Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipid profile was evaluated prospectively in 23 consecutive children, aged 3.2-14.9 years, admitted to the hospital with a febrile illness (pneumonia, upper respiratory tract infection, diarrhea, pyelonephritis, mononucleosis, appendicitis). The degree of dyslipidemia associated with fever was assessed using each child as his/her own control and by comparison with 93 non-febrile children who had no evidence of fever during the past six months. Total cholesterol decreased during the symptomatic phase of the disease. The magnitude and duration of its decrease appeared to be related to the degree and duration of fever. Low HDL-cholesterol and hypertriglyceridemia were observed during the late stage of the febrile disease and were still detected in the convalescent phase. This study suggests that in children, transient and sometimes prolonged lipid changes may occur in association with an infectious febrile disease. This effect is important for defining the appropriate timing for screening for dyslipidemias.
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PMID:Changes in lipid profile observed in children over the course of infectious disease. 811 Nov 76

Numerous studies in recent years had proved pathogenetic correlation of the intestinal ecological community, not only with diseases of the gastrointestinal tract but also with diseases such as atherosclerosis and hypertension, urolithiasis and pyelonephritis, gallstones and hepatitis. In its role in maintaining homeostasis an intestinal microflora isn't inferior to any other vital organs. All this allowed to distinguish it as an independent body. Recently, as one of the most important factors for the development of dyslipidemia scientists consider breaking the functional state of the liver, as well as changes in blood lipid spectrum and disturbance of cholesterol metabolism begins at the level of the hepatocyte. However, in 2001, Carneiro de Moura proposed a theory of violation of the microbial community in the colon as one of the ways to lipid metabolism. By reducing the detoxification function of intestinal microflora associated with Microecological disorders of various origins, the first "hit" is to the host liver--is on one side. On the other--the vast majority of microorganisms are characterized by a pronounced ability of bile acids deconjugation, and therefore the increased reproduction in the ileum of bacteria (especially anaerobic, with enhanced activity against deconjugation activity to related bile acids) and the formation of toxic endogenous bile salts, acids are important prerequisites for the occurrence of violations of all functions of the liver, including the activities of Kupffer cells and the whole system of mononuclear macrophages. In this regard, the formation and progression of dyslipidemia, regardless of the target organ must be closely linked with the digestive tract by micro. Schematically it can be represented as follows: violation of microecology intestine --> accumulation of endotoxin in the gut --> entry of endotoxins in portal vein to the liver --> RES of liver cell damage --> strengthening the pathological effects of toxicants other (non-microbial) origin --> dysfunction of hepatocytes --> dislipoproteidemiya.
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PMID:[Intestinal dysbiosis and atherogenic dyslipidemia]. 2049 50