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 is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
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PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

Estrogen replacement in menopause should be used for specific symptoms such as ovarian failure, hot flushes, vaginal atrophy, atrophy of the vulva, and atrophic urethritis. The dose should be as low as possible to be effective and perscribed for as short as time as possible, since there are possible risks of uterine cancer, breast cancer, increased blood pressure, gallstones, deep vein thrombosis, and thromboembolism. Estrogens should be administered to provide the maximum benefit with the minimum risk involved. Estrogens should not be given to patients with known contraindications such as: suspected breast or uterine cancer; undiagnosed genital bleeding; Dubin-Johnson syndrome; acute hepatic disease; previous or present thromboembolism; or severe thrombophlebitis. Careful evaluation should be made before administering estrogen to women with uterine myomata, hyperlipidemia, hypercholesterolemia, sevare varicose veins, chronic hepatic dysfunction, diabetes mellitus, porphyria, or severe hypertension.
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PMID:Estrogen replacement in the menopause. 39 Apr 56

The present study provides no evidence that the prevalence of gallstones is increased in patients with hyperlipidemia. During the first year of treatment with clofibrate, the incidence of new gallstones appears to increase 8-fold. Cholestyramine, in doses of 16 g per day, does not seem to increase the incidence of stones, either when given alone or with clofibrate. Further studies on the cumulative risk of clofibrate and the long-term effect of clofibrate on biliary lipid composition are necessary to adequately define the risk/benefit ratio of this medication--with or without bile acid sequestrants. It is highly desirable to ascertain whether the concurrent administration of agents such as chenodeoxycholic or ursodeoxycholic acids could beneficially affect bile lipid composition and hence protect against gallstone formation during the initial period of clofibrate treatment.
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PMID:Prevalence of gallstones in hyperlipidemia and incidence during treatment with clofibrate and/or cholestyramine. 75 1

Studies were carried out to determine effects of combined chemotherapy in patients with hyperlipidemia. In one study, 14 patients were treated first with colestipol and then with the combination of colestipol and clofibrate. In a second study, six patients were given clofibrate followed by addition of phytosterols. The following measurements were made in most patients: (1) plasma lipid concentrations, (2) fecal excretions of neutral steroids and bile acids, and (3) lipid composition of gallbladder bile. In six patients of the first study, hepatic secretion rates of biliary lipids and pool sizes of bile acids were also estimated. In the first study, colestipol alone caused a marked increase in fecal bile acids that resulted in a sizable decrease in plasma cholesterol concentrations (average 21 percent). In several patients, however, triglycerides were increased somewhat by colestipol. Despite interruption of the enterohepatic circulation of bile acids, the bile acid pool was not reduced, since a compensatory increase took place in bile acid synthesis. Also, except in one patient who developed gallstones following institution of colestipol, saturation of gallbladder bile with cholesterol was not markedly increased by this drug alone. Addition of clofibrate frequently produced a further decrement in plasma cholesterol, and the mild hypertriglyceridemia induced by colestipol was reversed. However, colestipol plus clofibrate usually caused a striking increase in saturation of gallbladder bile. Previous studies have shown that clofibrate causes a flux of cholesterol from tissue pools by simultaneously decreasing cholesterol synthesis and increasing its excretion. To further increase cholesterol excretion, phytosterols, which block cholesterol absorption, were added to clofibrate in the second study. Although phytosterols did not cause a further reduction in plasma cholesterol in these particular patients, they nevertheless greatly enhanced cholesterol excretion.
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PMID:Colestipol, clofibrate, and phytosterols in combined therapy of hyperlipidemia. 83 72

Pancreatitis occurring in late pregnancy and in the puerperium has been documented as an entity unrelated to cholelithiasis or hyperlipidemia. Canine pancreatic exocrine function has been studied during pregnancy and the puerperium. Pancreatic secretion was evaluated in eight pregnant female mongrel dogs prepared with Thomas duodenal and gastric fistulae, during pregnancy (corresponding to the third trimester in humans), during the puerperium, and several months after whelping. Basal secretion (volume and HCO3) was increased during pregnancy and the puerperium. The response to exogenous secretin (submaximal and maximal) was unchanged during pregnancy but decreased in the puerperium. Resting enzyme output was increased during pregnancy and the puerperium; the responses to cholecystokinin-pancreozymin during pregnancy were even more profoundly increased. Although the mechanism is speculative, these alterations in pancreatic function might contribute to the development of pancreatitis in pregnancy and the puerperium.
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PMID:Pancreatic exocrine secretion during and after pregnancy. 111 67

We have characterized the clinical and biochemical features of three siblings of a kindred with severe hypertriglyceridaemia due to apolipoprotein C-II (apo C-II) deficiency caused by the mutation described as apo C-IIHamburg. The clinical syndrome is characterized by recurrent pancreatitis in two of three affected individuals, with discrete hepatosplenomegaly in all three patients and cholelithiasis in one. Eruptive xanthomas and lipemia retinalis were absent. Plasma lipoproteins were characterized by fasting chylomicronaemia, reduced low density lipoproteins (LDL) and low high density lipoproteins (HDL). The marked hypertriglyceridaemia could be corrected promptly by infusion of normal plasma. Apolipoprotein C-II (apo C-II) levels in homozygotes were very low (0.01 mg dl-1), and mean apo C-II levels in heterozygotes were lower (2.08 +/- 0.11 mg dl-1) than in normal family members (3.38 +/- 0.75 mg dl-1). Lipoprotein lipase and hepatic triglyceride lipase activities in post-heparin plasma were normal. Zonal ultracentrifugation revealed a marked increase in triglyceride-rich lipoproteins and reduced LDL and HDL. LDL consisted of two fractions with higher hydrated density of the main fraction compared with normals with a trend to normalization on a fat-free diet. The molecular defect in the apo C-II Hamburg gene has been previously identified as a donor splice site mutation in the second intron. This leads to abnormal splicing of the apo C-II Hamburg mRNA and apo C-II deficiency in plasma. The mutation causes the loss of an HphI restriction enzyme site present in the normal apo C-II gene.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein C-II deficiency syndrome due to apo C-IIHamburg: clinical and biochemical features and HphI restriction enzyme polymorphism. 134 86

Laparoscopic cholecystectomy is increasingly being used in adults with gallbladder disease. Despite the exponential increase in the number of laparoscopic cholecystectomies performed in adults, there are very few reports of its use in children. It is thought that gallstone disease is rare in childhood. Since the introduction of ultrasonography, it is used almost routinely for evaluating children with abdominal pain, and cholelithiasis is being increasingly recognized in children. Since the beginning of 1991 we evaluated 7 children for biliary colic, and on sonography gallstones were demonstrated in all of them. 1 boy also had thalassemia and another hyperlipidemia; the other 5 developed symptoms of biliary colic without any history of hematological or other disease. 5 underwent laparoscopic cholecystectomy without complication. In the other 2 laparotomy was performed. In 1 suspected damage to the common bile duct during laparoscopy required direct visualization, but no damage was found. In the other, no gallbladder was identified on laparoscopy; laparotomy confirmed the diagnosis of congenital agenesis of the gallbladder with several technical modifications. We found laparoscopic cholecystectomy to be both safe and effective in children. Its advantages include shorter hospitalization, decreased postoperative discomfort and a much shorter interval between operation and return to normal activity.
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PMID:[Laparoscopic cholecystectomy in children]. 138 28

Hepatobiliary characteristics of untreated obese patients and those of patients reducing weight through very-low-calorie diets (VLCDs) are reviewed. In untreated obesity, hepatobiliary abnormalities are prevalent. Fatty change is common and may be related to insulin resistance. Moreover, portal inflammation and fibrosis are prevalent findings, also in the absence of alcohol abuse. The liver plays a key role in the hyperinsulinism and hyperlipidemia, and hepatic drug metabolism is influenced by enhanced glucuronidation and sulphatation. Predisposition to gallstone formation can be ascribed to increased biliary cholesterol secretion in concert with changed nucleating factors and altered gallbladder motility. Weight loss by VLCD reduces fatty change but may induce slight portal inflammation and fibrosis. Insulin resistance and pharmacokinetic abnormalities regress. During VLCD the risk of gallstone formation is markedly increased. The deleterious effects described of a rapid weight loss should draw some attention to the liver and biliary tract during VLCD treatment.
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PMID:Liver and gallbladder disease before and after very-low-calorie diets. 161 89

From 1981 to 1990, 14 of 70 patients hospitalized at our institution for severe acute pancreatitis were selected to undergo percutaneous drainage of pancreatic abscess, under computed tomographic (CT) scan guidance. Pancreatic abscess was defined, on contrast-enhanced CT scan, as an infected fluid collection without pancreatic necrosis. There were nine men and five women, ranging in age from 28 to 46 years. The main cause of pancreatitis was alcohol abuse (eight patients). Other causes were gallstones (two patients), hyperlipidemia (two patients), postoperative (one patient) and one unknown. Ranson criteria were available in ten patients and ranged from three to six. Percutaneous drainage was performed as the primary treatment in 13 patients and for removal of a residual collection postoperatively in one patient. In two critically ill patients, percutaneous drainage was performed as a temporizing measure. In 12 patients with well-limited hypodense collections, percutaneous drainage was expected to result in the definitive cure of the abscess. Pigtail drains (No. 14F), were inserted using local anesthesia and CT scan guidance. Two patients had two drains and 12 patients had only one drain. Two patients were definitively cured by percutaneous drainage and all other patients were operated upon for removal of infected necrosis. In this study, the lack of accuracy of contrast-enhanced CT scan in the diagnosis of peripancreatic necrosis is highlighted and that percutaneous drainage has a better efficiency in the treatment of residual collections postoperatively than as a primary treatment of infected fluid collections is illustrated.
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PMID:Failure of percutaneous drainage of pancreatic abscesses complicating severe acute pancreatitis. 173 73

Gemfibrozil is frequently used for lipid-lowering in familial combined hyperlipidaemia (FCHL) and in other forms of combined hyperlipidaemia. This therapy increases biliary cholesterol saturation, enhancing the risk for gallstone formation. Furthermore, in hypertriglyceridaemia, LDL cholesterol levels often tend to rise. We have explored the possibility that addition of a low dose of cholestyramine to gemfibrozil therapy obliterates these phenomena. Eighteen gallstone-free patients with definite (n = 5) or probable (n = 10) FCHL, or combined hyperlipoproteinaemia (n = 3) were randomized to a 6 week treatment with gemfibrozil, 600 mg b.i.d., or gemfibrozil 600 mg b.i.d. plus 4 g cholestyramine o.d. After 6 weeks the patients were crossed over to the alternative treatment. Plasma lipoproteins and biliary lipids were determined at baseline and at the end of each period. Institution of gemfibrozil treatment resulted in a decrease in plasma cholesterol by 15% (P less than 0.05) and in plasma triglycerides by 47% (P less than 0.05); HDL cholesterol increased by 18% (P less than 0.05). Addition of cholestyramine further decreased plasma and LDL total cholesterol by 9% (P less than 0.05). Total triglycerides and HDL cholesterol did not change. Gemfibrozil treatment was associated with a rise in the relative biliary concentration of cholesterol from 5.6 +/- 0.4 to 6.9 +/- 0.5 molar percent (P less than 0.01), and a parallel decrease in the relative concentration of bile acids, resulting in an increased cholesterol saturation of the bile, from 77 +/- 5 to 90 +/- 6% (P less than 0.05). This change was not observed during the combined therapy (mean cholesterol saturation, 82 +/- 4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gemfibrozil in familial combined hyperlipidaemia: effect of added low-dose cholestyramine on plasma and biliary lipids. 190 37


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