Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reasons of fat embolism as well as the following fat embolism syndrome are most likely long bone fractures, especially if the femur is participated. On the other hand there are cases, where a severe concussion of the entire body caused fat embolism. But it is also supposed, that intramedullary reaming as well as the insertion of knee- and hip-prostheses could be a releasing factor, because the applicated pressure on the medullary canal can cause a fat release in the systemic blood system. The morbidity depends on age and fracture, which is on fractures between 0.9 and 2%. The most affected group are people between 18 and 28 years of age. The fat embolism is manifesting at 46-60% of the patients in the first 24 hours and over 90% of the patients are affected in the first three days. If you look at the metabolic changes, you will find shortly after the fracturing process a rapid increase of free fatty acids (FFA), as well as an increase of the plasmatic enzyme levels (lipase, GPT, GOT, GLDH, LDH, etc.), catecholamines and glucocorticoids. In order to discuss the pathogenesis in a fairly complete way, you have to take different theories into consideration, because several parallel running processes--which are influencing each other--are leading to the syndrome. Infloating theory: Proceeding on the assumption that contents of the bone marrow are floating out of the fracture gap into the venous system and are leading to fat embolism in the lungs. Lipase theory: You can diagnose in 50-70% of the fracture patients an increase of the lipase level, which is correlating with the manifestation of the fat embolism. The lipase releases fat from the body depositories in addition to the fat, who is coming out of the fracture gap. Shock and coagulation theory: During shock the microcirculation is decelerated, the blood viscosity is increased and the suspension stability of the cellular blood components is decreased, which is leading to the sludging phenomenon. So the capillaries of the lungs and the brain are a kind of sludge filter of the blood, that is changed in its suspensions stability. Free fatty acids theory: Primary existing capillary defects are reasonable caused by free fatty acids (FFA). They are hydrolyzed of the neutral fats and are histotoxic for the walls of the blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Fat embolism and fracture, a review of the literature]. 135 89

Liposuction is a procedure that allows the surgical removal of excess adipose tissue in healthy individuals. Lipoplasty is commonly performed with few clinical side effects. However, with increased lipoaspirate volumes, complications have been reported. In addition, the abnormal appearance of fat cells in other tissues subsequent to lipoplasty has been reported in a small number of cases. The authors examined whether larger-volume lipoplasty, in the porcine model, resulted in disturbances in cardiac or pulmonary output levels, electrolytes, and liver chemistry analyses or alterations in organ histology. Nine adult porcine specimens were subjected to either lipoplasty (n = 6) with the superwet technique or no lipoplasty (n = 3). Using a Swan-Ganz catheter, cardiac output and pulmonary artery pressure measurements were obtained from initial placement before lipoplasty until 48 hours postoperatively. Blood analyte measurements were obtained. Upon euthanization, liver, kidney, and lung specimens were collected and tissue sections were prepared. No significant differences or trends were observed in cardiac parameters or blood analytes between control and experimental groups. Significant elevations in serum aspartate aminotransferase and alanine aminotransferase enzyme levels (p < 0.03) were observed in animals postoperatively (10 to 48 hours) subjected to lipoplasty compared with controls. Upon gross examination, the lung tissues of animals subjected to lipoplasty unexpectedly demonstrated patchy petechial hemorrhages on the pleural surface. Tissue sections revealed marked hemorrhagic congestion and evidence of pulmonary edema. Fat emboli were also identified within the pulmonary and renal systems.
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PMID:Hemodynamics, electrolytes, and organ histology of larger-volume liposuction in a porcine model. 1506 Mar 51

We previously demonstrated that pulmonary fat embolism was induced by elevation of the core body temperature, in rats with a fatty liver. The aim of the present examination was to investigate the core body temperature at which pulmonary fat embolism developed capillaries through exposure to a high temperature, in rats with a fatty liver. Following heat stress, pulmonary fat embolism was observed to a slight degree at a core body temperature of 41 and 42 degrees C, whereas the severity of pulmonary fat embolism was greatly increased and was classified as severe at a core body temperature of 43 degrees C. Moreover, the concentrations of aspartate aminotransferase and alanine aminotransferase within plasma were significantly increased at a core body temperature of 43 degrees C. These results clearly indicate that the development of pulmonary fat embolism could be related to hyperthermia at above 42 degrees C following heat stress, and that fat emboli may be derived from the fatty liver itself. It is thus likely that pulmonary fat embolism can be considered as one form of evidence of hyperthermia in an individual with a fatty liver.
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PMID:Relationship between pulmonary fat embolism and core body temperature in rats with a severe fatty liver. 1679 13