Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154251 (lipid disorder)
 795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 311 patients with primary acute pancreatitis, seven revealed major and seven minor lipid abnormalities on hospital admission. One pregnant woman suffered acute pancreatitis associated with Fredrickson type I hyperlipoproteinaemia. Twelve of the 13 men with types IV and V hyperlipoproteinaemia suffered alcohol abuse pancreatitis and represented 13.2 per cent of this aetiological group. However, only one of the 157 patients (0.6 per cent) with biliary disease had lipid abnormalities. Two of the 13 men died--the oldest, who had gallstones, and one with alcohol related disease. The remaining 11 were subject to follow-up (5-10 years). Six, who had improvement of their lipid abnormalities, had abstained from alcohol. The other five had a persistent lipid disorder, and all admitted continuing heavy alcohol ingestion. The clinical diagnosis of acute pancreatitis was supported by serum amylase elevation in only nine of the fourteen patients. Urinary amylase levels were consistent with the diagnosis in 11 of the 12 patients. Estimation of both serum and urinary amylase gave 100 per cent support to the clinical diagnosis of acute pancreatitis. Hyperlipidaemia associated with acute pancreatitis may be secondary to alcohol abuse but the possible role of HLP cannot be discounted. Urinary amylase is useful in diagnosing acute pancreatitis in the presence of hyperlipidaemia.
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PMID:Hyperlipidaemia, alcohol abuse and acute pancreatitis. 620 8

The influence of the efficacy of triglyceride and cholesterol correction on cardiovascular complications and mortality was analysed in a follow-up study with 260 patients with primary HLP (triglycerides before entry greater than 2.9 mmol/l and/or cholesterol greater than 7.8 mmol/l). The follow-up time was 67.4 +/- 27 months. It was hypothesised that reduction of elevated levels of triglycerides and/or cholesterol influenced favourably the incidence of angina pectoris, MI, stroke and total mortality. For ethical reasons, it was not possible to carry out the investigations with a control group. Therefore, we performed an internal comparison of 3 categories of lipid correction achieved during the trial (effective, moderate, insufficient). A substantial improvement of the lipid disorder was obtained by individualizing the therapy. Triglycerides and cholesterol decreased on average by 50% and 20%, respectively. The incidence of MI was 10 times higher than in the general population. With respect to the type of HLP, hypertriglyceridemia revealed a significantly higher incidence of MI compared with hypercholesterolemia and mixed HLP. The therapy variant was only of importance with respect to gallstone diseases accumulating in the CPIB-treated subgroups. We found a majority of cases with newly manifested angina pectoris and stroke in the group with moderate correction of both triglycerides and cholesterol. Patients with effective triglyceride and cholesterol correction suffered less frequently from MI than those with insufficient correction. This was also the case with secondary prevention in cases with MI prior to entry. There was no significant difference in the distribution of lipid categories at entry between those with and without recurrent infarction. In the group without reinfarction, however, the percentage with insufficient control diminished significantly. Associated risk factors such as hypertension, diabetes, smoking and obesity were of minor or no significance. In subjects with effective triglyceride correction, the total mortality was 0.97/1000 treatment months vs. 3.63 in insufficiently treated patients. The figures for MI mortality were 0.36 and 1.91, respectively.
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PMID:Reduced incidence of cardiovascular complications and mortality in hyperlipoproteinemia (HLP) with effective lipid correction. The Dresden HLP study. 649 44

Type I hyperlipoproteinemia (type I HLP) is a rare disorder of lipid metabolism characterized by fasting chylomicronemia and reduced postheparin plasma lipoprotein lipase (LPL) activity. Most cases of type I HLP are due to genetic defects in the LPL gene or in its activator, the apolipoprotein CII gene. Several cases of acquired type I HLP have also been described in the course of autoimmune diseases due to the presence of circulating inhibitors of LPL. Here we report a case of type I HLP due to a transient defect of LPL activity during puberty associated with chronic idiopathic urticaria (CIU). The absence of any circulating LPL inhibitor in plasma during the disease was demonstrated. The LPL genotype showed that the patient was heterozygous for the D9N variant. This mutation, previously described, can explain only minor defects in the LPL activity. The presence of HLP just after the onset of CIU, and the elevation of the LPL activity with remission of the HLP when the patient recovered from CIU, indicate that type I HLP was caused by CIU. In summary, we report a new etiology for type I HLP - a transient decrease in LPL activity associated with CIU and with absence of circulating inhibitors. This is the first description of this association, which suggests a new mechanism for type I HLP.
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PMID:Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia. 1057 67