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)

Certain fractures and/or dislocations of the femoral head are known to cause arterial injury and result in post-traumatic osteonecrosis. However, the more complex etiology of non-traumatic osteonecrosis is multifactorial and includes chemotherapy, radiotherapy, thermal injuries, and especially coagulopathies, which are now commonly observed in these patients. Intravascular coagulation with fibrin thrombosis begins in the capillaries and sinusoids of the intraosseous microcirculation, and residual venous thrombosis is more likely to occur if there is coexistent hypofibrinolysis. Coagulopathies are intermediary events, which are always activated by some underlying etiologic risk factor(s). Conditions capable of triggering intravascular coagulation include familial thrombophilia (resistance to activated protein C, decreased protein C, protein S, or antithrombin III, and hyperhomocystinemia), hyperlipemia and embolic lipid (alcoholism and hypercortisonism), hypersensitivity reactions (allograft organ rejection, immune complexes, and antiphospholipid antibodies), bacterial endotoxic (Shwartzman) reactions and various viral infections, proteolytic enzymes (pancreatitis), tissue factor release (inflammatory bowel disease, malignancies, neurotrauma, and pregnancy), and other thrombophilic and hypofibrinolytic disorders. Currently known risk factors for non-traumatic osteonecrosis of the femoral head are described briefly in this review article.
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PMID:[Epidemiological risk factors for non-traumatic osteonecrosis]. 1087 31

An antilipidemic effect of poseidonol was tested in 123 patients with ischemic heart disease, stable angina of effort (II-III functional class), 40 patients with secondary pyelonephritis and 40 patients with chronic hepatosis-hepatitis associated with chronic alcoholism or diabetes mellitus. The patients had also hyperlipidemia. A positive effect of poseidonol was established: cholesterol content fell by 25.4, 20.6 and 18.7%, respectively; triglycerides level decreased by 63, 42 and 21.4%, respectively; B-lipoproteins fell by 55.5, 36.9 and 13.1%, respectively. High density lipoproteins rose by 40.2, 27 and 69.9%, respectively. No adverse effects either on the liver or kidney functions were observed.
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PMID:[Poseidonol in the treatment of patients with hyperlipidemia]. 1122 Aug 93

Immigration from the former Soviet Union has been increasing. In 1990, there were 454,000 Russian immigrants living in the United States. Lifestyle habits prevalent in Russia, including smoking, alcoholism, and little preventive health, are compelling medical and economic reasons to understand the health status of this population. This study identified a cohort of Russian-born subjects living in Denver to characterize their cardiovascular risk profile. Using a risk assessment questionnaire, 204 Russian immigrants were screened. Seventy-one percent had Medicaid insurance; 14 percent were medically indigent. Those aged 55 to 64 years had a higher prevalence of hyperlipidemia (p < 0.04) and hypertension (p < 0.03) than U.S. counterparts; those age 20 to 34 and 65 to 74 years had a higher prevalence of hypertension (p < 0.00001). Almost half of the participants had two or more cardiac risk factors. Cardiac risk factor identification and intervention programs may help to reduce the health care costs for these patients.
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PMID:Russian immigrant cardiovascular risk assessment. 1137 Jan 89

Benign Symmetric Lipomatosis (Madelung's disease) is a rare disease, characterized by massive fatty deposits in the neck, the shoulders, and the upper extremities. The deformity is associated with chronic alcohol use, malignant tumors of the upper airways, neuropathy, diabetes mellitus, hyperlipidemia, and other metabolic disorders. Although the deformity is prone to recurrence, surgical removal via lipectomy or liposuction provides the only way of palliation. This paper describes the treatment of a 51-year-old man with a history of alcoholism and liver cirrhosis. He reported masses in his cervical and facial regions that had gradually enlarged over a period of 6 years. He also developed respiratory symptoms due to the fatty compression of his upper airways. Our experience with ultrasound-assisted liposuction for the palliative treatment of this disease is reported.
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PMID:Ultrasound assisted liposuction for the palliative treatment of Madelung's disease: a case report. 1142 8

Osteonecrosis has been increasingly associated with HIV disease throughout the 1990s, and the incidence appears to be rising. The hip is most commonly involved and often bilaterally. Although anecodotal reports suggest an association between osteonecrosis and highly active antiretroviral therapy, controlled epidemiologic studies do not support a direct link. Many patients with osteonecrosis have established risk factors, some of which may be related to HIV disease or its therapy, including corticosteroid use and hyperlipidemia. Alcoholism, hypercoagulability, megesterol acetate use, immune reconstitution, and other factors may also contribute. Plain radiographs and magnetic resonance imaging are the cornerstones of diagnosis. Management is dependent on the stage of bone disease and ranges from observation to total joint arthroplasty. Clinicians may help to prevent HIV-associated osteonecrosis by encouraging patients to limit their exposure to the established risk factors for the disease.
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PMID:Osteonecrosis in HIV disease: epidemiology, etiologies, and clinical management. 1247 64

Ethanol toxicity on liver is a function of duration of alcoholism, amount of daily intake of alcohol and patient's nutrition. The threshold of alcohol toxicity on the liver is about 40 g of ethanol daily in men and 20-30 g in women, however liver cirrhosis develops in no more than 8-20% of patients exceeding this values. Ethanol is oxidized in the liver to acetaldehyde--a compound considerably more toxic than ethanol itself. Despite small amount of alcohol dehydrogenase (ADH) found in gastric mucosa, the metabolism of ethanol in this site may have an important hepatoprotective effect. The oxidation of ethanol is associated with a change of hepatocyte redox homeostasis, which leads to a number of metabolic disorders such as lactic acidosis, hyperlipidaemia and hyperuricaemia. Chronic ethanol consumption does not influence ADH activity, but has a profound stimulatory effect on microsomal enzymes, in particular cytochrome CYP2E1. This fact is responsible for development in alcoholic liver associated with rise of oxygen consumption, excessive production of free radicals and increased metabolism of ethanol, vitamin A and testosterone. Ethanol and acetaldehyde have a deleterious effect, both the direct and indirect, on hepatocytes e.g., generating radical oxygen species and damaging intestinal mucosal barrier. Cellular oxidative stress that is caused by both an excess of free radicals and the antioxidatives' deficiency (glutathion, vitamin E, phosphatidylcholine), may be the principal factor responsible for progression of alcoholic liver disease. Among other factors accelerating alcohol-related liver lesion there are certain drugs, high fat diet, infection with HCV and genetic factors (female sex, enzymatic polymorphic forms of ADH and ALDH, hemochromatosis). Great importance in pathogenesis of necrotic and inflammatory hepatic events is being attributed to portal endotoxaemia and cytokines induced within the liver, in particular TNF-alpha and interleukin 8. These cytokines play a key role in development of alcoholic hepatitis, which clinical severity ranges from subclinical to fatal forms. Apart from abstinence, the treatment of alcohol liver disease is based on hyperalimentation, since alcoholism is generally associated with protein malnutrition. In severe forms of alcohol hepatitis corticosteroids are recommended.
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PMID:[Alcoholic liver disease]. 1290 Dec 71

The human biological mechanisms show a predictable clinical variability in time, which has allowed a deeper reevaluation of present-day medical practices, regarding the circadian rhythm (CR) and the mechanisms that produce the supported variations in all biological levels. We have made a study aiming to relate the CR and onset of the neurological clinic situation due to the encephalic vascular lesion, correlating with modifying risk factors. Fifty three patients were studied, 50,94% female (n=27) and 49,50% male (n=26), at average age 66.4 years old. Four intervals of six hours each (0-6; 6-12; 12-18; 18-24) were used to analyze the frequency of the ictus and the incidence in each interval. We found an incidence of 6(11.32%) patients in the 0-6 hs interval; 21 (39.62%) patients in the 6-12 hs interval; 10(18.86%) patients in the 12-18 hs interval; 16 (30.18%) patients in the 18-24 interval. A correlative study with the risk factors has shown that arterial hypertension [(81.25%)] and smoking habit [ (56.25)] were predominant during the 18-24 hs interval, while sedentary [11(52.38%)] stress [11(52.38%)] diabetes [(47.61%)] hyperlipidemia [8 (38.09%)] and alcoholism [8 (38.09%] were predominant during the 6-12 hs interval; and cardiac diseases in the 12-18hs interval.
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PMID:[Circadian rhythm and encephalic vascular disease: a correlative study with risk factors]. 1523 33

Since avascular necrosis of the bone was first described in a HIV infected patient in 1990, its incidence has increased, especially in recent years. The hip is most commonly involved and often bilaterally. We report a series of 5 cases of avascular necrosis of the bone in patients with HIV infection. Both hips were involved in 4 of the cases. All of them were receiving highly active antiretroviral treatment when avascular necrosis of the bone was diagnosed, and 4 of them presented at least one risk factor. The risk factors found in our series were: hyperlipidemia, use of corticosteroids and alcoholism. We cannot rule out antiretroviral treatment as a risk factor for avascular necrosis of the bone. Case-control studies published have not identified antiretroviral treatment as a risk factor probably due to small size of the samples.
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PMID:[Avascular necrosis of the bone in patients with HIV infection: an emergent problem]. 1686 26

Poor glycaemic control and the duration of diabetes mellitus are known to accelerate development and progression of neuropathy. Diabetic co-morbidities: hypertension and hyperlipidaemia, have been postulated to associate with development of neuropathy. A diabetic foot with low temperature and frequent exposure to low temperature environment has recently been hypothesized to be at higher risk to develop early neuropathy. This cross-sectional study is undertaken to identify risk factors for diabetic neuropathy and the association between foot temperature and development of diabetic neuropathy by using simple clinical examination in the outpatient setting. From April 18, to April 30, 2005, universal sampling method was used to select 134 diabetic patients (type 1 or type 2 for >1 year) with peripheral neuropathy. Excluded are those with chronic alcoholism, drug-induced neuropathy, dietary history of vitamin B deficiency and family history of porphyria and hereditary sensorimotor neuropathy. The patient's duration of diabetes, glycaemic control status and the presence of co-morbids: hypertension and hyperlipidemia, were recorded. The temperature of the foot was measured by using thermo buddy. Of 134 patients representing Malaysian ethnic distribution with an equal number of males and females, 20.1% were in the age group of 61 to 65 years and, 85.1% and 67.9% belonged to lower socioeconomic and educational groups respectively. Associations between diabetic neuropathy and glycaemic control (p = 0.018) and duration of diabetes (p < 0.05) were significant. However, hypertension, hyperlipidaemia and low foot temperature were not significantly associated with development of diabetic neuropathy. Poor glycaemic control is significantly associated with diabetic neuropathy. Foot temperature alteration is merely an effect of autonomic neuropathy with a cold foot is attributed to co-existing peripheral arterial disease.
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PMID:Alteration of foot temperature in diabetic neuropathy: is it another piece of puzzle? 1704 21

Stroke is one of the leading causes of death and certainly the major cause of disability in the world. WHO has estimated that between 1990 to 2020 the world will witness an increase in stroke mortality of 78% in woman and 106% in man. Much of this increase will be in developing countries which are witnessing rapid change in lifestyle and nutrition, hypertension, diabetes mellitus, smoking, atrial fibrillation, hyperlipidemia, Homocysteinemia, and alcohol are the most significant modifiable risk factors of stroke. Of these, hypertension, diabetes, smoking, hyperlipidemia, homocysteinemia and alcoholism are obviously affected by lifestyle and nutrition. However, whilst epidemiology studies have noted an association of nutritional practice with stroke risk, further research is needed to show how nutritional interventions can be effective in stroke prevention.
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PMID:Nutrition and stroke. 1739 17


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