Health-related quality of life and factors affecting it in type-2 diabetic nephropathy patients: a cross sectional observational study

Background: Diabetes is known to worsen the health related quality of life (HRQoL). The aim of the study was to analyze a comprehensive set of potential determinants of HRQoL in a sample of patients suffering from diabetic nephropathy.Method: 60 patients were enrolled and divided into different groups on the basis of stage of diabetic nephropathy. HRQoL was evaluated using generic and disease- specific questionnaires. Generic instrument included SF-36 and diseases-specific instruments used were D-39 (Diabetes-39) and ADS (appraisal diabetes scale). The scores of these questionnaires were analyzed for their association with various demographic factors.Results: It was observed that quality of life deteriorated with the progression of diabetic nephropathy. On the basis of SF-36 score HRQoL was found to be dependent on, age, HbA1c level, presence of positive family history of diabetes and alcohol consumption. On the other hand D-39 scores showed significant association between HRQoL and various demographic factors such as gender, blood pressure, alcoholic consumption and blood sugar levels. According to ADS scores, HRQoL showed association with alcohol consumption and blood sugar levels.Discussion: HRQoL is associated with multiple factors but high linkage is demonstrated by socio-demographic factors and diabetic complications. A patient centred approach should be helpful to prevent deterioration of HRQoL and thus will decrease the burden of diabetes. A regular checkup and early detection of diabetic nephropathy and its management could further delay the decline in quality of life of these patients

Effect of sodium tungstate on obesity induced cardiac hypertrophy and oxidative stress

Obesity was induced by high fat diet (30 % fat by weight). Wistar rats of 225-250 g were kept on high fat diet to induce obesity for 90 days. Sodium tungstate (2 mg/ml, in drinking water) was administered for 90 days. Obesity was assessed by measuring % age change in body weight, WHR ratio, adiposity index and obesity index. Left ventricular cardiac hypertrophy was assessed in terms of left ventricular weight, left ventricular wall thickness, left ventricular protein content and left ventricular collagen content. Oxidative stress was measured in terms of levels of thiobarbituric acid reactive substances (TBARS), superoxide anion generation (SAG) and level of reduced glutathione. Sodium tungstate significantly attenuated the increase in body weight adiposity index, obesity index, TBARS, SAG and reduced glutathione, whereas no significant change was observed the parameters of cardiac hypertrophy. So, it can be concluded that sodium tungstate significantly attenuated high fat diet induced obesity and oxidative stress but no significant decrease was observed in the parameters of cardiac hypertrophy.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Effect of sodium tungstate on obesity induced cardiac hypertrophy and oxidative stress

Obesity was induced by high fat diet (30 % fat by weight). Wistar rats of 225-250 g were kept on high fat diet to induce obesity for 90 days. Sodium tungstate (2 mg/ml, in drinking water) was administered for 90 days. Obesity was assessed by measuring % age change in body weight, WHR ratio, adiposity index and obesity index. Left ventricular cardiac hypertrophy was assessed in terms of left ventricular weight, left ventricular wall thickness, left ventricular protein content and left ventricular collagen content. Oxidative stress was measured in terms of levels of thiobarbituric acid reactive substances (TBARS), superoxide anion generation (SAG) and level of reduced glutathione. Sodium tungstate significantly attenuated the increase in body weight adiposity index, obesity index, TBARS, SAG and reduced glutathione, whereas no significant change was observed the parameters of cardiac hypertrophy. So, it can be concluded that sodium tungstate significantly attenuated high fat diet induced obesity and oxidative stress but no significant decrease was observed in the parameters of cardiac hypertrophy.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Modulation of impact of obesity in pathological and physiological cardiac hypertrophy by orlistat

High fat diet (30 % fat) was used to induce obesity in rats. Male wistar rats were kept at high fat diet for 90 days and subjected to partial abdominal aortic constriction (PAAC) at 62nd day and continued upto 90th day. Similarly rats were kept at high fat diet for 90 days and subjected to chronic swimming training (CST) at 46th day and continued upto 90th day. Obesity was assessed by measuring body weight, WHR ratio, obesity index and adiposity index. Cardiac hypertrophy was assessed by measuring left ventricular weight, left ventricular weight to body weight, left ventricular wall thickness, cardiomyocyte diameter, left ventricular protein content and left ventricular collagen content. Mean arterial blood pressure (MABP) was also recorded. Oxidative stress was assessed in terms of thiobarbituric acid reactive species (TBARS) level, superoxide anion generation level and reduced glutathione level in left ventricular tissue. Obesity, cardiac hypertrophy and oxidative stress were increased in high fat diet groups. Orlistat, lipase inhibitor, significantly attenuated the impact of obesity in experimental cardiac hypertrophy. Furthermore orlistat significantly attenuated the oxidative stress. So it can be concluded that by decreasing the impact of obesity, orlistat significantly attenuated the extent of cardiac hypertrophy.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Modulation of impact of obesity in pathological and physiological cardiac hypertrophy by orlistat

High fat diet (30 % fat) was used to induce obesity in rats. Male wistar rats were kept at high fat diet for 90 days and subjected to partial abdominal aortic constriction (PAAC) at 62nd day and continued upto 90th day. Similarly rats were kept at high fat diet for 90 days and subjected to chronic swimming training (CST) at 46th day and continued upto 90th day. Obesity was assessed by measuring body weight, WHR ratio, obesity index and adiposity index. Cardiac hypertrophy was assessed by measuring left ventricular weight, left ventricular weight to body weight, left ventricular wall thickness, cardiomyocyte diameter, left ventricular protein content and left ventricular collagen content. Mean arterial blood pressure (MABP) was also recorded. Oxidative stress was assessed in terms of thiobarbituric acid reactive species (TBARS) level, superoxide anion generation level and reduced glutathione level in left ventricular tissue. Obesity, cardiac hypertrophy and oxidative stress were increased in high fat diet groups. Orlistat, lipase inhibitor, significantly attenuated the impact of obesity in experimental cardiac hypertrophy. Furthermore orlistat significantly attenuated the oxidative stress. So it can be concluded that by decreasing the impact of obesity, orlistat significantly attenuated the extent of cardiac hypertrophy.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Effect of sodium tungstate on obesity induced cardiac hypertrophy and oxidative stress

Obesity was induced by high fat diet (30 % fat by weight). Wistar rats of 225-250 g were kept on high fat diet to induce obesity for 90 days. Sodium tungstate (2 mg/ml, in drinking water) was administered for 90 days. Obesity was assessed by measuring % age change in body weight, WHR ratio, adiposity index and obesity index. Left ventricular cardiac hypertrophy was assessed in terms of left ventricular weight, left ventricular wall thickness, left ventricular protein content and left ventricular collagen content. Oxidative stress was measured in terms of levels of thiobarbituric acid reactive substances (TBARS), superoxide anion generation (SAG) and level of reduced glutathione. Sodium tungstate significantly attenuated the increase in body weight adiposity index, obesity index, TBARS, SAG and reduced glutathione, whereas no significant change was observed the parameters of cardiac hypertrophy. So, it can be concluded that sodium tungstate significantly attenuated high fat diet induced obesity and oxidative stress but no significant decrease was observed in the parameters of cardiac hypertrophy.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Case Reports1. A Late Presentation of Loeys-Dietz Syndrome: Beware of TGFβ Receptor Mutations in Benign Joint Hypermobility

Background: Thoracic aortic aneurysms (TAA) and dissections are not uncommon causes of sudden death in young adults. Loeys-Dietz syndrome (LDS) is a rare, recently described, autosomal dominant, connective tissue disease characterized by aggressive arterial aneurysms, resulting from mutations in the transforming growth factor beta (TGFβ) receptor genes TGFBR1 and TGFBR2. Mean age at death is 26.1 years, most often due to aortic dissection. We report an unusually late presentation of LDS, diagnosed following elective surgery in a female with a long history of joint hypermobility. Methods: A 51-year-old Caucasian lady complained of chest pain and headache following a dural leak from spinal anaesthesia for an elective ankle arthroscopy. CT scan and echocardiography demonstrated a dilated aortic root and significant aortic regurgitation. MRA demonstrated aortic tortuosity, an infrarenal aortic aneurysm and aneurysms in the left renal and right internal mammary arteries. She underwent aortic root repair and aortic valve replacement. She had a background of long-standing joint pains secondary to hypermobility, easy bruising, unusual fracture susceptibility and mild bronchiectasis. She had one healthy child age 32, after which she suffered a uterine prolapse. Examination revealed mild Marfanoid features. Uvula, skin and ophthalmological examination was normal. Results: Fibrillin-1 testing for Marfan syndrome (MFS) was negative. Detection of a c.1270G > C (p.Gly424Arg) TGFBR2 mutation confirmed the diagnosis of LDS. Losartan was started for vascular protection. Conclusions: LDS is a severe inherited vasculopathy that usually presents in childhood. It is characterized by aortic root dilatation and ascending aneurysms. There is a higher risk of aortic dissection compared with MFS. Clinical features overlap with MFS and Ehlers Danlos syndrome Type IV, but differentiating dysmorphogenic features include ocular hypertelorism, bifid uvula and cleft palate. Echocardiography and MRA or CT scanning from head to pelvis is recommended to establish the extent of vascular involvement. Management involves early surgical intervention, including early valve-sparing aortic root replacement, genetic counselling and close monitoring in pregnancy. Despite being caused by loss of function mutations in either TGFβ receptor, paradoxical activation of TGFβ signalling is seen, suggesting that TGFβ antagonism may confer disease modifying effects similar to those observed in MFS. TGFβ antagonism can be achieved with angiotensin antagonists, such as Losartan, which is able to delay aortic aneurysm development in preclinical models and in patients with MFS. Our case emphasizes the importance of timely recognition of vasculopathy syndromes in patients with hypermobility and the need for early surgical intervention. It also highlights their heterogeneity and the potential for late presentation. Disclosures: The authors have declared no conflicts of interes

Estimating global injuries morbidity and mortality : methods and data used in the Global Burden of Disease 2017 study

Background: While there is a long history of measuring death and disability from injuries, modern research methods must account for the wide spectrum of disability that can occur in an injury, and must provide estimates with sufficient demographic, geographical and temporal detail to be useful for policy makers. The Global Burden of Disease (GBD) 2017 study used methods to provide highly detailed estimates of global injury burden that meet these criteria. Methods: In this study, we report and discuss the methods used in GBD 2017 for injury morbidity and mortality burden estimation. In summary, these methods included estimating cause-specific mortality for every cause of injury, and then estimating incidence for every cause of injury. Non-fatal disability for each cause is then calculated based on the probabilities of suffering from different types of bodily injury experienced. Results: GBD 2017 produced morbidity and mortality estimates for 38 causes of injury. Estimates were produced in terms of incidence, prevalence, years lived with disability, cause-specific mortality, years of life lost and disability-adjusted life-years for a 28-year period for 22 age groups, 195 countries and both sexes. Conclusions: GBD 2017 demonstrated a complex and sophisticated series of analytical steps using the largest known database of morbidity and mortality data on injuries. GBD 2017 results should be used to help inform injury prevention policy making and resource allocation. We also identify important avenues for improving injury burden estimation in the future

Alcohol use and burden for 195 countries and territories, 1990-2016 : a systematic analysis for the Global Burden of Disease Study 2016

Background Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions. With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older. Methods Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs. We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health. Findings Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2.2% (95% uncertainty interval [UI] 1.5-3.0) of age-standardised female deaths and 6.8% (5.8-8.0) of age-standardised male deaths. Among the population aged 15-49 years, alcohol use was the leading risk factor globally in 2016, with 3.8% (95% UI 3.2-4-3) of female deaths and 12.2% (10.8-13-6) of male deaths attributable to alcohol use. For the population aged 15-49 years, female attributable DALYs were 2.3% (95% UI 2.0-2.6) and male attributable DALYs were 8.9% (7.8-9.9). The three leading causes of attributable deaths in this age group were tuberculosis (1.4% [95% UI 1. 0-1. 7] of total deaths), road injuries (1.2% [0.7-1.9]), and self-harm (1.1% [0.6-1.5]). For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27.1% (95% UI 21.2-33.3) of total alcohol-attributable female deaths and 18.9% (15.3-22.6) of male deaths. The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0.0-0.8) standard drinks per week. Interpretation Alcohol use is a leading risk factor for global disease burden and causes substantial health loss. We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero. These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.Peer reviewe

Global injury morbidity and mortality from 1990 to 2017 : results from the Global Burden of Disease Study 2017

Correction:Background Past research in population health trends has shown that injuries form a substantial burden of population health loss. Regular updates to injury burden assessments are critical. We report Global Burden of Disease (GBD) 2017 Study estimates on morbidity and mortality for all injuries. Methods We reviewed results for injuries from the GBD 2017 study. GBD 2017 measured injury-specific mortality and years of life lost (YLLs) using the Cause of Death Ensemble model. To measure non-fatal injuries, GBD 2017 modelled injury-specific incidence and converted this to prevalence and years lived with disability (YLDs). YLLs and YLDs were summed to calculate disability-adjusted life years (DALYs). Findings In 1990, there were 4 260 493 (4 085 700 to 4 396 138) injury deaths, which increased to 4 484 722 (4 332 010 to 4 585 554) deaths in 2017, while age-standardised mortality decreased from 1079 (1073 to 1086) to 738 (730 to 745) per 100 000. In 1990, there were 354 064 302 (95% uncertainty interval: 338 174 876 to 371 610 802) new cases of injury globally, which increased to 520 710 288 (493 430 247 to 547 988 635) new cases in 2017. During this time, age-standardised incidence decreased non-significantly from 6824 (6534 to 7147) to 6763 (6412 to 7118) per 100 000. Between 1990 and 2017, age-standardised DALYs decreased from 4947 (4655 to 5233) per 100 000 to 3267 (3058 to 3505). Interpretation Injuries are an important cause of health loss globally, though mortality has declined between 1990 and 2017. Future research in injury burden should focus on prevention in high-burden populations, improving data collection and ensuring access to medical care.Peer reviewe