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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the first experiment, rats fed diet containing Phenoclor DP6 at a level of 100 ppm (wet weigh) were sacrificed after 1, 3, 8, 15 and 30 days of treatment. Metabolic alterations such as enlarged liver, increased protein and lipid liver contents and hyperlipemia were established within 8 days. The glucid metabolism and muscle metabolic parameters show a low sensibility to DP6 treatment. In the second experiment, rats fed diet containing Phenoclor DP6 (100 ppm) for 15 days were subsequently removed from the experimental diet and placed on control diet. The metabolic alterations described above disappear within 52 days after removal DP6 diet, although the remaining liver PCB stays elevated. These data attest the early effect of DP6 exposure in rats and the reversibility of induced metabolic alterations.
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PMID:[Effect of polychlorinated biphenyls in the rat. IV - Metabolic alterations and residual effects of DP6 dietary exposure (author's transl)]. 10 29

A female patient with the following symptoms has been observed: complete absence of subcutaneous fat on the arms and legs, well developed adipose tissue on the trunk and face, severe hyperlipidemia, eruptive xanthomas, insulin resistant diabetes mellitus with lack of ketoacidosis, hepatomegaly and elevated basal metabolic rate. The patient thus exhibited all characteristics of lipatrophic diabetes (Lawrence type of diabetes). The mother and a sister of the patient were found to have the same peculiar appearance and a slight hyperlipidemia but no diabetes mellitus. The combination of this type of partial lipodystrophy with severe hyperlipidemia, insulin resistant diabetes mellitus without ketoacidosis and elevated basal metabolic rate was further observed in 2 unrelated patients without known familial occurrence. Thus partial lipodystrophy of the extremities is another, previously undescribed, syndrome associated with the Lawrence type of diabetes mellitus. In the 1 family the syndrome of lipodystrophy and hyperlipidemia is dominantly inherited. Besides the autosomal recessively inherited syndrome of congenital generalized lipodystrophy there is a heterogenous group of dominantly inherited syndromes with various types of lipodystrophy.
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PMID:Lipodystrophy of the extremities. A dominantly inherited syndrome associated with lipatrophic diabetes. 17 Jan 90

Experimental models for hyper-beta-lipoproteinemia were established in rats and the effects of certain hypolipidemic drugs were studied with these models. In the hyperlipemia induced in rats by feeding a high cholesterol diet, Y-9738 [ethyl 2(4-chlorophenyl)-5-ethoxy-4-oxazoleacetate] produced a dose-dependent reduction of serum cholesterol: such hypolipidemic activity was estimated to be about 7 times as great as that of clofibrate. On the other hand, clofibrate induced hepatomegaly at 100 mg/kg, whereas Y-9738 did not at this dosage, which is about 10 times the effective dose. Hyperlipemia induced by high cholesterol and thiouracil was characterized by increased beta-lipoprotein (heparin-calcium and disc electrophoresis). In this model, Y-9738 showed a dose-dependent lowering effect on beta-lipoprotein cholesterol with a marked decrease in the beta/alpha lipoprotein ratio. A tendency was noted for alpha-lipoprotein to be increased. In contrast, clofibrate exerted no effect on this hyper-beta-lipoproteinemia. These results suggest that the above models may be of value in exploring hyper-beta-lipoproteinemia and that Y-9738 may be more useful than clofibrate in the therapy of hyperlipemia.
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PMID:Experimental hyper-beta-lipoproteinemia and its amelioration by a novel hypolipidemic agent. 20 4

Of three siblings affected with cholesterol ester storage disease, two died at ages 7 and 9 years, respectively, with hepatic scarring and portal hypertension. Lipid storage was documented in both patients, as were esophageal varices and aortic plaques in the older child. The third affected sibling, followed to 13 years of age, has hepatomegaly, hyperlipidemia, short stature, adrenal calcification, and acid lipase deficiency. Leukocyte extracts demonstrated deficiency of acid lipase in this patient. This autosomal recessive condition may be allelic with Wolman disease with a more malignant course in this family than in most reported cases.
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PMID:Cholesterol ester storage disease: clinical, biochemical, and pathological studies. 85 64

Nephrotic mixed hyperlipidemia may be associated with accelerated coronary artery disease. To investigate the response of experimental nephrotic hyperlipidemia to therapy, a 2(4) factorial study of sodium clofibrate and beta-benzalbutyrate, halofenate and oxandrolone (250, 150, 100 and 10 mg/kg/day, respectively) was carried out. Nephrotic syndrome was induced by a single i.p. injection of puromycin aminonucleoside (90 mg/kg) in 80 female white rats of average weight 160 g. Oxandrolone proved to be significantly hypotriglyceridemic in combined therapy (average fall, 38%; P less than .05), and also lowered serum total cholesterol and phospholipid concentrations (23% and 21% falls, P less than .01) and less than .05), due largely to synergistic interactions with clofibrate-like drugs. Hypocholesteremic effects (23 and 22% average falls) were also significant for halofenate (P less than .01) and clofibrate (P less than .05) . Serum triglyceride levels actually rose significantly (P less than .05) with drug combinations containing beta-benzalbutyrate. Clofibrate and its analogs (halofenate and beta-benzalbutyrate) produced significant hepatomegaly (mean responses of +18, +18 and +10%, respectively) whereas oxandrolone produced significant hepatic shrinkage (-10%)(P less than .05). Secondary effects (drug interactions) were also found; hypotriglyceridemic synergism (effects more than additive) occurred between oxandrolone and clofibrate or its analogs (P less than .05), whereas antagonism (effects less than additive) was observed within the clofibrate-like group (P less than .01 or less .05).
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PMID:Efficacy and interactions of oxandrolone, halo-fenate and clofibrate in a factorial study on experimental acute nephrotic hyperlipidemia. 117 Dec 21

A familial syndrome of partial lipodystrophy inherited as a dominant trait is reported. Subcutaneous fat loss was confined to the extremities and trunk. Diabetes mellitus, hyperlipidemia, hepatomegaly and renal disease were very prevalent in this family. Metabolic studies were performed on 3 members. In vivo tests suggested that the remaining fat tissue responded normally to stimulators and inhibitors of lipolysis. In vitro incubation of the dystrophic fat tissue of one patient suggested that the intracellular pathways of lipid and glucose metabolism were normal. The pattern of subcutaneous loss of adipose tissue observed in this family may be due to sympathetic nervous system overactivity of certain non-contiguous dermatomes.
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PMID:Metabolic studies in familial partial lipodystrophy of the lower trunk and extremities. 120 25

The macroscopic and microscopic findings of a case of Zieve's syndrome are described (fatty liver, icterus, hyperlipemia and hemolytic anemia in chronic alcoholism). The outstanding macroscopic finding is milky turbidity of the blood in arterial and venous vascular channels as well as hepatomegaly and anaemia of internal organs. A prominent feature of the histological picture is the high-grade lipaemia of the large and small vessels (arteries and veins), capillary occlusions resembling fat embolism in all organs and severe diffuse fatty metamorphosis of the liver. Circulatory disorders and the cause of death are discussed.
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PMID:[Morphological findings in Zieve's syndrome (author's transl)]. 121 21

Report of a 10-year-old boy with congenital hypoplasia of the intrahepatic bile ducts, the socalled MacMahon-Thannhauser-Syndrome. The patient had been suffering from a varying degree of jaundice since his 2nd day of life and from pruritus since his 21st month of life. Furthermore, he had hepatomegaly, a systolic cardiac murmur, hypogenitalism, retarded growth, and finally hypertension. Transitory xanthomas existed between 1 3/4 and 2 3/4 years of age. Signs of persistent intrahepatic cholestasis was manifested by increased levels of bilirubin and bile acids in serum as well as raised activities of leucine aminopeptidase, gamma-glutamyl transpeptidase and alkaline phosphatase. Pathological values of serum glutamic dehydrogenase pointed to a persistent destruction of liver cells. Without treatment, the activities of vitamin K dependent clotting factors were decreased. Cholesterol, phosphatides and triglycerides in serum were increased and lipoprotein-X was detectable. Aortography revealed stenosis of both renal arteries. An exploratory laparotomy and 5 liver biopsies led to the diagnosis of hypoplasia of the intrahepatic bile ducts. Therapeutic trials with steroids and the anion exchange resin "cholestyramine" were ineffective. Phenobarbital relieved the pruritus. Parenteral administration of fat soluble vitamins restored the activity of vitamin K dependent clotting factors to normal. The high blood pressure fell significantly due to treatment with adelphan. The etiology of hypoplasia of the intrahepatic bile ducts is unknown. It may be a malformation or an obliteration secondary to inflammation. In our patient, narrowing of the renal arteries, increase of plasma-renin activity and hypertension were probably secondary to hyperlipidemia. It has been suggested that hyperlipemia secondary to cholestasis may be due to a disturbance of lipoprotein metabolism. A review of reports on 118 patients suffering from intrahepatic bile ducts hypoplasia is included.
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PMID:[Hypertension and bilateral stenosis of the renal artery associated with congenital hypoplasia of the intrahepatic bile ducts (author's transl)]. 124 84

A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions.
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PMID:Alcoholism-induced bone necrosis. 151 11

Dietary intake of technical hexachlorocyclohexane (HCH) by albino mice for 2 weeks (at 400 and 800 ppm) resulted in hyperlipemia. Significant increase in triglycerides, phospholipids and cholesterol fractions of blood was observed in these animals. Dietary intake of gamma-isomer of HCH for 2 weeks (at 200 ppm) did not have any effect on blood lipid profile, but at 400 ppm level produced higher contents of phospholipids and cholesterol. The hepatomegaly produced by dietary technical HCH or gamma-HCH was not accompanied by fatty metamorphosis of liver. Hypertriglyceridemia caused by HCH was accompanied by lower triglyceride levels in liver, suggesting a possible higher rate of secretion from liver.
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PMID:Dietary hexachlorocyclohexane induced changes in blood and liver lipids in albino mice. 169 97


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