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)

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13

The incidence of deep-vein thrombosis was studied in 146 consecutive Korean patients who had a cementless total hip replacement with a porous-coated anatomic prosthesis. All of the patients had discontinued taking aspirin, aspirin-containing compounds, or other antiplatelet medications fourteen days before admission to the hospital for the operation. Deep-vein thrombosis was diagnosed by roentgenographic venography, and pulmonary embolism, by perfusion lung-scanning. There was an unusually low incidence (10 per cent) of deep-vein thrombosis in this series. In contrast to other reports, we did not identify a relationship between deep-vein thrombosis and so-called risk factors such as advanced age, number of venous valves (more than five) in the lower extremity, abnormal coagulation-assay data, certain diseases, or preoperative limitation of mobility. In addition, hypertension, blood group, surgical approach, and choice of cemented or cementless total hip replacement did not seem to affect the incidence of deep-vein thrombosis. There was a low incidence of deep-vein thrombosis in patients in whom obesity, prolonged immobilization postoperatively, varicose veins, and hyperlipemia were not factors.
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PMID:Low incidence of deep-vein thrombosis after cementless total hip replacement. 339 86

Fat overload syndrome is a rare complication of intravenous fat emulsion therapy. It is characterized by sudden elevation of the serum triglyceride level, fever, hepatosplenomegaly, coagulopathy, and variable end-organ dysfunction. The illness is generally discrete, and symptoms regress as the lipemia clears. The transient nature of the syndrome has allowed only speculation as to its pathogenesis. The authors report an autopsy study of a child who died during an acute episode of fat overload and document the causative role of fat sludging in the associated end-organ failure. In addition, they offer evidence that the coagulopathy, previously an enigma, results from primary fibrinolysis, possibly caused by release of tissue plasminogen activators from the damaged endothelial cells.
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PMID:Fat overload syndrome. An autopsy study with evaluation of the coagulopathy. 339 63

One hundred and one patients below 45 years and showing objective signs of cerebral ischemia were studied retrospectively for pathogenic factors. Twelve were below 15 years; the male to female ratio was 1:1. Factors known as predisposing (heart disease, hypertension, hyperlipemia, diabetes mellitus or infectious diseases) and other possible factors (e.g. trauma, abuse) were found in 41 patients. Among women using contraceptive pills there might be an increased risk of development of cerebral thrombosis, but the material was not large enough to warrant statistical analysis. In 64 patients one or more abnormal coagulation values were found, the most frequent being a deficient vessel wall fibrinolysis, which was noted in 38%. We therefore consider it worthwhile to investigate the fibrinolytic defence mechanism of the vessel wall in patients with cerebral thrombosis, since it is possible to treat this condition with specific fibrinolytic stimulating agents.
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PMID:Coagulation studies in children and young adults with cerebral ischemic episodes. 732 67

1) In two patient with excessive hyperlipidemia diet in the post-partum days resulted in a rapid reduction of the high neutral fats in the serum which were 6,150 mg/dl and 6,290 mg/dl respectively. In one patient the hyperlipidemia was reduced by diet during the pregnancy. The course of the pregnancies and the puerperium were uneventful. Complications during delivery were not related to the hyperlipidemia. Coagulation defects were not tested.--2) Excessively high serum lipid values of the mother only had a minor influence on the serum lipid values of the mother only had a minor influence on the serum lipid values of the infants. The infants had slightly elevated values compared to controls. One infant was tested at age 7 months and showed definitely elevated lipids with higher values than neonatally. A familial hyperlipidemia was confirmed in this case.--3) The milk fat values (Total Cholesterol and Neutral fats) were not influenced by the hyperlipidemia. Breast feeding was therefore safe.--4) Both infants of the mothers with hyperlipidemia had neonatal hyperbilirubinaemia with values of maximal 16.2 mg% and 16.7 mg% which required phototherapy.
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PMID:[Excessive hyperlipidemia during pregnancy (author's transl)]. 740 9

Aetiologic factors (gallstones, hyperlipidemia I-IV, hypertriglyceridaemia) make their occurrence, mainly, in the third trimester of gestation. Two cases of acute pancreatitis in pregnancy are described; in both cases patients referred healthy diet, no habit to smoke and no previous episode of pancreatitis. An obstructive pathology of biliary tract was the aetiologic factor. Vomiting, upper abdominal pain are aspecific symptoms that impose a differential diagnosis with acute appendicitis, cholecystitis and obstructive intestinal pathology. Laboratory data (elevated serum amylase and lipase levels) and ultrasonography carry out an accurate diagnosis. The management of acute pancreatitis is based on the use of symptomatic drugs, a low fat diet alternated to the parenteral nutrition when triglycerides levels are more than 28 mmol/L. Surgical therapy, used only in case of obstructive pathology of biliary tract, is optimally collected in the third trimester or immediately after postpartum. Our patients, treated only medically, delivered respectively at 38th and 40th week of gestation. Tempestivity of diagnosis and appropriate therapy permit to improve prognosis of a pathology that, although really associated with pregnancy, presents high maternal mortality (37%) cause of complications (shock, coagulopathy, acute respiratory insufficiency) and fetal (37.9%) by occurrence of preterm delivery.
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PMID:[Acute pancreatitis and pregnancy]. 813 93

Nephrotic syndrome is a disease which accompanies hypoproteinemia, edema, hyperlipidemia and coagulopathy. This syndrome has also been recognized in pediatric patient. We experienced recently a case of 11-year-old girl, who had insertion of a plasma exchange catheter because of secondary hyperlipidemia due to nephrotic syndrome. She suffered soon from a severe SVC obstruction by thrombosis grown up around the catheter and an emergency thrombectomy was planned under the cardiopulmonary bypass. Renal function was maintained preoperatively, in comparison with nephrotic syndrome in adult where some problems in perioperative management, such as difficulties in tracheal intubation, choice of anesthetic drugs, blood and fluid management, monitoring without CVP and weaning from ventilator are observed. Induction was carried out carefully under spontaneous breathing and the anesthetic method we used consisted of balanced technique using N2O, O2, fentanyl and pancuronium bromide with moderate hyperventilation. Intraoperative course was uneventful and the patient was extubated on the second day after the operation without any neurological defects.
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PMID:[Perioperative management of pediatric patient with vena cava superior thrombosis complicated with nephrotic syndrome]. 818 25

Intravascular coagulation of the intraosseous microcirculation (capillaries and venous sinusoids) progressing to generalized venous thrombosis, and less commonly retrograde arterial occlusion, now appears to be the cause of nontraumatic osteonecrosis. However, this coagulopathy is only an intermediary event, which is 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), 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 prothrombotic and hypofibrinolytic conditions.
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PMID:Coagulopathies and osteonecrosis. 1008 10

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

We reported a 68-year-old man with anti-phospholipid antibody syndrome who presented slowly progressive pure motor monoparesis(PMM) in left upper extremity as a sign of cerebral infarction. He had history of hypertension and hyperlipidemia. He first noticed clumsiness in left fingers, then weakness of left fingers with drop hand developing gradually in 2 to 6 weeks. He began to feel difficulty in raising left upper arm in 8 weeks and was admitted to our hospital. On admission, he exhibited severe weakness in distal portion and moderate weakness in proximal portion of left upper extremity. Deep tendon reflexes were slightly hyperactive in left side. Muscle strength of right upper extremity and bilateral lower extremities were normal. There was no sensory and autonomic abnormality. Laboratory examination revealed high titer of anti-cardiolipin IgM antibody. Brain MRI demonstrated a small cortical infarction in the right precentral gyrus. Cerebral angiography revealed severe stenosis in right common carotid artery. Other examinations including EMG were unremarkable. PMM in left upper extremity was considered to be caused by the ischemic lesion in the precentral motor cortex. Slowly progressive course might be explained by the hypovolemic factor due to the marked stenosis in right common carotid artery, poor collateral circulation, and abnormal coagulation caused by anti-phospholipid antibody syndrome.
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PMID:[A case of antiphospholipid antibody syndrome with cerebral infarction showing slowly progressive pure motor monoparesis in unilateral upper extremity]. 1121 63


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