Articles

In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies efficacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (efficacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really efficacy drugs strategy that show a profile of efficacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?

Hypertension and blood pressure are closely related, and hypertension is directly related with stroke. There are different type of blood pressures such as basal, diastolic, maximum, mean arterial, systolic, mean central venous. The present report examines the determinants of systolic blood pressure for two different groups of cardiac patients. One group of cardiac patients is those who underwent dobutamine stress echocardiography, and the other group is Worcester heart attack study. Many systolic blood pressure determinants, their effects, and correlations have been focused in the current report.

The global obesity epidemic that was previously reported [1,2] is now to worsen with obesity to double in 73 countries around the world [3,4]. Improving the health of obese individuals by dietary restriction, anti-obese foods and increased physical activity [1] has not reduced the global obesity epidemic. Obesity is linked to nonalcoholic fatty liver disease (NAFLD) [5,6] with complications relevant to the metabolic syndrome and cardiovascular disease [7]. Appetite control has become critical to endocrinology and metabolism with the apelinergic pathway and nuclear receptor Sirtuin 1 (Sirt 1) now connected to the endocrine system [8] and critical to metabolism. The apelin-Sirt 1 interaction involves nitric oxide (NO) [9] that is now considered as the defect [10] in the interaction between the peptide apelin and calorie sensitive gene Sirt 1 involved in NO imbalances in the adipose tissue, liver and the brain.

High blood pressure (HBP) is a strong, independent and etiologically relevant risk factor for cardiovascular and therefore, the leading cause of preventable deaths worldwide. Hypertension has high medical and social costs. Due to its many associated complications, the use of medical services create high costs with medications which represent almost half of the estimated direct expenses. Free distribution of more than 15 medications for HyPERtension and DIAbetes (HIPERDIA program) clearly shows the important role of drugs in the Brazilian Government’s effort to tackle these two diseases. Notwithstanding, the prevalence of HBP is rising in parallel with other NCDs. It is known that HBP results from environmental and genetic factors, and interactions among them. Our ancestors were often faced with survival stresses, including famine, water and sodium deprivation. As results of natural selection, the survival pressures drove our evolution to shape a thrifty genotype, which favored/promoted energy-saving and sodium/water preservation. However, with the switch to a sodium- and energy-rich diets and sedentary lifestyle, the thrifty genotype and ancient frugal alleles, are no longer advantageous, and may be maladaptive to disease phenotype, resulting in hypertension, obesity and insulin resistance syndrome. Low-grade chronic inflammation and oxidative stress would be the underlying mechanisms for these diseases. HBP is often associated with unhealthy lifestyles such as consumption of high fat and/or high-salt diets and physical inactivity. Therefore, alternatively to medicine drugs, lifestyle and behavioral modifications are stressed for the prevention, treatment, and control of hypertension. A lifestyle modification program (LSM) involving dietary counseling and regularly supervised physical activity (“Move for Health”) has been used for decades, in our group, for NCDs primary care. Retrospective (2006-2016) data from 1317 subjects have shown the top quartile of blood pressure(142.2/88.5mmHg) differing from the lower quartile (120.6/69.2mmHg) by being older, with lower schooling, lower income and, lower physical activity and aerobic capacity. Additionally, the P75 showed higher intake of CHO, saturated fat and sodium along with lower-diet quality score with a more processed foods. They showed higher body fatness and prevalence of metabolic syndrome along with higher pro-inflammatory and peroxidative activities and insulin resistance. In this free-demand sample, the HBP rate was 51.2% for SBP and 42.7% for DBP. The rate of undiagnosed HBP was 9.8% and only 1/3 of medicated patients were controlled for HBP. After 10 weeks of LSM the HBP normalization achieved 17.8% for SBP and 9.3% for DBP with a net effectiveness of 8.5% and 2.4%, respectively. The reduction of HBP by LSM was followed by increased aerobic conditioning and reduced intake of processed foods along with decreased values of BMI, abdominal fatness, insulin resistance, pro-inflammatory and peroxydative activities. Importantly, once applied nationwide this LSM would save HBP medication for 3.1 million of hypertensives at an economic saving costs of US$ 1.47 billion a year!

Type 2 diabetes is a common disease in these days and day by day it is arising. The main focus of the study was to investigate association of packed cell volume (PCV), Mean Corpuscular Volume (MPV), Mean Corpuscular Hemoglobin Concentration (MCHC), Red Cell Distribution Width (RDW) with glycemic marker HbA1c. So that PCV, MPV, MCHC, RDW could be used as a predictor of glucoregulation in type 2 diabetes instead of HbA1c value. This study included 87 DMT2 patients, which divided into two groups, A (n=41, presence in diabetics≤6.5-6.9%) and B (n=46, target in diabetes≥7.0%), according to HbA1c values. Spearsman correlation co-efficients were calculated to evaluate the relationship between RBC count, MCHC, RDW with random blood sugar (RBS) and PCV, MCV, MCHC with HbA1c value. Binominal logistic regression analysis was performed to estimate the relationship between glycemic control, as dichotomous outcome of MCHC, RDW, PCV, and MCV as the main prognosticator. MCHC and RDW were significantly higher in the group B compared to the group A. RDW and MCHC may be applied as the auxiliary indicators of deterioration of glucoregulation.

Several experimental studies performed since 1975, using smooth muscles richly innervated by sympathetic nerves to exclude the autonomic influence of adjusting reflex (rodent vas deferens), showed that L-type voltage-activated Ca2++ channels (VACC) blockers completely inhibited neurogenic contractions induced by electrical field stimulation (EFS) in high concentrations (>10-6 M), but paradoxically increased these EFS-contractions in low concentrations (<10-6 M), suggesting that other mechanisms than only autonomic adjusting reflex are involved in these paradoxical effects. In 2013, we showed that these paradoxical effects of L-type VACC blockers, named by us “calcium paradox” phenomenon, were potentiated by drugs which increase cytosolic cAMP concentration ([cAMP] c-enhancers), such as rolipram, IBMX and forskolin, indicating that this sympathetic hyperactivity drug-induced is due to interaction of the Ca2+/cAMP intracellular signaling pathways (Ca2+/cAMP interaction). Then, the pharmacological manipulation of this interaction produced by combination of the L-type VACC blockers used in the antihypertensive therapy, and [cAMP] c-enhancers used in the antidepressive therapy, could represent a potential cardiovascular risk for hypertensive patients due to sympathetic hyperactivity. Then, we discussed the role of Ca2+/cAMP interaction for antihypertensive pharmacotherapy.

Background: Hypoparathyroidism is well known to occur in thalassemia major patients, but it is thought to be uncommon and its incidence is considered to be decreasing with improvements in chelation therapy. The objective of this study was to assess the prevalence of parathyroid dysfunction in the first decade of life of the patients with thalassemia major. Patients and Methods: Ninety children with beta-thalassemia major (55 males and 35 females) with a mean age of 7.17±3.78 years (1-13 years) and age and sex matched control group of 60 healthy children (36 males and 24 females) with a mean age 6.98±3.66 years (1-13) years. Serum parathyroid hormone (PTH), serum total Calcium (Ca), serum phosphorus (P), serum alkaline phosphatase (ALP), serum 25-hydroxyvitamin D (25-OHD) and serum ferritin levels were measured. Result: PTH levels were higher than normal range in 23 (25.6%) patients with a mean value of 75.2±31.3 µg/mL compared to those having normal range level (35.3±15.2 µg/mL). Ca levels were found low in 11 patients (12.2%), and P levels were found high in 2 (2.22%) and low in 4 (4.44%) patients while high ALP levels were found in 6 (6.67%) patients. 25-OHD levels were low in all patients with a mean value of 24.95±5.82. Conclusion: Reports in the literature indicate that parathyroid dysfunction due to iron overload generally occurs in 2nd or 3rd decade of patients with thalassemia major. However, our study shows that PTH due to iron overload may develop in a significant number of thalassemia major patients, therefore, all thalassemics should be carefully watched for endocrine organ function such as hyperparathyroidism might occur even in the first decade of the patients with thalassemia major.

Hypertension is a complex disorder involving multiple organ systems and the primarily modifiable risk factor for heart disease, which is the leading cause of death among both men and women in the World. Although both men and women develop hypertension, distinct gender differences in the incidence and severity of hypertension are well established where men have a higher incidence of hypertension compared with women of the same age until the sixth decade of life [1,2]. Despite gender differences in human hypertension, the treatment guidelines do not differ by gender [3]. Even if the causes of hypertension are complex and are related to genetic factors, lifestyle, diet structure, and environmental factors including air pollution [4], coupled with the potential determinants of hypertension, sex differences in hypertension-which exist in human populations-are attributed to both biological and behavioural factors. The biological factors include sex hormones, chromosomal differences, and other biological sex differences that are protective against hypertension in women. These factors become prominent in adolescence and persist through adulthood until women reach menopause. Behavioural risk factors for hypertension include high body mass index, smoking, and low physical activity.

Background: Vitamin D deficiency in pregnancy increases several risks of breastfed mothers. To prevent these adverse events, vitamin D supplementation during pregnancy and lactation is recommended, but suggested dose ranges vary. Objective: To determine whether vitamin D3 1,800 IU/d supplementation in lactating mothers improves the vitamin D status of their breastfed infants. Materials and Methods: A randomized, placebo–controlled trial with Thai pregnant women was conducted. Lactating mothers (n=72) and their breastfed infants with insufficient maternal 25 hydroxyvitamin D (25(OH)D) levels in the third trimester were randomly assigned to two groups, one of which received 1,800 IU/d vitamin D supplementation and the other a placebo. Maternal serum 25(OH)D during lactation, cord blood, and 6-week breastfed infant serum were measured using LC-MS/MS. Results: Mean maternal age (±SD) was 27±5 years, and pre-gestational BMI was 22.29±5 kg/m2. Maternal serum 25(OH)D at baseline was 22.29±7.15 nmol/L. At 6 weeks, both maternal 25(OH)D and infant 25 (OH)D levels had increased significantly in the vitamin D supplement group of mothers and infants (68.30±15.40, 40.40±12.56 nmol/L) compared to those in placebo groups (55.15±13.57, 24.28±17.20 nmol/L) (p <0.001, p<0.001). The changes in infant 25(OH)D levels increased substantially in the vitamin D supplement group but decreased in placebo(17.49±16.27 ng/ml compared to -1.34±19.23 nmol/L in the placebo group, p<0.001). The change of maternal 25(OH)D were positively correlation to the change of 25(OH)D level in breastmilk mothers and infants by r=0.697, p<0.001 and r=0.379, p=0.003 respectively. Conclusions: Vitamin D3 supplementation to breastfed mother during lactation can increase serum 25(OH)D level in Thai breastfed mother and infants. Further work is needed to determine the optimum duration of vitamin D supplementation to normalized breastfed infants with 25(OH)D level >75 nmol/L.

Objective: To examine the association between adverse social determinants of health (SDH) and missed well-child visits and the interaction with the level of caregiver social support. Methods: This is a secondary data analysis of data collected from a SDH screening program conducted during well-child visits with referral, navigation and follow-up services for patients. We included 573 adult caregivers who accompanied patients aged 0-5 years to well-child visits and completed the screening from August 2017 to May 2018. The caregivers reported financial hardship, food insecurity, housing challenges, childcare difficulty, transportation issues, insurance difficulty, job difficulty, and education needs. Our primary outcome was a no-show (i.e., missed) to a well-child visit. Social support was dichotomized as low or high. Results: Among 573 patients who completed the screening, 335 patients (76.4%) had at least one social need. Financial hardship (p = 0.006), housing instability (p = 0.002), and no/poor childcare (p = 0.03) were associated with missed well-child visits. In multivariable regression analysis, having Medicaid (aOR = 1.91 [1.17-3.10]) and unstable housing (aOR = 6.79 [1.35-34.70]) were both associated with missed well-child visits. However, when social support was added to the multivariable logistic model, both Medicaid and unstable housing were no longer associated with missed well-child visits. Conclusion: Adverse SDH such as financial hardship, housing instability, and childcare difficulty were associated with missed well-child visits. However, with the addition of social support, this association was no longer significant. This study supports the hypothesis that high social support may mitigate the association between well-child visits among families experiencing adverse SDH.