Recomendaciones dietéticas para las dislipemias. ANEXO DISLIPEMIAS: Guía para la prescripción del .. – himar perez Dieta: Dislipemia – Hipercolesterolemia – Prevención Arteriosclerosis. Circulation ; Lago F. Dislipemias. Guias clinicas ;2 (41). Available at: ra. com/ Mahley RW. Bersot TP.
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It is the best journal to keep up to date with endocrine pathophysiology both in the clinical and in the research field. It publishes the best original articles of large research institutions, as well as prestigious reviews. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two receding years.
SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal’s impact.
SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. There are studies showing a strong association between thyroid dysfunction and increased cardiovascular risk due to lipid profile changes. The purpose of this study was to assess the degree of association and predictive power of thyroid-stimulating hormone TSH levels in relation to lipid profile changes, identifying the TSH cut-off point beyond which lipid changes occur.
A cross-sectional, retrospective study in Quito Ecuador was conducted from January to December on patients first attending the endocrinology department.
A total of histories were analyzed, and a No association was found between sex and cholesterol or between sex and low density lipoprotein LDL. TSH levels show a statistically significant association to total cholesterol and LDL levels, but are not a good clinical predictor in this process.
A cut-off point beyond which replacement therapy should be started to prevent occurrence of dyslipidemia cannot therefore be established. Thyroid hormone deficiency may occur as clinical or subclinical hypothyroidism. The role of thyroid hormones on the cardiovascular system is crucial, and a strong association has been found between thyroid hormones and both lipid profile and atherosclerotic disease as predictors of cardiovascular risk.
Studies conducted in hypothyroid patients have reported high levels of total and low density lipoprotein LDL cholesterol and decreased levels of high density lipoprotein HDL cholesterol as compared to euthyroid controls. The pathophysiological mechanism accounting for the atherogenic process consists of a decreased affinity of LDL for its receptors, decreased biliary excretion of cholesterol, and decreased lipoprotein lipase activity, resulting in the prolongation of the half-lives of total and LDL cholesterol.
It should be borne in mind that cardiovascular disease is the leading cause of disability and early death worldwide, and makes a substantial contribution to the high costs of health care.
Atherosclerosis is the main condition, related to coronary artery disease and a significant increase in morbidity and mortality. Dyslipidemia is one of the five significant risk factors for the development of cardiovascular diseases, 16,17 and hypothyroidism is the second leading endocrinological disease causing dyslipidemia after diabetes mellitus. It should also be noted that a study where patients were distributed into groups based on their severity of dyslipidemia found the greatest proportion of patients with subclinical hypothyroidism in the group with the highest serum cholesterol levels, which confirmed that subclinical hypothyroidism is a risk factor for atherosclerosis and myocardial infarction.
National Health and Nutrition Examination Survey NHANES III showed higher cholesterol and LDL levels in patients with subclinical hypothyroidism as compared to euthyroid patients, but after adjustment for variables such as sex, race, age, and the concomitant use of oral lipid lowering drugs, hypothyroidism was not related to an abnormal lipid profile.
The main controversy in the vast majority of studies on the adequate time to start hypothyroid treatment is focused on the TSH cut-off value below which hormone replacement therapy should be started in order to normalize lipid levels. The presence or absence of antibodies and the risk-benefit of treatment should also be considered.
The purpose of this study was to establish the degree of clinical and statistical association of TSH levels and lipid profile, what the contribution of replacement therapy as an intervention to prevent the occurrence of dyslipidemia would be, and the ideal cut-off point for starting such therapy. This was a retrospective, cross-sectional study enrolling all patients attending the endocrinology department of the General Army Hospital No.
Thyroid hormone and lipid profile tests of all patients were requested during their first visit, and clinical histories from patients who had complete results for thyroid function, anthropometrics, LDL cholesterol, and total cholesterol were also selected for the research.
Patients attending the endocrinology outpatient clinic whose clinical history included all variables proposed in the case report form were considered to be eligible, while patients having a concurrent disease as the causative factor of lipid changes, pregnant women, and patients already receiving lipid lowering treatment before being diagnosed with hypothyroidism were excluded from the study.
dislipemiqs Data were collected by reviewing clinical histories. These mainly consisted of progress notes of the first visit and results obtained at the laboratory of the Military Hospital. In the first stage, a univariate analysis was performed. Continuous variables were summarized with measures of central tendency and dispersion.
Linear regression with Pearson’s R 2 coefficient was used for this purpose.
The receiver operating characteristics ROC curve was used to measure the clinical predictive power of the association between TSH and dyslipidemia.
All clinical histories from patients attending the endocrinology department of the Military Hospital from January to December were reviewed, and TSH tests were requested.
There were clinical histories that met this criterion. Of these, clinical histories not including the results of lipid and thyroid profiles, height or weight were excluded, leaving histories. Exclusion criteria, as reported in the methodology, were met by clinical histories. A total of clinical histories were therefore used for the final analysis. The median age of the patients was 51 years IQR [second interquartile]: One hundred and twelve subjects Median age was similar across diagnoses Table Diagnosis in relation to age and sex.
As regards anthropometric data, median height was cm IQR: Diagnosis in relation to lipid changes and anthropometric values. Mean total cholesterol levels and diagnosis. Mean LDL cholesterol levels and diagnosis. Dyslipidemia according to the criteria given in the subjects and methods section was found in patients No significant difference was found in sex distribution in these age groups OR: No significant difference was seen either in TSH levels between both age groups.
A significant difference was however seen in total and LDL cholesterol levels and BMI, with higher values found in subjects older than 50 years Table TSH levels, dyslipidemia, and body mass index by age group. No association was found between sex and total cholesterol or between sex and LDL cholesterol.
Linear regression of TSH-total cholesterol. Linear regression of body mass index-TSH. Receiver operating characteristics curve for the discriminant power of TSH in dyslipidemia. Since a clinical association was not found between TSH levels and lipid profile changes, the next planned step, namely the determination of the cut-off point for TSH beyond which treatment would be started, was not warranted. This study showed a statistical association between TSH levels and lipid profile changes.
It may therefore be stated that TSH level is a risk factor for the development of lipid changes, but is not a good clinical predictor of such changes. However, this association has no clinical implications for prediction, as it is shown by the analysis of the ROC curve. In studies on clinical predictors, it is very important to distinguish between the existence of an association between two variables and the strength of such an association with its attendant clinical implications.
In fact, it has been shown that in many studies where a statistical association has been found between two variables, the association loses predictive power when it is converted into confirmatory and exclusionary powers.
This is precisely what happened in this study: However, the strength of this association was very weak, and it had therefore no value as a clinical predictor.
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This was the reason why assessment of the cut-off point made no sense. It should be noted that this does not mean that TSH is no longer significant as a risk factor for dyslipidemia.
However, it should be used for primary prevention, not for taking treatment decisions. It is significant that 8 out of every 10 histories reviewed were of female patients, which agrees with the results of previous studies. It should be stressed that the study was conducted at the Army Hospital, where the majority of patients are male. This confirms the predominance of thyroid disease in females.
The increasing prevalence of subclinical hypothyroidism was also confirmed by the higher prevalence rates reported in patients between the fifth and sixth decades of life.
A predominance of patients with clinical hypothyroidism was also found, but it should be noted that the highest total cholesterol and LDL cholesterol levels were seen in patients with subclinical thyroid disease with highly significant p values, in whom a TSH cut-off value of 5. These figures agree with the results of other studies and suggest that, despite the low predictive power for dyslipidemia of TSH discussed in prior paragraphs, lipid profile should be tested in patients with TSH levels higher than the cut-off point found.
Mention should be made of the worldwide controversy about the relationship between subclinical hypothyroidism and dyslipidemia.
Prevalence rates of hypothyroidism were shown to be 7. Dyslipidemia is one of the five risk factors for the development of cardiovascular disease, 13 and hypothyroidism is the second leading endocrinological disease causing dyslipidemia dslipemias diabetes mellitus. Different views also exist regarding screening in the general population. The American Thyroid Association recommends TSH measurements from the age of 35 dislipemiws and every five years thereafter in asymptomatic adults, while the U.
Preventive Services Task Force questions screening, particularly in men, who have a much lower incidence of subclinical hypothyroidism as compared to older women.
Their main argument, however, is that studies do not lead to clear conclusions as to whether early treatment does or does not decrease morbidity and mortality or improves quality of life in these cases. This agrees with the findings reported in fitserra environment. Studies in patients with hypothyroidism showed prolongation of the half-life of LDL cholesterol due to decreased catabolism, an effect which is reversible upon the administration of hormone treatment.
Additional data from human fibroblasts confirm that T3 induces an increased degradation of LDL cholesterol, which is a direct mediator of the increase in the number of LDL receptors with no change in LDL affinity for these receptors.
Research on patients with hypothyroidism showed an increase in LDL cholesterol half-life secondary to decreased catabolism, an effect that is reversible with replacement therapy. It needs therefore to be confirmed whether or not LDL cholesterol levels decrease when replacement therapy is started with levothyroxine despite the absence of lipid lowering treatment. This study is the first retrospective research conducted in our country to assess the association between subclinical hypothyroidism and lipid profile.
It provides data about TSH levels that cause lipid changes in our environment, although it should be borne in mind that they are not the best predictor for the occurrence of such changes. It is also expected to be the basis for future prospective studies. One of the limitations of this study was its retrospective nature. In addition, data for the clinical histories were recorded by other people.
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It should be stressed that many medical charts were excluded from the study because they did not include the data required for the analysis. A significant disadvantage that should be mentioned is the lack of lipid profile results in patients diagnosed with subclinical hypothyroidism, probably because of a lack of awareness about the correlation between the disease investigated and dyslipidemia.
A bias that should be taken into account is that a majority of the study population from the Military Hospital belonged to the middle and upper middle classes, and the study results can therefore only be extrapolated to populations with the same socioeconomic characteristics. This research, which was conducted in order to find an association between TSH levels and lipid profile changes, will serve as the basis for future prospective research where long-term monitoring of patients may allow for analyzing parameters that could not be studied in a retrospective study such as this.
It will also be appropriate to consider studies that allow for establishing the prevalence of cardiovascular risk factors in relation to subclinical hypothyroidism, with regard to blood pressure levels, cardiac muscle hypertrophy, the size of atheromatous plaque at the aortic level, the development of peripheral fisterga, and the influence of associated factors such as smoking and diabetes mellitus, taking into account that subclinical hypothyroidism is a marker of nephropathy and coronary artery disease in diabetic patients.
The clinical implications of this study are very important, because it helps us to understand diwlipemias true value of TSH measurements in patients with suspected subclinical hypothyroidism. In fact, based on the results obtained, there would appear to be no point in dislipemiae TSH levels when making the decision whether or not to start replacement therapy to prevent dyslipidemia. The study was fully financed by the authors. The authors state that they have no conflicts of interest.