ABSTRACT
Background: The burden of diabetes-related deaths reached two million in 2019 globally. Accessibility to health care services and adherence to follow-up and therapy are key to improving outcomes for diabetic patients. We aimed to assess outpatient department (OPD) service utilization and diabetes-related hospitalizations over a period of 44 months. Methods: A retrospective cohort study was conducted on OPD visits and hospitalizations recorded between January 1, 2018, and August 31, 2021, at the St Luke Catholic Hospital (Ethiopia). All diabetic patients were included in the analysis. A linear regression model was used for univariate analysis of OPD visits and hospitalizations and their association with potential predictors. The autoregressive integrated moving average (ARIMA) method was applied to both the time series of OPD visits and hospitalizations. Potential predictors were sociodemographic factors, COVID-19 cases, mean monthly temperature and precipitations. Results: In the time series analysis, OPD visits increased over time (P < 0.01) while hospitalizations were stable. The time series model was ARIMA (0,1,1) for OPD visits and ARIMA (0,0,0) for hospitalizations. There were 1685 diabetes OPD patients (F = 732, 43%). Females had an average of 16% fewer OPD accesses per month (P < 0.01) and a lower number of hospitalizations per month (P = 0.03). There were 801 patients missing follow-up (48%). The time between follow-up increased with age (P < 0.01). OPD visits decreased differently by geographic area as COVID-19 cases increased (P < 0.01). There were 57 fewer forecast OPD visits per month on average using COVID-19 cases as ARIMA regressor. The odds ratio (OR) of new diagnosis at hospitalization was lower in patients with type 2 diabetes (OR = 0.26, 95% CI = 0.14-0.49, P = 0.02). Conclusions: Despite an increase in OPD visits for diabetic patients over the study period, the number of losses at follow-up and diagnoses at hospitalization remains high. Female sex, older age, and COVID-19 were associated with impaired OPD service accessibility. Primary health care should be implemented to achieve better health coverage and improve diabetes management.
Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Humans , Female , Ethiopia/epidemiology , Retrospective Studies , COVID-19/epidemiology , COVID-19/therapy , Outpatients , Emergency Service, Hospital , Hospitalization , Ambulatory Care , HospitalsABSTRACT
PURPOSE OF REVIEW: To examine the state of the art on the pathogenesis of endothelial dysfunction in the microcirculation of patients with obesity, focusing on the complex relationship between the consolidated and the novel mechanisms involved in this alteration. RECENT FINDINGS: Human obesity is associated with vascular endothelial dysfunction, caused by a reduced nitric oxide availability secondary to an enhanced oxidative stress production. Pro-inflammatory cytokine generation, secreted by perivascular adipose tissue, is a major mechanism whereby obesity is associated with a reduced vascular NO availability. Vasculature also represents a source of low-grade inflammation and oxidative stress which contribute to endothelial dysfunction in obese patients. Recently, a direct influence of arginase on endothelial function by reducing nitric oxide availability was demonstrated in small vessels from patients with severe obesity. This effect is modulated by ageing and related to the high levels of vascular oxidative stress. Oxidative stress, inflammation, and enzymatic pathways are important players in the pathophysiology of obesity-related vascular disease. The identification of new therapeutic approaches able to interfere with these mechanisms will result in more effective prevention of the cardiovascular complications associated with obesity.
Subject(s)
Endothelium, Vascular/physiopathology , Obesity/physiopathology , Humans , Inflammation , Nitric Oxide/metabolism , Oxidative StressABSTRACT
Arterial hypertension remains the world's leading mortality risk factor and despite overwhelming evidence that blood pressure-lowering strategies greatly reduce the cardiovascular risk, a substantial proportion of hypertensive individuals worldwide fail to achieve an optimal blood pressure control under treatment. Among the causes responsible for the gap existing between blood pressure lowering potential of the different antihypertensive treatments and real-life practice is the presence of drug-induced hypertension. Many therapeutic agents or substances may directly favour an increment of blood pressure values or counteract the blood pressure lowering effects of antihypertensive drugs. Excessive water and sodium retention, direct vasoconstriction or sympathomimetic activation are major mechanisms of action of such substances. The present manuscript will review medications and other substances that may increase blood pressure, also suggesting the choice of the more appropriate antihypertensive agents to employ when withdrawal of the substance or drug causing an elevation of blood pressure values is not possible.
Subject(s)
Antihypertensive Agents/therapeutic use , Arterial Pressure/drug effects , Drug-Related Side Effects and Adverse Reactions/drug therapy , Hypertension/drug therapy , Antihypertensive Agents/adverse effects , Clinical Decision-Making , Drug-Related Side Effects and Adverse Reactions/diagnosis , Drug-Related Side Effects and Adverse Reactions/etiology , Drug-Related Side Effects and Adverse Reactions/physiopathology , Humans , Hypertension/chemically induced , Hypertension/diagnosis , Hypertension/physiopathology , Risk Factors , Treatment OutcomeABSTRACT
Reactive oxygen species (ROS) are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. Physiologically, ROS generation is counteracted effectively by the rate of elimination. In hypertension, a ROS excess occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. Angiotensin II, the active peptide of the renin-angiotensin-system (RAS), is a significant stimulus for ROS generation within the vasculature. It was also documented that at the level of subfornical cerebral regions an inappropriate RAS stimulation may lead to an increased vascular sympathetic activity. More recently, in conditions of fetal undernutrition, it was also proposed an increased vascular sympathetic activity secondary to inappropriate RAS activation, leading to the development of hypertension in adult life. The present review will discuss the complex interaction between RAS activation, vascular ROS generation and increased sympathetic outflow in hypertension.
Subject(s)
Angiotensin II/metabolism , Blood Pressure , Blood Vessels/innervation , Hypertension/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolism , Renin-Angiotensin System , Sympathetic Nervous System/metabolism , Animals , Brain/metabolism , Brain/physiopathology , Humans , Hypertension/etiology , Hypertension/physiopathology , Risk Factors , Signal Transduction , Sympathetic Nervous System/physiopathologyABSTRACT
A patient was a heavy smoker and drinker, so during his life has developed three cancers: larynx, liver and lung. These cancers can be linked to his bad lifestyle. We believe that it is very important to insist upon health education which can reach the entire population, so that illnesses related to a mistaken lifestyle can be reduced.