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)

Case reports since 1957 implicate corticosteroids in excess of physiologic requirements as a cause of nontraumatic osteonecrosis. Both laboratory and clinical studies demonstrate marked alterations in lipid metabolism with hyperlipemia, fatty liver and systemic fat embolism. Intra-arterial infusion of fat produces embolic vascular obstruction, focal marrow necrosis and osteocytic death in the femoral head of the rabbit. Induced hypercortisonism in rabbits produces severe hyperlipemia, fatty liver, systemic fat emboli, terminal vascular obstruction in bone and associated areas of osteocytic death representing avascular necrosis. Osteoporosis develops without fracture. Histologic evidence of vasculitis, thrombosis, or microfracture is lacking. The specific biochemical pathway of corticosteroid lipid alterations is unknown.
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PMID:The role of fat embolism in the etiology of corticosteroid-induced avascular necrosis: clinical and experimental results. 63 8

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

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

Like the liposomes of certain intravenous fat emulsions associated with embolic effects in acutely ill patients, chylomicrons and very low density lipoproteins (VLDL) show calcium-dependent agglutination by C-reactive protein (CRP). It is suggested that non-traumatic fat embolism may be caused by agglutination of chylomicrons and VLDL by high levels of plasma CRP. This mechanism may also cause acute pancreatitis in patients with types I, IV, and V hyperlipidaemia, and avascular necrosis of bone in patients with corticosteroid-induced hyperlipidaemia.
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PMID:Pathogenesis of non-traumatic fat embolism. 289 46

Chylomicrons show calcium-dependent agglutination by C-reactive protein (CRP). This has been suggested as a mechanism by which fat embolism may occur in the absence of trauma. It may also play a role in the pathogenesis of acute pancreatitis in patients with types I and V hyperlipidaemia.
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PMID:Fat macroglobule formation from chylomicrons and non-traumatic fat embolism. 323 65

In several cases of fatal blunt-trauma injuries or after exposure to severe burning, large-drop fatty substances, discernible to the naked eye, were found in the venous blood of the right ventricle. Thin-layer chromatographic separation of the extracted lipids demonstrated an increase in the triglyceride fraction. Analysis of the fatty acids by means of combined gas chromatography/mass spectrometry showed a shift towards oleic acid. The distribution pattern of the molecular weights was determined by means of DCI-mass spectrometry in order to characterize the triglycerides in detail. The total chemical findings indicated that the visible lipids present in the right ventricle had predominantly derived from the adipose tissues. In cases of post mortem burning (without vital traumata) no typical pulmonary fat embolism had developed despite massive lipemia in the venous blood.
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PMID:[Large droplet lipids in blood in the right ventricle]. 342 2

Aseptic osteonecrosis is observed in 25% of cases after renal transplantation. This etiological variety of osteonecrosis is unusual in that it is frequently bilateral and has multiple localisations. Apart from the classical radiological signs, attention in attracted by isolated images of osteocondensation in the metaphyses and/or the diaphyses suggesting massive bony infarction and the appearances of fatigue fractures observed frequently (14%). In 43% of cases, the obvious necrosis was proceeded by early bone pain, around the 7 th day, during massive administration of corticosteroids in the prevention or cure of graft resection. This finding suggested to us that the best time to observe ischemia of the bone or marrow is very early and led us to undertake an experimental study in the rabbit. Two series of New Zealand White rabbits were treated with massive doses of corticosteroid and sacrificed between the 3rd and the 21st day. The treated animals presented an early peak of hyperlipemia from the 7th day onwards, and diffuse lesions of hepatic and renal steatosis. Fat emboli associated with appearances of parietal thrombosis were observed in most cases. In the same animals, there were also appearances of stage I or stage II necrosis. Referring to the description of bone marrow necrosis in stages by Arlet and Ficat, there was observed in all the series, a frequency of marrow lesions of all stages much higher in treated animals (16 out of 20) than in controls. Only one lesion of stage I was observed in controls; the difference was highly significant. (0,000001 < p < 0,00001). If one only considers necroses of stage II and III (10/20 in the treated group nil in controls) the frequency was still significant p < 0.001. The preliminary results of the fixation of tetracycline are reported.
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PMID:[Cortisone-induced osteonecrosis: knowledge acquired from observations in man and comparison with the results of animal experimentation]. 700 46

Autologous fat injection for soft tissue augmentation in the face is claimed to be a safe procedure. However, there are several case reports in the literature where patients have suffered from acute visual loss and cerebral infarction following fat injections into the face. Acute visual loss after injection of various substances into the face is a well-known complication of such interventions. We report two further patients who suffered from ocular and cerebral embolism after fat injections into the face. For the intravasation of fat particles there are three preconditions: well-vascularized tissue, fragmentation of parenchyma, and, especially, a local increase in pressure in the affected tissue. Fat injections into the face lead to an acute local increase in pressure in highly vascularized tissue. We assume that fragments of fatty tissue reach ocular and cerebral arteries by reversed flow through branches of the carotid arteries after they are introduced into facial vessels. The manifestation of fat embolism appears either immediately after the fat injection or after a latency period. Fat embolism can remain subclinical and may not be recognized, or the clinical features may be misinterpreted. To minimize the risk of such a major complication, fat injections should be performed slowly, with the lowest possible force. One should avoid fat injections into pretraumatized soft tissue, for example, after rhytidectomy, because the risk of intravasation of fat particles may be higher. Metabolic disturbances such as hyperlipidemia may also contribute to the clinical manifestation of fat embolism Routine funduscopic examinations after fat injections into the face could help to provide data for future estimation of the patient's general risk.
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PMID:Autologous fat injection for soft tissue augmentation in the face: a safe procedure? 961 80

The patient was an 88-year-old woman with a 10-year history of hypertension. She was suspected to have been hit by a car. At the time of the event, she was conscious and able to stand on her own and had no obvious injuries. She was sent home, but she lapsed into unconsciousness and was nonresponsive after 2 hours. She was sent to the hospital, and her heartbeat and breathing stopped. After half an hour of rescue attempts, her heartbeat did not recover, and she was declared dead. During the autopsy, a small subcutaneous hemorrhage was observed below the right knee joint. No obvious internal organ injuries or bone fractures were observed. The deceased also had mild atherosclerosis in the coronary arteries and an old cerebral infarction in the right cerebellum. The tissue histopathological tests showed distinct fat embolism in multiple organs, including the brain, lungs, kidneys, liver, and pancreas. A postmortem blood biochemistry test of the heart blood showed that the levels of low-density lipoprotein, cholesterol, triglycerides, and free fatty acids in the blood were increased, and the level of C-reactive protein was elevated. According to the autopsy results, the direct cause of death was multiorgan fat embolism. This case suggests that aging, hypertension, and hyperlipidemia may be risk factors for nontraumatic fat embolism under stressful conditions.
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PMID:Nontraumatic Multiple-Organ Fat Embolism: An Autopsy Case and Review of Literature. 3237 96