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)

We propose a rapid enzymatic micromethod for the specific determination of lipase (EC 3.1.1.3) activity in serum and duodenal fluid. Free linoleic acid produced during 10-min incubation of 10 mul of sample with 1 ml of substrate (trillinolein emulsion) at 30 degrees C is converted by lipoxygenase (EC 1.99.2.1), in a coupled reaction, to its hydroperoxide, which is measured photometrically after solubilizing the reaction mixture in ethanol. Lipase activity is calculated from the rate of hydroperoxide formation, with linoleic acid as primary standard. The velocity of the reaction is greatest at pH 8.8, 35-37 degrees C, and a deoxycholate concentration of 3.6 mmol/liter. The energy of activation is 6.7 kcal/mol. The differing "apparent" Km values obtained for lipase in undiluted serum (4 X 10(-5) mol/liter) and in albumin-based diluents (1 X 10(-5) mol/liter) indicate the presence of a competitive inhibitor in the serum matrix. We detected no lipase activity in urine. Results by the proposed method correlate well with those by a copper soap extraction method (r = 0.95), but values are significantly higher for pancreatitis patients' sera (slope 1.6). The linear dynamic range extends to 1000 U/liter. Hemolysis, lipemia, and hyperbilirubinemia do not interfere. The normal range is 40-60 U/liter. Lipase activity of pancreatitis patients generally exceed 1000 U/liter during the acute phase and 250 U/liter for as long as 10 days after it.
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PMID:Lipoxygenic micromethod for specific determination of lipase activity in serum and duodenal fluid. 1 45

Oxyhemoglobin dissociation curves were performed from blood of subjects with pancreatitis associated with Type V and Type I hyperlipoproteinemia. The hemoglobin-oxygen affininty was markedly increased with P50 varying from 22.3 to 17.7 mmHg. As the hyperlipoproteinemia subsided the clinical and laboratory signs of pancreatic affection disappeared. The increased hemoglobin-oxygen affinity and decreased flow of red cells due to hyperchylomicronemia in the microcirculation may lead to tissue hypoxia, which may act as a precipitating injurious factor leading to pancreatitis during severe hyperlipemia.
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PMID:Increased hemoglobin-oxygen affinity in patients with pancreatitis associated with type I and V hyperlipoproteinemia. 2 74

Lipemic serum from three patients with acute pancreatitis and type IV hyperlipemia was fractionated into very-low-density lipoproteins and clear serum. Amylase activity (determined by the Phadebas method) in the component fractions did not exceed that in the original lipemic serum. Addition of these fractions or VLDL and chylomicrons from asymptomatic patients with hyperlipemia to nonlipemic serum from patients with "routine acute pancreatitis" did not inhibit amylase activity or alter the electrophoretic mobility of amylase isoenzymes. Therefore the normal amylase activity often observed in hyperlipemic pancreatitis does not result from an inhibition of amylase activity by serum lipoproteins.
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PMID:Possible mechanisms of normal amylase activity in hyperlipemic pancreatitis. 20 33

The history of a 27-year-old woman with 10 years of episodic abdominal pain and the development of calcific pancreatitis secondary to hyperlipoproteinemia is presented. The relationship between familial and alcoholic hyperlipidemia and pancreatitis is discussed as well as the mechanism of injury to the pancreas.
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PMID:Calcific pancreatitis in a patient with type 5 hyperlipoproteinemia. 22 44

Definite inherited defect in hereditary pancreatitis (HP) is not known. A new kindred with 3 definite and 6 suspected cases of HP was investigated for possible inherited abnormalities. No aminoaciduria (except for a slight rise in urinary histidine in one patient) and no hyperparathyroidism, hyperlipidemia, or chromosomal abnormality was present. An increase in serum IgM level of a polyclonal type was noted in 3 definitely affected sisters and also in 2 nonaffected members. Serum alpha-1-antitrypsin and serum trypsin inhibition were normal. However, very marked dilatation and ectasia of the pancreatic duct were found in the propositus. Reviewing the data from this family and previously described kindreds, it is postulated that the genetic abnormality in HP encompasses a wide variety of structural and anatomical defects in the sphincter of Oddi or the pancreatic ductal system. These predispose to intermittent obstruction of the duct with concomitant activation of enzymes and ductal metaplasia. In suspected cases an early effort should be made to outline the pancreatic duct as the defect may be amenable to surgery.
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PMID:Inherited defect in hereditary pancreatitis. 30 62

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.
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PMID:Pancreatitis and renal disease. 31 21

Although it is widely known that patients with severe hyperlipemia may have pancreatitis, it is not generally appreciated that such patients may have recurrent abdominal pain of variable character and intensity not due to pancreatitis. Review of 35 patients followed in our clinic for 1--11 years showed that 54% had recurrent abdominal pain, while only 29% had pancreatitis. Although mild pain occurred frequently with plasma triglycerides in the 2000--5000 mg/dl range, triglycerides over 6000 mg/dl were often associated with severe pain and physical findings which necessitated hospitalization, often led to the misdiagnosis of pancreatitis and other intra-abdominal catastrophes and resulted in multiple unnecessary diagnostic studies and operations. When recognized, the pain subsided within 48 hours upon cessation of oral intake and treatment with intravenous electrolyte solutions. Furthermore, effective treatment of the hyperlipemia prevented both the attacks of severe pain and the pancreatitis which otherwise occurred (or recurred) in a significant fraction of the patients. These data confirm the existence of hyperlipemic abdominal crisis as a distinct entity and testify to the importance of recognizing this syndrome in order to avoid the occurrence of acute pancreatitis and the performance of unnecessary and potentially harmful surgery.
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PMID:The natural history and surgical significance of hyperlipemic abdominal crisis. 48 15

Hyperlipemia was revealed in 3 of 26 patients who died from an acute destructive pancreatitis. The level of lipids was as high as 2000--5000 mg%. Hyperlipemia when combined with destructive pancreatitis should be considered to be a poor prognostic sign.
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PMID:[Pancreatitis and hyperlipemia]. 50 37

Ten episodes of massive transaminase increase with hepatic necrosis were observed in 7 patients after infusion of megluminioglycamide (Biligram). The patients were 3 men and 4 women aged 49 to 65 years with biliary tract disease (n = 1), recurrent pancreatitis (n = 1), hyperlipidaemia and minimal toxic liver damage (n = 1), pyelonephritis (n = 1), , arteriitis (n = 1), and pseudo-LE (n = 1). In 6 patients there was an increase of the alkaline phosphatase without icterus before the investigation and a slight increase of transaminases in 3 patients. After infusion of 100 ml of Biligram in 5 patients and of 200 ml in 2 patients there was an abrupt increase of GPT (98-2202 U/l) with a lesser increase of GOT. The alkaline phosphatase activity remained unchanged. Three patients showed symptoms such as upper abdominal pain, fever erythema, or conjunctivitis. Histologically all patients showed centrolobular necroses. Transaminases should be checked 2 days after intravenous cholangiograms. In patients with a definite increase reexposure should be avoided.
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PMID:[Hepatic necroses after infusion cholangiography (author's transl)]. 63 57

We studied the relationship between pregnancy and pancreatitis together with reviewing the bibliography after having had 4 cases. As far as the aetiology is concerned there does not seem to be a mechanical factor associated with the pregnant uterus but a vesicular factor (gall bladder) of stasis and hypersecretion, with hyperlipidaemia of pregnancy and pancreatic oversecretion in pregnancy, all of which are finally associated with a neuro-vegetative lack of tone and with the part played by certain drugs that are often prescribed in pregnancy. The fetal prognosis is relatively good except for the risks of premature delivery. Management of a case of acute severe pancreatitis is difficult to work out. All the same, the treatment should be above all conservative, which means medical. Surgery should be reserved for those cases with definite indications such as progressive deterioration in spite of medical treatment with the knowledge beforehand that it will not make much difference to the final prognosis.
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PMID:[Pregnancy and severe pancreatitis (author's transl)]. 64 18


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