhomocysteinemia was detected in 28 patients (27%). In univariate analysis, it was associated with hepatitis C virus infection, treatment with mycophenolate mofetil, and greater serum levels of alkaline phosphatase, gamma-glutamyl transpeptidase, urea, and creatinine. In multivariate analysis, only greater serum levels of creatinine (P =.006) were associated with hyperhomocysteinemia. Treatment with folic acid resulted in a decrease in fasting serum homocysteine levels in 9 of the 10 patients tested (P =.01). Hyperhomocystinemia, associated with renal dysfunction, is a frequent finding in liver transplant recipients. Treatment with folic acid may reduce fasting homocysteine levels.
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PMID:Hyperhomocysteinemia in liver transplant recipients: prevalence and multivariate analysis of predisposing factors. 1098 61

Based on titration microcalorimetry and Caco-2 cell line transfection studies, it has been suggested that the A54T of the FABP2 gene plays a significant role in the assimilation of dietary fatty acids. However, reports were divergent with regard to the in vivo interaction between this polymorphism and postprandial lipemia. We therefore determined the influence of this intestinal fatty acid-binding protein polymorphism on intestinal fat transport using the human jejunal organ culture model, thus avoiding the interference of various circulating factors capable of metabolizing in vivo postprandial lipids. Analysis of DNA samples from 32 fetal intestines revealed 22 homozygotes for the wild-type Ala-54/Ala-54 genotype (0.83) and 10 heterozygotes for the polymorphic Thr-54/Ala-54 genotype (0.17). The Thr-encoding allele was associated with increased secretion of newly esterified triglycerides, augmented de novo apolipoprotein B synthesis, and elevated chylomicron output. On the other hand, no alterations were found in very low density lipoprotein and high density lipoprotein production, apolipoprotein A-I biogenesis, or microsomal triglyceride transfer protein mass and activity. Similarly, the alanine to threonine substitution at residue 54 did not result in changes in brush border hydrolytic activities (sucrase, glucoamylase, lactase, and alkaline phosphatase) or in glucose uptake or oxidation. Our data clearly document that the A54T polymorphism of FABP2 specifically influences small intestinal lipid absorption without modifying glucose uptake or metabolism. It is proposed that, in the absence of confounding factors such as environmental and genetic variables, the FABP2 polymorphism has an important effect on postprandial lipids in vivo, potentially influencing plasma levels of lipids and atherogenesis.
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PMID:The polymorphism at codon 54 of the FABP2 gene increases fat absorption in human intestinal explants. 1148 82


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