16 research outputs found
Juxta Cortical Tibia Metastatic Deposition in Gastric Cancer: A Case Report
We report a 41 years old man with rapidly growing and tender lump on the anteromedial surface of tibia. The patient had the history of gastrectomy and gastrojejunostomy due to gastric carcinoma. On admission, the Simple X-ray of lower extremity disclosed a slight thinning of the anterior cortex of tibia without cortical destruction. The whole-body bone scan with 99mTC MDP revealed activity of lesion in all 3 phases. The histopathological evaluation showed an infiltration of bone with tumor cells. Review No the literature revealed in previous cases of skeletal metastasis from gastric cancer in the tibia like this
Sprengel's Deformity Associated with Musculoskeletal Dysfunctions and Renal Anomalies: A Case Report
Background. Sprengel's deformity is a rare congenital anomaly of the shoulder girdle. The deformity is due to failure of descent of the scapula in intrauterine life. Case Presentation. We report a case of unilateral Sprengel's deformity associated with several other musculoskeletal and renal disorders consisting of absence of pectoralis major, weakness of trapezius and serratus anterior muscles, one kidney agenesis, and severe hydronephrosis of the other kidney in a 7-year-old boy. Conclusion. Sprengel's deformity can be associated with other musculoskeletal abnormalities and it is much more than a cosmetic problem
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Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021
BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation
EFFECT OF LEFT ATRIA SIZE ON P-WAVE DISPERSION: A STUDY IN PATIENTS WITH PAROXYSMAL ATRIAL FIBRILLATION
Abstract INTRODUCTION: Paroxysmal atrial fibrillation (AF) is a common arrhythmia encountered in clinical practice. Experimental and human mapping studies have demonstrated that perpetuation of AF is due to the presence of multiple reentrant wavelets with various sizes in the right and left atria. P-wave dispersion (PWD), defined as the difference between the maximum and minimum P-wave duration, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (AF). This study was undertaken to examine the effect of left atria (LA) dimension on P-wave dispersion in unselected patients with PAF compared to healthy controls. METHODS: In this study, 40 consecutive patients with PAF (25 male, 15 female, mean age 45 ± 9 years) and 40 age and gender matched healthy controls (25 male, 15 female, mean age 46 ± 10 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECG. The difference between the maximum and minimum P wave duration was calculated and defined as P wave dispersion (PWD = Pmax - Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). RESULTS: P-wave dispersion in patients with PAF and normal LA diastolic diameter (LAD) was longer than in controls with normal LA size (51±9 vs. 34±8 ms, P < 0.002). P-wave dispersion increased in patients with PAF (60±14 vs. 50±7 ms, P < 0.001) and controls (39 ± 9 vs. 33 ± 9 ms, P < 0.004) with increased LAD. In the PAF group, P-wave dispersion correlated with LAD (r = 0.40, P = 0.001) and LA diastolic volume (r = 0.62, P < 0.001). On multivariate logistic regression analysis, only P-wave dispersion retained significance on development of PAF. CONCLUSION: P-wave dispersion increased in patients with PAF and normal LA size. In controls with increased LA size, P-wave dispersion increased but did not reach the levels attained in patients with PAF. These findings can be explained by the changes in LA microarchitecture which concurrently decreased atrial myocardial contraction, increased P-wave dispersion and predisposed to PAF. Keywords: coronary calcification, inflammation, risk factors, h-CRP.</p
Implantable cardioverter-defibrillator in a patient with dextrocardia situs inversus
Background: Dextrocardia is a congenital anomaly, which may have coexistent coronary artery disease (CAD), arrhythmias and conventional indications for device therapy. However, the implantation of transvenous leads can be technically challenging and the approach needs to be tailored to the patient's individual anatomy.
Case presentation: A 54-year-old male with dextrocardia situs inversus and ischemic left ventricular dysfunction developed ventricular tachycardia and fibrillation. Therefore, left- sided approach, dual chamber implantable cardioverter-defibrillator (ICD) was applied using a conventional method and standard equipment after complete evaluation of cardiac anatomy and vascular assessment.
Conclusion: Electrical device implantation in patients with dextrocardia is possible after obtaining complete information about anatomy and/or coexisting congenital abnormalities, which helps in obtaining appropriate implantation approach
Etiology of syncope in hospitalized patients
Background: Syncope is a common clinical problem which can be remarkably debilitating and associated with high health care costs. Syncope is a clinical syndrome with many potential causes. The aim of the study was to determine the etiologies of patients with syncope in the emergency department (ED) of a referral and general university hospital.
Methods: One hundred sixty-five consecutive patients aged more than 18 years old with syncope were admitted to the emergency department of Ayatollah Rouhani Hospital. Initially organized, systematic approach included detailed medical history and structured questionnaires for history taking, physical examination, ECG and cardiac monitoring, cardiology and neurology were done. Advanced diagnostic tests were carried out if the etiology of syncope remained unexplained.
Results: Out of the 165 patients who presented to the ED between February 2012 and February 2013, 124 had definition of syncope. The mean age of male patients was 59.5±19.8, 58. The etiology of syncope was diagnosed in 104 (83%) patients. Neurocardiogenic syncope was found in 36 (29.03%) patients, cardiac arrhythmias in 40 (32.25%) patients, and acute coronary syndrome in 8 (6.45%) patients. There are some infrequent etiologies like intracranial hemorrhage in 5 patients, aortic stenosis in 4 patients, hypertrophic cardiomyopathy and aortic dissection in 3 patients, Brugada and pulmonary embolism in 2 patients and carotid hypersensitivity in one patient.
Conclusion: We found that cardiac arrhythmias and neurocardiogenic type are the frequent causes of syncope. In about one-sixth of the patients, no etiology was found. Approximately one-third of patients had traumatic syncope
Association of vitamin D deficiency and premature coronary artery disease
Background: Evidence suggests hypovitaminosis D is associated with increased risk of coronary artery disease (CAD) and its extent and related risk factors. However, some investigations have produced contrary results. Therefore, we aimed to evaluate the association between serum vitamin D levels and the severity of premature coronary artery involvement. Methods: This randomized prospective, case-control study was conducted in Babol from April 2013 to June 2017. We collected the demographic data and measured serum 25-OH-D levels of 294 patients (age≤50 years) diagnosed with CAD with coronary angiography as case group as well as 438 age and sex-matched controls. CAD severity was assessed using the Gensini score. Statistical analyses were used to assess the associations and p<0.05 was considered as significant. Results: The mean serum level of 25-OH-D was 13.12±11.13 and 18.28±8.34 in case and control groups, respectively (P=0.036). In the case group, mean serum vitamin D levels were significantly lower among hypertensives (P=0.018), those with a family history of CVD (P=0.016) and those who used aspirin (P=0.036). The mean Gensini score of patients in the case group was 45.02±23.62 and was higher among men (P=0.022). There was a weak significant correlation between the serum vitamin D levels and the Gensini score (P=0.001 & R=-0.543). The mean Gensini score was not significantly different between patients with deficient (47.02±22.78), insufficient (26.0±21.72) and sufficient (39.0±43.84) vitamin D levels (P>0.05). Conclusion: The results showed that the lower levels of vitamin D is associated with increased risk and extent of coronary artery involvement as well as some of the risk factors of CAD, including male gender, hypertension and positive family history for CVD