Вплив антигіпертензивної терапії на рівень сечової кислоти у хворих на артеріальну гіпертензію з гіперурикемією

Артеріальна гіпертензія (АГ) є найбільш поширеним хронічним захворюванням у світі і значною мірою визначає високу смертність та інвалідність від серцево-судинних і церебро-васкулярних захворювань. При цитуванні документа, використовуйте посилання http://essuir.sumdu.edu.ua/handle/123456789/2723

Untargeted Metabolomic Analysis of Sjögren–Larsson Syndrome Reveals a Distinctive Pattern of Multiple Disrupted Biochemical Pathways

Sjögren–Larsson syndrome (SLS) is a rare inherited neurocutaneous disease characterized by ichthyosis, spastic diplegia or tetraplegia, intellectual disability and a distinctive retinopathy. SLS is caused by bi-allelic mutations in ALDH3A2, which codes for fatty aldehyde dehydrogenase (FALDH) and results in abnormal lipid metabolism. The biochemical abnormalities in SLS are not completely known, and the pathogenic mechanisms leading to symptoms are still unclear. To search for pathways that are perturbed in SLS, we performed untargeted metabolomic screening in 20 SLS subjects along with age- and sex-matched controls. Of 823 identified metabolites in plasma, 121 (14.7%) quantitatively differed in the overall SLS cohort from controls; 77 metabolites were decreased and 44 increased. Pathway analysis pointed to disrupted metabolism of sphingolipids, sterols, bile acids, glycogen, purines and certain amino acids such as tryptophan, aspartate and phenylalanine. Random forest analysis identified a unique metabolomic profile that had a predictive accuracy of 100% for discriminating SLS from controls. These results provide new insight into the abnormal biochemical pathways that likely contribute to disease in SLS and may constitute a biomarker panel for diagnosis and future therapeutic studies

Metabolic and endocrine aspects of coronary disease

The early history, the nature and the incidence of coronary atherosclerosis and ischaemic heart disease have been reviewed. Evidence has been presented to suggest that there are aetiological factors which favour the development of ischaemic heart disease without influencing the incidence of coronary atherosclerosis. The close relationship of cholesterol metabolism to coronary atherosclerosis and to ischaemic heart disease has been emphasised. The circulating lipids and lipoproteins have been studied in health in relation to age and sex. They were abnormal in the majority of patients with ischaemic heart disease, particularly in those under the age of 50. Analysis of the circulating lipids and lipoprotein could aid the solution of an equivocal diagnosis in young subjects suspected of having ischaemic heart disease. The effects of endogenous hormones and the action of administered hormones on the circulating lipids and lipoproteins have been described in detail. Hormones can also influence the fluid state of the blood and the tonicity and metabolism of arteries. It has been postulated that the homeostasis of cholesterol metabolism, of the fluid state of the blood and of arterial metabolism could be disturbed by alteration of the physiological endocrine balance. The thesis has been proposed that an endocrine imbalance could contribute to the development of coronary atherosclerosis and of ischaemic heart disease. The relationship of this thesis to existing theories of the aetiology of ischaemic heart disease has been considered in detail. Finally, some therapeutic implications of these metabolic and endocrine aspects of coronary disease have been considered

Coronary thrombosis: a study of 128 cases with special reference to its relationship to angina pectoris

It is observed from this study that angina pectoris and coronary thrombosis are the different phases of the same process being caused by anoxaemia of heart muscle. The underlying factor in both the conditions 154. excluding the precipitating factors is the same i.e. atherosclerosis of coronary arteries Atheromatous changes in angina pectoris however are more or less of a uniform nature, resulting usually in narrowing of the lumen of these vessels, whereas in coronary thrombosis the changes are generally of a patchy type with or without much narrowing of the caliber of coronary arteries. The precipitating factors no doubt are different, but while coronary thrombosis is caused in a person with Sclerotic coronary arteries at rest, Angina pectoris results in the same individual in excitement and with exertion

Uric acid, metabolism, neuro-endocrine-immune complex, 258 s.

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A qualitative study exploring the experiences of access and pathways to health care among BME community groups residing in Ayrshire

A review of the literature showed that Black and minority ethnic (BME) communities carry a disproportionately higher burden of illness than the general population and experience greater inequalities in health and health care provision. A growing body of research confirms that BME groups are under-represented in research. The main objective of the present study was to gain insights into the perspectives of BME community groups' experiences of accessing general and sexual health care services in Ayrshire. Semi-structured interviews were conducted with 11 participants, n = 5 men (age range: 32-65; mean age = 52.4 years), and n = 6 women (age range: 27-60; mean age = 47.67 years). Data were analysed employing Interpretative Phenomenological Analysis (IPA). The analysis is illustrated through the use of four super-ordinate themes: ‘It’s a Trust Thing’, ‘Minding the Gap(s)’, ‘Sexual Health: a Culture of Silence’, and ‘Personal Perception of Risk’. The findings both support and add to the existing trust literature by presenting a heuristic model of trust, and by showing that participants trust is dynamic in character, has a role, and serves various roles and functions that impact decisions about accessing health services. Significant gaps in knowledge about available health services and unique communication challenges that prevent full access to health care and health promotion information were found, resulting in unmet needs. Analysis charted culturally driven factors that prohibit discussions about sexual health concerns and found complex cognitions involved in the personal perception of risk that was meaningfully understood by participants that direct towards understanding risk in terms of a heuristic model. The implications for clinical practice, health promotion, health service development, and the direction of future research will be discussed.awd_pdtunpub2619_ethesesunpu

Gout and Metabolic Disease: Investigation of Potential Relationship in the New Zealand Population

Hyperuricaemia, pathologically defined as the presence of higher levels of serum urate, results from a compromise in the delicate balance between the production and excretion of urate primarily in the liver and the kidneys, respectively. Hyperuricaemia is a prerequisite for gout, a painful inflammatory arthritis. The symptoms of gout arise from the body’s immune response to monosodium urate crystals that accumulate in the synovial fluid of the joints. Hyperuricaemia and gout are complex traits. A number of genetic loci confer risk to develop hyperuricaemia. Genome-wide association studies (GWAS), an indispensable tool in population genetics, has identified at least twenty eight genomic loci that contain variants affecting serum urate concentration. Gene-environment interactions also play a significant role in this context. Exogenous factors such as the intake of purine-rich foods increase the frequency of gout flares. Population-specific genetic effects on gout are as evident, if not more, as for other complex phenotypes. The prevalence of gout is much higher in the New Zealand Polynesian population compared to other populations. Approximately 7% of New Zealand Māori and Pacific Island people and 3% of New Zealand Europeans are affected by gout. The coexistence of metabolic conditions with gout, usually called gout-comorbidities, adds another level of complexity. However, not many studies have attempted to address the causal relationship between these traits. In fact, my research project was instigated as an attempt to study the causal associations between gout and its comorbidities and fill in some gap in the scientific literature. The research was, however, limited to three metabolic conditions/comorbidities of gout – imbalanced iron homeostasis, metabolic syndrome and disrupted lipid metabolism. My study shows an association between increased serum ferritin and the risk of gout and seeded an idea that the consumption of iron-rich diet may play a role in increasing the frequency and severity of gout flares. Genetic association analysis using two variants in the HFE gene was done to confirm the association between ferritin and urate, which showed positive association in a smaller dataset and provoked the idea to investigate the causality, if it exists, between gout and iron metabolism. Using the robust ‘Two-sample Mendelian randomisation’ approach and exploiting summary statistics data from two large GWA studies, I was able to find an evidence of a causal effect of iron on urate metabolism, but not urate on iron metabolism. In the context of the metabolic syndrome, the role of variants within/near the ADRB3, MC3R, MC4R and ADTRP genes were investigated. The positive effects identified for these variants supported the possible involvement of obesity and insulin resistance-related genes in gout pathophysiology. With the help of gene sequencing-based rare variant analyses, several novel population-specific association signals were found within the coding regions of two lipid-related genes, LRP2 and A1CF. Polynesian-specific novel genetic effects were identified to be predictive for gout for common variants within the LRP2 gene. Rare variants within the LRP2 gene were also identified and a higher prevalence of non-synonymous polymorphisms that can increase the risk of hyperuricaemia was observed in European individuals compared to Polynesians. These results indicated LRP2 to contribute to the difference in gout prevalence between Māori and Pacific Island individuals compared to the New Zealand European population. Collectively, my study reports a causal role of iron and ferritin in increasing serum urate concentration and the involvement of imbalanced iron homeostasis in hyperuricaemia. Also, positive genetic associations indicated that genes contributing to metabolic syndrome and lipid metabolism can increase the risk of gout, and also have population-specific effects for the Polynesian and European ancestral groups in New Zealand