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Women with overweight, mixed hyperlipidemia, intolerance to glucose and diastolic hypertension  [PDF]
Ruth-Maria Korth
Health (Health) , 2014, DOI: 10.4236/health.2014.65064
Abstract: Primarily healthy women who attended a practice of General Medicine were examined and coded data were evaluated using two statistical methods (n = 248, aged 36 ± 14 years). It was found that participants with LDL-related (mixed) hyperlipidemia showed higher blood pressure, a higher proportion of alcohol problems and/or smoking compared to normolipidemic women (p ≤ 0.05). These hyperlipidemic women who reported alcohol problems and/or smoking more often showed proteinuria and/or hematuria, rise of LDL/HDL, critical fasting blood glucose and lower HDL-cholesterol compared to hyperlipidemic women reporting healthy lifestyle (p ≤ 0.05). Likewise, high triglycerides were associated with rise of blood pressure and intolerance to glucose (p ≤ 0.05) and also with elevated total cholesterol. Alcohol-related hypertriglyceridemia overlapped with diastolic hypertension, rise of body weight and urine pathology, lowering of HDL-cholesterol and critical fasting blood glucose. The motivating message was that women with mixed hyperlipidemia and healthy lifestyle had functionally renal endothelium and healthy HDL-related baseline measures. Altogether, LDL-related hyperlipidemia and/or high triglycerides were correlated with diastolic hypertension whereby critical alcohol consumption declined renal endothelium and lowered HDL-cholesterol implicating baseline strategies to neutralize early risk factors.
Plasma kinetics of an LDL-like nanoemulsion and lipid transfer to HDL in subjects with glucose intolerance
Bertato, Marina P;Oliveira, Carolina P.;Wajchenberg, Bernardo L.;Lerario, Antonio C.;Maranh?o, Raul C.;
Clinics , 2012, DOI: 10.6061/clinics/2012(04)08
Abstract: objective: glucose intolerance is frequently associated with an altered plasma lipid profile and increased cardiovascular disease risk. nonetheless, lipid metabolism is scarcely studied in normolipidemic glucose-intolerant patients. the aim of this study was to investigate whether important lipid metabolic parameters, such as the kinetics of ldl free and esterified cholesterol and the transfer of lipids to hdl, are altered in glucose-intolerant patients with normal plasma lipids. methods: fourteen glucose-intolerant patients and 15 control patients were studied; none of the patients had cardiovascular disease manifestations, and they were paired for age, sex, race and co-morbidities. a nanoemulsion resembling a ldl lipid composition (lde) labeled with 14c-cholesteryl ester and 3h-free cholesterol was intravenously injected, and blood samples were collected over a 24-h period to determine the fractional clearance rate of the labels by compartmental analysis. the transfer of free and esterified cholesterol, triglycerides and phospholipids from the lde to hdl was measured by the incubation of the lde with plasma and radioactivity counting of the supernatant after chemical precipitation of non-hdl fractions. results: the levels of ldl, non-hdl and hdl cholesterol, triglycerides, apo a1 and apo b were equal in both groups. the 14c-esterified cholesterol fractional clearance rate was not different between glucose-intolerant and control patients, but the 3h-free-cholesterol fractional clearance rate was greater in glucose-intolerant patients than in control patients. the lipid transfer to hdl was equal in both groups. conclusion: in these glucose-intolerant patients with normal plasma lipids, a faster removal of lde free cholesterol was the only lipid metabolic alteration detected in our study. this finding suggests that the dissociation of free cholesterol from lipoprotein particles occurs in normolipidemic glucose intolerance and may participate in atherogenic signaling.
Q&A: Food additive intolerance
Margitta Worm
BMC Medicine , 2011, DOI: 10.1186/1741-7015-9-115
Abstract: Both, IgE-mediated allergy, but also food additive intolerance are mast cell dependent reactions. The release of mast cell mediators like histamine, leukotrienes and others leads to the onset of the above mentioned clinical symptoms, which cannot be distinguished concerning the underlying mechanisms. In the case of an allergic reaction, crosslinking of membrane bound IgE via an allergen is inducing mast cell degranulation. In food additive intolerance a direct action of the additive on the mast cells is proposed, however the exact mechanisms are not known.The most common food additives to which patients are intolerant are sulfite, sodium benzoate and food colorings. In addition, histamine is often accused of inducing intolerance reactions, however its exact role as an intolerance reaction as such requires more clarification.It is estimated that 0.1 - 1.5% of the population may suffer from food additive tolerance. So far the data suggest that intolerance reactions occur more frequently in older patients rather than in young children Further, it is known that drug intolerance towards acetylsalicylic acid (ASA) occurs more frequently in asthmatic patients. However, whether this is also true in respect to the prevalence of food intolerance in asthmatics remains to be determined.The risk of developing an allergy to my knowledge does not solely depend on age but rather depends on the allergen and the specific exposure situation of an individual. The lifetime risk for a food allergy probably does decrease rather than increase over time. However, in the case of food additive intolerance, this decrease of the risk over time might not be true. A possible explanation for this might be a change of the gastrointestinal barrier function. In addition the presence of additional cofactors, which can trigger such reactions (intake of drugs like ACE-inhibitors, physical activity, in-take of alcohol), makes the onset of food additive intolerance in later life more likely.As mentioned a
Disaccharide intolerance  [PDF]
Radlovi? Nedeljko
Srpski Arhiv za Celokupno Lekarstvo , 2010, DOI: 10.2298/sarh1012777r
Abstract: Disaccharide intolerance presents a pathogenic heterogeneous and most complex clinical entity. It usually occurs due to primary or secondary deficit of disaccharide activity, and rarely because of disorders of absorption or monomer metabolism. Symptomatology of disaccharide maldigestion and/or malabsorption depends on the severity of the basic disorder, the level of its overload and the patient’s age. In the youngest children, due to a rapid gastrointestinal transit and a low compensatory capacity of the colon, osmotic-fermentative diarrhoea forms the basis of clinical features. Diarrhoeal disorder can be occasionally so intensive that it disturbs not only water and electrolytic balance, but also the nutritive status of the child. In older children and adults, as well as in milder forms of the disorder, the symptomatology, most often without diarrhoea, is dominated by abdominal colic, loud peristaltic sounds, meteorism and increased flatulence. Metabolic disorders followed by conversion disorders of galactose and fructose into glucose are characterized by a hypoglycaemic crisis, as well as by various multisystemic damages due to the deposit of toxic metabolic products. The diagnosis of gastrointestinal forms of disaccharide intolerance is based on the pathologic clinical and laboratory response during the overload test, while that of the metabolic form is based on the confirmed presence of specific enzyme and/or genetic defect. Treatment of disaccharide intolerance is based on the elimination diet. Besides, in the secondary forms of the disorder, it is also necessary to apply the treatment of the basic disease.
Genetic determinants of statin intolerance
Jisun Oh, Matthew R Ban, Brooke A Miskie, Rebecca L Pollex, Robert A Hegele
Lipids in Health and Disease , 2007, DOI: 10.1186/1476-511x-6-7
Abstract: COQ2 genotypes, based on two single nucleotide polymorphisms (SNP1 and SNP2) and a 2-SNP haplotype, all showed significant associations with statin intolerance. Specifically, the odds ratios (with 95% confidence intervals) for increased risk of statin intolerance among homozygotes for the rare alleles were 2.42 (0.99 to 5.89), 2.33 (1.13 to 4.81) and 2.58 (1.26 to 5.28) for SNP1 and SNP2 genotypes, and the 2-SNP haplotype, respectively.These preliminary pharmacogenetic results, if confirmed, are consistent with the idea that statin intolerance which is manifested primarily through muscle symptoms is associated with genomic variation in COQ2 and thus perhaps with the CoQ10 pathway.Large clinical trials over the past two decades have unequivocally established the benefit of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) inhibitors – or "statins" – in the primary and secondary prevention of coronary heart disease (CHD) [1]. Reduction of plasma low-density lipoprotein (LDL) cholesterol with statins has revolutionized clinical cardiology; this family of drugs is generally well-tolerated, easy to administer, and has very good patient acceptance. However, the potential for adverse effects exists. From clinical trials, the statin discontinuation rate due to adverse events ranges between 1 and 5% [1]. Frequently reported adverse effects include gastrointestinal complaints, rashes, dizziness, pruritus and headache [2]. Statin-related skeletal muscle disorders range from benign myalgias – such as non-specific muscle aches or joint pains without elevated serum creatinine kinase (CK) concentration – to true myositis with >10-fold elevation of serum CK [3]. The incidence of muscle aches and pains with statin monotherapy ranges from 1 to 7%, whereas severe myopathy, defined as >10-fold elevation of serum CK with muscle pains, weakness and tenderness, occurs in up to 0.5% of patients [3]. Life-threatening rhabdomyolysis with muscle necrosis and subsequent electrolyte alterations,
Effect of Acute Smoking on Diastolic Function
M A Akbarzadeh,M E Ghaidari,Sh Yazdani,M Asadpour Piranfar
Iranian Cardiovascular Research Journal , 2010,
Abstract: Background: Smoking is a known risk factor of atherosclerosis, endothelial dysfunction, athermanous plaque rupture, unstable coronary syndrome and sudden cardiac death. Methods: The present study comprised 40 randomly selected healthy male hospital staff without a history of hypertension or cardiac or pulmonary disease. Participants were divided into two groups. The first group included 20 professional smokers (at least 5 pack/year till the time of study) and the second group consisted of 20 non-professional smokers defined as 0.5 pack/ year or less till the time of study. Participants were instructed not to smoke for 6 hours before the study. Patients underwent echocardiography before smoking. The participants were then asked to smoke a whole cigarette. After smoking, echocardiography was repeated within 7 to 15 minutes. Echocardiographic indices of diastolic function (E wave, A wave, Ea, E/A ratio and deceleration time) were measured before and after smoking.Results: There was no statistically significant difference in the baseline measures in both groups before smoking and also there was no significant difference between measures in the two groups after smoking. The analysis of the pooled data from two groups showed that, smoking resulted in significant increase of heart rate (P<0.001). A wave, E wave, Ea, E/A ratio and deceleration time changed significantly after smoking (P<0.001, P=0.027, P=0.011, P<0.001 and P<0.001 respectively). Conclusion: Smoking of only a cigarette in both professional and nonprofessional smokers, resulted in the same significant diastolic dysfunction. Background: Smoking is a known risk factor of atherosclerosis, endothelial dysfunction, athermanous plaque rupture, unstable coronary syndrome and sudden cardiac death. Methods: The present study comprised 40 randomly selected healthy male hospital staff without a history of hypertension or cardiac or pulmonary disease. Participants were divided into two groups. The first group included 20 professional smokers (at least 5 pack/year till the time of study) and the second group consisted of 20 non-professional smokers defined as 0.5 pack/ year or less till the time of study. Participants were instructed not to smoke for 6 hours before the study. Patients underwent echocardiography before smoking. The participants were then asked to smoke a whole cigarette. After smoking, echocardiography was repeated within 7 to 15 minutes. Echocardiographic indices of diastolic function (E wave, A wave, Ea, E/A ratio and deceleration time) were measured before and after smoking.Results: There w
Change Intolerance in Spanning Forests  [PDF]
Deborah Heicklen,Russell Lyons
Mathematics , 2001,
Abstract: Call a percolation process on edges of a graph change intolerant if the status of each edge is almost surely determined by the status of the other edges. We give necessary and sufficient conditions for change intolerance of the wired spanning forest when the underlying graph is a spherically symmetric tree.
Early diastolic filling dynamics in diastolic dysfunction
Gerard J King, Jerome B Foley, Faisal Almane, Peter A Crean, Michael J Walsh
Cardiovascular Ultrasound , 2003, DOI: 10.1186/1476-7120-1-9
Abstract: The relationship between early passive diastolic transmitral flow and peak early mitral annular velocity in the normal and in diastolic dysfunction was studied. Two groups comprising 22 normal controls and 25 patients with diastolic dysfunction were studied.Compared with the normal group, those with diastolic dysfunction had a lower E/A ratio (0.7 ± 0.2 vs. 1.9 ± 0.5, p < 0.001), a higher time-velocity integral of the atrial component (11.7 ± 3.2 cm vs. 5.5 ± 2.1 cm, p < 0.0001), a longer isovolumic relaxation time 73 ± 12 ms vs. 94 ± 6 ms, p < 0.01 and a lower rate of acceleration of blood across the mitral valve (549.2 ± 151.9 cm/sec2 vs. 871 ± 128.1 cm/sec2, p < 0.001). They also had a lower mitral annular relaxation velocity (Ea) (6.08 ± 1.6 cm/sec vs 12.8 ± 0.67 cm/sec, p < 0.001), which was positively correlated to the acceleration of early diastolic filling (R = 0.66), p < 0.05.This investigation provides information on the acceleration of early diastolic filling and its relationship to mitral annular peak tissue velocity (Ea) recorded by Doppler tissue imaging. It supports not only the premise that recoil is an important mechanism for rapid early diastolic filling but also the existence of an early diastolic mechanism in normal.The study of left ventricular filling dynamics has only recently received the same attention historically associated with systolic dynamics. Doppler Tissue Imaging (DTI) is fundamental in this assessment as it allows for the determination of systolic and diastolic velocities in the myocardium [1,2]. A number of studies have proposed that recorded mitral annular displacement and velocity in both systole and diastole may be used as indicators of overall cardiac performance [3,4].In normal left ventricular relaxation after systole, the peak mitral annular velocity (Ea) recorded by DTI precedes the peak early passive diastolic transmitral flow (E) recorded by conventional pulsed wave (PW) Doppler ultrasound. In situations where this relax
The Impact of Statin Intolerance in Lipid Clinic Patients  [PDF]
Kate Williams, Vinita Mishra
International Journal of Clinical Medicine (IJCM) , 2015, DOI: 10.4236/ijcm.2015.65040
Abstract:
Context: Cardiovascular disease is a very common and serious problem in the western world. Statin drug therapy is used in primary, secondary prevention and familial hypercholesterolemia. However, these are frequently associated with adverse effects, causing poor adherence and thus putting patients at risk for future cardiovascular events. Aim: The objective of this study was to review the statin intolerance in lipid patients and to assess the impact of alternative lipid lowering therapy on lipid parameters and cardiovascular outcome in statin intolerant patients. Methodology: 50 patients attending the out-patient lipid clinic of our hospital with statin intolerance were identified. Clinical data on the study patients were gathered retrospectively relating to statin intolerance and the clinical effectiveness of alternative lipid lowering therapy on lipid parameters and cardiovascular outcome. Results: Rosuvastatin was the most intolerable whereas pravastatin or fluvastatin was the most tolerable statin in our study patients. Myalgia was the commonly reported adverse effect of statin. The low dose statin monotherapy or combination of low dose statin and ezetemibe was the most tolerable alternative lipid lowering therapy in statin intolerant patients. After an average period of 10 months of initiation of alternative lipid lowering therapy; combination of low dose statin plus ezetimibe showed the largest reduction in serum total cholesterol and low-density lipoprotein (LDL) cholesterol levels. Conclusions: Pravastatin should be preferred in statin intolerant patients. A combination of low dose statin plus ezetimibe appeared to be the most tolerable and clinically effective therapy in statin intolerant patients.
Adult hereditary fructose intolerance  [cached]
Mohamed Ismail Yasawy, Ulrich Richard Folsch, Wolfgang Eckhard Schmidt, Michael Schwend
World Journal of Gastroenterology , 2009,
Abstract: Hereditary fructose intolerance (HFI) is an under-recognized, preventable life-threatening condition. It is an autosomal recessive disorder with subnormal activity of aldolase B in the liver, kidney and small bowel. Symptoms are present only after the ingestion of fructose, which leads to brisk hypoglycemia, and an individual with continued ingestion will exhibit vomiting, abdominal pain, failure to thrive, and renal and liver failure. A diagnosis of HFI was made in a 50-year-old woman on the basis of medical history, response to IV fructose intolerance test, demonstration of aldolase B activity reduction in duodenal biopsy, and molecular analysis of leukocyte DNA by PCR showed homozygosity for two doses of mutant gene. HFI may remain undiagnosed until adult life and may lead to disastrous complications following inadvertent fructose or sorbitol infusion. Several lethal episodes of HFI following sorbitol and fructose infusion have been reported. The diagnosis can only be suspected by taking a careful dietary history, and this can present serious complications.
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