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)

In most cases, primary liver carcinoma in tropical areas remains an hepatoma. The high incidence of this malignant tumor of the liver in some regions, and especially in black Africa, is still unexplained. As compared with the form found either in the European or in the North-African, this hepatoma shows special features since it occurs in younger people (35 years), follows a bursting-out course and is precipitously associated not to an alcoholic cirrhosis but to a post-hepatitic one. An humoral syndrome leading to a presomptive diagnosis consists of hypoglycemia, hypercholesterolemia, hyperlipemia, and high blood level of alcaline phosphatases. In 85% of the cases, these tumors secrete an alpha fetoprotein determined by radioimmunoassay. A major etiologic factor is the oncogenous activity of hepatitis virus B which could be either an induction factor or a "co-factor" which would initiate, facilitate or increase the activity of the carcinogen. In this respect, aflatoxin has to be regarded as a "co-factor" too. The best treatment, when it is possible, is an exeresis carried out through a partial hepatectomy. If such a surgical intervention is unadvisable, chemotherapy is the only possibility. Immunization against viral hepatitis has raised hope for the prophylaxis of hepatoma. But it will not be possible to evaluate it before the year 2.000.
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PMID:[Primary liver cancer in the tropical environment. Classical and current data]. 619 92

1. A relationship is established between different doses of intraperitoneally injected streptozotocin (SZ) and the degree of hyperglycemia and hyperlipemia. 2. Changes in serum level of glucose, cholesterol, triglycerides and NEFA were determined after intraperitoneal administration of three different doses (55 mg, 85 mg and 125 mg/kg body weight) of SZ. Cholesterol level was significantly (P less than 0.001) elevated after 72 hrs only in the animals which received 85 mg/kg and 125 mg/kg SZ. 3. Dose dependent changes in NEFA and triglycerides could be observed after 24 hrs of SZ administration. 4. Diabetic animals consistently showed triphasic blood sugar response, initial hyperglycemia at 5-7 hrs, profound hypoglycemia in between 8-12 hrs and finally an irreversible hyperglycemic state by 24 hrs and onwards. 5. Liver and muscle glycogen were continuously decreased except a significant rise at 12 hrs coinciding with hypoglycemic phase. During the experimental period SZ treated rats continuously lost weight, while control animals progressively gained weight. In summary these changes indicated that diabetogenicity is dose dependent and the severity can be judged by elevated lipid metabolites.
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PMID:Dose dependent alteration in lipid and carbohydrate metabolites in streptozotocin induced diabetic rats. 621 69

Glycogen storage disease type Ib has all the clinical manifestations of glycogen storage disease type Ia such as hepatomegaly, growth retardation, bleeding tendency, hypoglycemia, hyperlactacidemia, hyperuricemia, hyperlipidemia, impaired platelet function plus neutropenia. The overall glucose-6-phosphatase activity in disrupted microsomes from liver is normal whereas glucose-6-phosphate translocase, the first enzyme in the glucose-6-phosphate transport system is absent. There is no glucose-6-phosphatase activity in vivo. Recent results show that in granulocytes the glucose-6-phosphate-dependent hexosemonophosphate-shunt is impaired.
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PMID:Glycogen storage disease type Ib. 631 72

Type IB Glycogen storage disease (GSD) is a new variant of type I Glycogen storage disease. It is characterized by same clinical findings: hepatomegaly, fasting hypoglycemia, hyperlipidemia, hyperuricemia, lactic acidosis, renal enlargement, short stature; but it distinguish for normal glucose-6-phosphatase hepatic activity in vitro. The involvement is in G-6-P transport system. Recently has been described in some patients with GSD IB, neutropenia and defective neutrophil mobility. In this report the authors described two family cases of GDS IB that one characterized by severe neutropenia.
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PMID:[Neutropenia in glycogenesis I B]. 659 20

380 diabetic patients with hyperlipidaemia and undergoing treatment with sulphonylureas or insulin were given 200 mg bezafibrate t.i.d for 3 months after a control period of 4 weeks. After cessation of treatment a follow-up examination was performed a further 4 weeks later. 194 treatment centres took part in the investigation. Total cholesterol fell by 17%, triglycerides by 36% and HDL-cholesterol rose by 15% during the treatment period. In addition, a glucose-lowering effect was seen which led to a definite improvement in the control of diabetes both with glibenclamide and with insulin. The degree of glucose reduction was most marked in moderately or poorly controlled diabetics. There was no correlation between the triglyceride reduction and the glucose reduction. After cessation of bezafibrate treatment the cholesterol, triglyceride and fasting glucose increased again and the HDL-cholesterol diminished. However, they did not reach pretreatment values. Bezafibrate was well tolerated, hypoglycaemia or hypoglycaemic reactions were not observed.
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PMID:[Improvement in diabetes control by treatment with bezafibrate]. 674 68

Deficiency of glucose-6-phosphatase in Type I glycogen storage disease (GSD) results in hypoglycemia and excessive accumulation of glucose-6-phosphate. As a result, lactic acid, uric acid, and lipids are formed as end-products. The formation of these metabolites are discussed with an emphasis on monitoring therapeutic progress. In addition, hyperlipidemia and associated changes in apolipoproteins are considered as indices of the clinical course.
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PMID:Secondary metabolic changes in von Gierke's disease (Type I glycogen storage disease). 675 28

Individuals with type Ia glycogen storage disease (glucose-6-phosphatase deficiency) frequently develop hepatic adenomas. Potential complications involving these adenomas include malignant transformation and hemorrhage. Five of 9 patients with this disease had evidence of hepatic filling defects on radionucleotide liver scan when first evaluated at our hospital. Dietary therapy aimed at preventing hypoglycemia was begun in 7 of the 9 patients. Prevention of hypoglycemia resulted in the correction of all of the metabolic abnormalities (lactic acidosis, hyperlipidemia, hyperuricemia, and growth retardation). Treatment also corrected the marked elevation in plasma glucagon concentrations. A disappearance of the hepatic lesions occurred in 2 of the treated patients, and a marked reduction in size of the adenoma occurred in the third patient. The hepatic filling defects remained present in the two untreated patients. None of the affected patients receiving dietary therapy have developed hepatic adenomas. One of these patients is now 22 yr old and has received dietary therapy for 7 yr. Early dietary therapy seems to be effective in preventing development of adenomas as well as inducing their resolution.
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PMID:Regression of hepatic adenomas in type Ia glycogen storage disease with dietary therapy. 694 8

Four Asian babies presenting with type I glycogen storage disease during the early weeks of life are described. In one child the symptoms, metabolic acidosis, and hypoglycaemia were so easily controlled that the diagnosis was not entertained, leading to a late diagnosis. In another child the diagnosis was reached only by investigation of a fortuitously detected hyperlipidaemia. The 3 babies in whom early treatment was started are thriving, and in one, the liver histology was so normal that doubt was cast on the diagnosis initially.
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PMID:Glycogen storage disease (type I) presenting in the neonatal period. 695 21

Optimal control of diabetes should achieve not only euglycemia and normal levels of glycosylated hemoglobin but also absence of the reversible concomitants of diabetes such as red cell rigidity, hyperlipidemia, increased capillary permeability, enlargement of the kidneys, proteinuria, etc. Unfortunately, in most patients consistent euglycemia cannot be assured even with two daily injections of insulin. However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia.
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PMID:Parameters of good control in diabetes mellitus. 699 74

Glucose Tolerance Factor (GTF) is synthesized in vivo from absorbed dietary chromium, and acts as a physiological enhancer of insulin activity, binding to insulin and potentiating its action about three-fold. Since GTF is well absorbed orally, the development of sufficiently concentrated and stable supplementary sources of this agent may enable convenient and physiologically appropriate pharmacological modulation of insulin activity. A review of the numerous physiological actions of insulin suggests a number of therapeutic applications for GTF, in such diverse ailments as diabetes mellitus, hyperlipidemia, reactive hypoglycemia, obesity, cancer, protein malnutrition or malabsorption, endogenous depression, Parkinsonism, hypertension and cardiac arrhythmias. GTF supplementation may also have value in preventive medicine.
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PMID:The therapeutic potential of glucose tolerance factor. 700 27


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