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)

Protein-restricted diets are widely used in the dietary management of uremia. These diets are undoubtedly effective in ameliorating many aspects of the uremic syndrome. However, there is no consensus as to whether diets providing less than 0.6 g/kg per day of protein are nutritionally adequate and capable of preventing the wasting syndrome. Wasting is common in the adult patient with renal insufficiency as is growth failure in the uremic child. There is some evidence that wasted patients do less well on hemodialysis and are more prone to infection. Experimental studies in uremic animals point ot diminihsed efficiency of utilization of protein, increased gluconeogenesis from animo acids, and increased catabolism of protein in the fasting state; in addition, the metabolism of a number of individual amino acids is altered in uremia. In view of these multiple abnormalities, it would seem unwise to routinely provide less than the Recommended Daily Allowances of protein. More recent developments, i.e., supplementation of essential amino acids and perhaps alpha keto acids, may provide useful alternatives. One important aspect of dietary management, i.e. prevention of hyperlipidemia, has attracted surprisingly little attention so far. Therapy with protein restricted diets in nondialyzed uremic patients has to compete with other modalities of treatment currently available, i.e., hemodialysis and transplantation, in providing optimal medical rehabilitaiton of the patient.
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PMID:Protein restriction in the conservative management of uremia. 68 83

The patients belonged to three different families and were products of consanguineous marriage. The neurological symptoms and signs in these patients began in infancy or childhood and included gait disturbance, horizontal nystagmus, distention tremor of the hands, muscular wasting and sensory impairment of the hands and legs. CT-scan and/or MRI showed atrophy of the cerebellum. Serum biochemical analyses revealed hypoalbuminemia with hyperlipidemia. There were no abnormalities in the heart, liver, kidney, gastrointestinal tract, or endocrine systems. The autopsy revealed degenerative changes in the spinal cord including posterior column and lateral pyramidal tract, as well as in the peripheral nerves and cerebellar cortex. Although we have speculated that the disease presented here would be a clinical variants of Friedreich's disease, it would make a new clinical entity because there was no report about the association to hypoalbuminemia and hyperlipidemia with spinocerebellar degeneration.
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PMID:[A hereditary ataxia associated with hypoalbuminemia and hyperlipidemia--a variant form of Friedreich's disease or a new clinical entity?]. 129 49

Cancer patients have increased insulin resistance in skeletal muscles and probably also in the liver. The insulin production in response to a glucose challenge is decreased. This is associated with decreased glucose uptake in peripheral tissues and increased gluconeogenesis from amino acids, lactate, and glycerol. The correlation between the insulin response to a glucose challenge and the activities of glycolytic and oxidative rate-limiting enzymes in muscle tissue suggests a common denominator for these metabolic alterations. The most prominent feature in alteration of lipid metabolism is a reduction of body fat, probably dependent on increased lipolysis. The released fatty acids are oxidized outside the tumor mass. Species characteristics may be important for the degree of hyperlipidemia. Wasting of the skeletal muscle mass is caused by decreased protein synthesis and probably increased degradation. Anorexia can induce but not entirely explain this altered protein metabolism. Decreased physical activity may be another important factor for the depressed protein synthesis. Total parenteral nutrition (TPN) improves the muscle protein synthesis. The mechanism behind increased fractional degradation of muscle proteins in vitro is not clear, but it may be coupled to increased cathepsin D activity.
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PMID:Metabolism in peripheral tissues in cancer patients. 680 27

Glucocorticoids, when administered over prolonged periods of time, cause protein wasting, osteoporosis, elevation of total cholesterol, and carbohydrate intolerance. Human GH is a potent anabolic agent known to stimulate protein synthesis and osteoblast activity. Chronic hypercortisolemia is associated with impaired GH secretion. The aim of our study was to evaluate the effects of short term administration of human recombinant GH on bone and fuel metabolism in patients receiving chronic glucocorticoid treatment and with suppressed GHRH-stimulated GH peaks (< 10 micrograms/L). We studied nine nonobese adult patients more than 70 yr of age (seven females and two males; age range, 41-68 yr; body mass index, 26 +/- 1.3 kg/m2) undergoing long term glucocorticoid therapy for nonendocrine diseases. After a 3-day stabilization period in the hospital, several parameters were evaluated in all patients: 1) protein, 2) bone, 3) lipid, 4) carbohydrate metabolism, and 5) immune system function under baseline conditions. At 1800 h on the fifth day of hospitalization, the patients began treatment with a daily sc injection of 0.1 IU/kg (0.037 mg/kg) recombinant human GH (Humatrope, Eli Lilly Co.) for 7 days. GH administration caused a significant increase in nitrogen balance (from -0.12 +/- 0.04 to -0.03 +/- 0.02 g/kg.day; P < 0.05), osteocalcin, carboxy-terminal propeptide of type I procollagen, and carboxy-terminal telopeptide of type I collagen with respect to basal levels. After GH administration, total, high density lipoprotein, and low density lipoprotein cholesterol levels were significantly lowered, and serum triglyceride levels were increased in all patients. Normal blood glucose levels during GH administration were observed in our patients concomitantly with a slight increase in insulin secretion. After GH treatment, the T-helper/T-suppressor cell ratio significantly increased with respect to basal levels (2.5 +/- 0.4 vs. 2.2 +/- 0.3; P < 0.05). Our data suggest that in patients receiving chronic glucocorticoid treatment, GH administration may significantly antagonize several side-effects of long term glucocorticoid administration, such as protein wasting, osteoporosis, and hyperlipidemia.
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PMID:Effects of recombinant human growth hormone (GH) on bone and intermediary metabolism in patients receiving chronic glucocorticoid treatment with suppressed endogenous GH response to GH-releasing hormone. 782

In three patients, a 36-year-old HIV seropositive homosexual man and two women aged 35 and 59 years who had acquired HIV infection through heterosexual contact, signs of lipodystrophy developed after prolonged anti-HIV triple therapy. The observed syndrome is seen after prolonged use of HIV protease inhibitors: it is characterized by peripheral fat wasting, central fat accumulation, hyperlipidaemia and insulin resistance. Typically the subcutaneous fatty tissue disappears resulting in prominent zygomata, veins and muscles and thinning of extremities and buttocks. In addition to abdominal fat accumulation, there have been reports on the occurrence of a dorsocervical fat pad, the so-called buffalo hump. Lipodystrophy caused by protease inhibitors is a risk factor for cardiovascular disease. Recognition of the syndrome is essential for adequate follow-up and possible treatment.
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PMID:[Lipodystrophy and 'buffalo hump' during treatment with HIV protease inhibitors]. 1006 60

The triad of human immunodeficiency virus (HIV) infection, nutritional status and immune function are intimately related, each factor having effects on the others. The dominant effect in this three-way relationship is the effect of HIV infection on nutritional status, an effect which, until the advent of potent anti-retroviral drugs, has been manifest primarily as wasting. Recently, more complex metabolic abnormalities have become apparent, particularly fat redistribution syndromes, hyperlipidaemia and hypercholesterolaemia. For the converse effect, the effect of nutritional state on HIV disease progression, there is good evidence that clinical outcome is poorer in individuals with compromised nutrition. However, the beneficial effects of nutritional support have been more difficult to demonstrate. For macronutrients, effective macronutrient supply improves survival in severely-malnourished individuals and may have beneficial effects in less-severely-affected individuals. Micronutrient deficiencies appear to be involved in modifying clinical HIV disease and may also be associated with enhanced mother-to-child transmission of virus, particularly in developing countries. Intervention trials in this setting are currently under way. In conclusion, the interaction of HIV infection and nutrition is of great importance not just because of the major impact that HIV infection has on nutritional state, but also because strategies to improve nutritional status, both quantitatively and qualitatively, may have a beneficial effect on the clinical and immunological course of the disease.
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PMID:Nutrition and immune function in human immunodeficiency virus infection. 1060 11

The introduction of HAART has changed the nutritional status of HIV patients. In the pre-protease inhibitor (PI) era, more than 60% of HIV-positive persons presented with protein energy malnutrition (PEM) and vitamin and mineral deficit. This caused progressive physical-metabolic wasting (wasting syndrome/cachexia) and increased susceptibility to opportunistic infections and drug toxicity. PEM was a concurrent cause in 80% of deaths attributed to AIDS. Since 1996, the year in which PIs were introduced, the number of patients dying as a result of AIDS has decreased by two thirds, and cachexia is no longer the AIDS terminal phase in developed countries. But different patterns of nutritional status changes have appeared in association with the use of newer anti-HIV therapies and with longer survival of HIV-infected patients. A new clinical and laboratory syndrome--lipodystrophy syndrome--now affects patients receiving PI-based therapy. This syndrome consists of changes in body shape that are caused by an abnormal redistribution of fat. Fat accumulates in the abdominal area (truncal and visceral obesity), in the axillary pads (bilateral symmetric lipomatosis), and in the dorsocervical pads ("buffalo hump," "bull neck") but decreases in the legs, arms, and nasolabial and cheek pads (peripheral lipodystrophy). Hyperlipidemia and insulin resistance are also frequently present (metabolic syndrome X). Pathogenic mechanisms of lipid and fat tissue disturbances are discussed in this article, and the clinical approach to patient management and therapeutic options for lipodystrophy and lipid dysmetabolism is evaluated.
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PMID:Reversal of cachexia in patients treated with potent antiretroviral therapy. 1088 68

Currently available protease inhibitors are associated with development of a group of metabolic disorders. These include a peripheral lipodystrophy syndrome in which there is fat wasting in the face, arms, and legs; fat accumulation in the abdomen, dorsocervical region, and/or breasts (women only); as well as hyperlipidemia, hypercholesterolemia, and insulin resistance. A review of 15 observational studies and case reports shows that the incidence of the peripheral lipodystrophy syndrome increases with time of exposure to protease inhibitors, with a >60% incidence seen after 1 year of continuous treatment. Protease inhibitors are hypothesized to cause this syndrome by impairing conversion of retinoic acid to cis-9-retinoic acid (leading to impaired peripheral fat storage, sequestration of body fat to central adipocytes, and hyperlipidemia) and by inhibiting low-density lipoprotein receptor-related protein (LRP), thus preventing postprandial chylomicron clearance and further contributing to hyperlipidemia. Recent in vitro data suggest that more than one pathway contributes to the lipodystrophy syndrome and that pathways may differ among protease inhibitors. Although the central fat accumulation, hyperlipidemia, and insulin resistance components of this syndrome may reverse after discontinuation of protease inhibitor therapy, it is not known whether complete normalization of fast-wasted body regions is possible. Prospective controlled studies are needed to define whether protease inhibitors currently under development are less prone to produce the lipodystrophy syndrome.
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PMID:Metabolic disorders among HIV-infected patients treated with protease inhibitors: a review. 1112 25

Nutritional alterations are common in HIV infection. Early studies documented weight loss and protein depletion, a finding associated with body cell mass depletion in untreated patients. The application of highly active antiretroviral therapy has led to a decreased incidence of malnutrition, although altered body fat distribution and metabolic alterations, including hyperlipidemia and insulin resistance, are common sequelae. The development of malnutrition is multifactorial and occurs through changes in caloric intake, nutrient absorption, or energy expenditure. Clinically, malnutrition develops as a result of either starvation or cachexia. Other hormonal and endocrinologic alterations include hypercortisolemia and hypogonadism. The rationale for providing nutritional support to AIDS patients is based upon the assumptions that nutrition status can be improved and that such improvements have clinical benefits. The results of hypercaloric feeding studies, including the use of appetite stimulants, indicate that weight gain is possible but that the weight gained is predominantly fat. In contrast, anabolic agents and resistance training exercise have been shown to promote body cell mass repletion and skeletal muscle gain. Cytokine inhibitors also have been evaluated for the treatment of wasting in HIV infection. Development of combination therapies, preventive therapies, and efficient and cost-effective therapies are current tasks in the field.
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PMID:Nutritional alterations associated with HIV infection. 1112 32

Highly active antiretroviral therapy in HIV-1 infected patients is associated with a lipodystrophy syndrome, characterized by wasting of peripheral fat, central adiposity, hyperlipidaemia and insulin resistance. The CT findings are presented and the differential diagnosis is discussed.
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PMID:CT appearances of HIV-related lipodystrophy syndrome. 1138 59


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