Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P < .01), while a positive association with adiponectin concentrations was found (r = .7, P < .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.

Vitamin D deficiency is associated with cardiometabolic risk factors (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We studied 50 obese patients (body mass index [BMI]: 43.5 ± 9.2 kg/m(2)) and 36 normal weight participants (BMI: 22.6 ± 1.9 kg/m(2)). The prevalence of vitamin D deficiency (25-hydroxyvitamin D, 25(OH)D < 50 nmol/L) was 88% among obese patients and 31% among nonobese individuals; 25(OH)D levels were lower in the obese group (27.3 ± 13.7 vs 64.6 ± 21.3 nmol/L; P < .001). There was a negative correlation between vitamin D level and anthropometric indicators of obesity: BMI (r = -0.64; P < .001), waist circumference (r = -0.59; P < .001), and body fat percentage (r = -0.64; P < .001) as well as with fasting plasma insulin (r = -0.35; P < .001) and homeostasis model assessment of insulin resistance (r = -0.35; P < .001). In conclusion, we observed a higher prevalence of vitamin D deficiency among obese participants and this was associated with a proatherogenic cardiometabolic risk profile.

CSL could serve as a useful biomarker of early atherosclerosis in obese persons without previous history of cardiometabolic disorders but the final conclusion requires further testing.

Among the non-communicable diseases, cardiovascular disorders are the leading cause of morbidity and mortality in both the developed and the developing countries. The spectrum of risk factors is wide and their understanding is imperative to prevent the first and recurrent episodes of myocardial infarction, stroke or peripheral vascular disease which may prove fatal or disabling. This book has tried to present an update on risk factors incorporating new research which has thrown more light on the existing knowledge. It has also tried to highlight regional diversity addressing such issues. It will hopefully be resourceful to the cardiologists, general practitioners, family physicians, researchers, graduate students committed to cardiovascular risk prevention.

Introduction. Adrenal insufficiency results from the inadequate adrenocortical conjunction. Adrenal insufficiency can be primary, secondary and tertiary one. The most common cause of adrenal suppression is the effect of exogenous therapy with glucocorticoids. Glucocorticoids. Corticosteroids are used in treatment of endocrine and non-endocrine diseases. They are applied as a substitution therapy in the patients with primary and secondary adrenal insufficiency. Due to their immunosuppressive and anti-inflammatory characteristics, they are used to treat a wide range of diseases. They are usually divided according to the length and size of the effect i.e. how they are applied. Adrenal Insufficiency. Glucocorticoid therapy may lead to a number of adverse effects such as a disorder in glucose metabolism, osteoporosis or frequent infections. Adrenal suppression is the most common complication resulting from corticosteroid application. The function of the hypothalamus-pituitary-adrenal axis may be inhibited for months after the treatment cessation. There are several predictors of potential glucocorticoid-induced adrenal suppression. Diagnosing Adrenal Insufficiency. The most frequent symptoms and signs of adrenal insufficiency are fatigue, nausea and vomiting, hyponatremia, hyperpigmentation or hypotension. Algorithm for the diagnosis of adrenal insufficiency must be followed in clinical practice. Reduction in Glucocorticoid Therapy. Reduction or complete cessation of the therapy is indicated when the maximum therapeutic benefit has been achieved or when considerable side effects, such as diabetes mellitus, severe hypertension, osteoporosis i.e. adrenal insufficiency, develop. Conclusion. Numerous synthetic glucocorticoids have been developed to be used in everyday clinical practice and they can be administered systemically or locally. A lot of side effects are associated with chronic administration of glucocorticoids. In order to avoid complications, it is recommended to administer intermediate-acting glucocorticoids every second day. In addition, the patients must be monitored carefully and glucocorticoid therapy should be discontinued gradually to prevent adrenal insufficiency or reactivation of the disease under therapy.

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Introduction: Obesity is associated with wide variety of electrocardiographic (ECG) abnormalities. Prolonged QTc interval is common in obesity and it represents a delayed ventricular repolarisation which is associated with ventricular arrhythmias, syncope and sudden cardiac death. The aim of our study is to evaluate the effects of weight reduction on QTc interval in obese subjects. Materials and Methods: The study included 74 obese subjects aged 41.78 ± 10.70 years, treated with a lowcalorie diet (800 kcal/day) for two weeks. All patients underwent a standard resting 12-lead surface ECG before and after the treatment. QTc intervals were corrected by Bazett's formula. Results: The average loss in body weight was 10.26 ± 3.63%, and the average reduction in body mass index was 9.39 ± 4.23%. There were statistically significant differences for all electrocardiographic parameters (p<0.01) except for the QTc dispersion (p>0.05) before and after the treatment with low-calorie diet. Heart rate was also statistically significant reduced after the low-calorie diet treatment. Prevalence of prolonged QTc interval was 24.32% before and 9.21% after the treatment. Conclusion: The results show that obesity causes prolongation of QTc interval. Significant weight reduction of about 10% leads to favorable electrocardiographic changes and significant shortening of the QTc interval.

The patients with type 1 diabetes were found to have a low level of inflammatory activity manifested by the increased values of CRP, IL-6 and TNF-alpha.