Adnexal Torsion Recurrence ‐ Is the Adnexal Twist Degree a Risk Factor? A Retrospective Cohort Study

Author(s):  
Yossi Bart ◽  
Aya Mohr‐Sasson ◽  
Shayan Yousefi ◽  
Michal Goldenberg ◽  
Raanan Meyer ◽  
...  
2020 ◽  
pp. 107110072097126
Author(s):  
Jack Allport ◽  
Jayasree Ramaskandhan ◽  
Malik S. Siddique

Background: Nonunion rates in hind or midfoot arthrodesis have been reported as high as 41%. The most notable and readily modifiable risk factor that has been identified is smoking. In 2018, 14.4% of the UK population were active smokers. We examined the effect of smoking status on union rates for a large cohort of patients undergoing hind- or midfoot arthrodesis. Methods: In total, 381 consecutive primary joint arthrodeses were identified from a single surgeon’s logbook (analysis performed on a per joint basis, with a triple fusion reported as 3 separate joints). Patients were divided based on self-reported smoking status. Primary outcome was clinical union. Delayed union, infection, and the need for ultrasound bone stimulation were secondary outcomes. Results: Smoking prevalence was 14.0%, and 32.2% were ex-smokers. Groups were comparable for sex, diabetes, and body mass index. Smokers were younger and had fewer comorbidities. Nonunion rates were higher in smokers (relative risk, 5.81; 95% CI, 2.54-13.29; P < .001) with no statistically significant difference between ex-smokers and nonsmokers. Smokers had higher rates of infection ( P = .05) and bone stimulator use ( P < .001). Among smokers, there was a trend toward slower union with heavier smoking ( P = .004). Conclusion: This large retrospective cohort study confirmed previous evidence that smoking has a considerable negative effect on union in arthrodesis. The 5.81 relative risk in a modifiable risk factor is extremely high. Arthrodesis surgery should be undertaken with extreme caution in smokers. Our study shows that after cessation of smoking, the risk returns to normal, but we were unable to quantify the time frame. Level of Evidence: Level III, retrospective cohort study.


2016 ◽  
Vol 20 (4) ◽  
pp. 321-328 ◽  
Author(s):  
Jae Hung Jung ◽  
Song Vogue Ahn ◽  
Jae Mann Song ◽  
Se-Jin Chang ◽  
Kwang Jin Kim ◽  
...  

Author(s):  
Sumyia Mehrin M. D. Abulkalam ◽  
Mai Kadi ◽  
Mahmoud A. Gaddoury ◽  
Wallaa Khalid Albishi

Background: The association between tuberculosis (TB) and diabetes mellitus (DM) is re-emerging with the epidemic of type II diabetes. Both TB and DM were of the top 10 causes of death.[1] This study explores diabetes mellitus as a risk factor for developing the different antitubercular drug-resistant (DR) patterns among TB patients.  Methods: A retrospective cohort study has been conducted on all TB cases reported to the King Abdul Aziz University Hospital, Jeddah, between January 2012 to January 2021. All culture-confirmed and PCR-positive TB cases were included in this study. Categorical baseline characteristic of TB patient has been compared with DM status by using Fisher's exact and Pearson chi-square test. The univariable and multivariable logistic regression model was used to estimate the association between DM and different drug resistance patterns.  Results: Of the total 695 diagnosed TB patients, 92 (13.24%) are resistant to 1st line anti TB drugs. Among 92 DR-TB patients, 36 (39.13%) are diabetic. The percentage of different patterns of DR-TB with DM, in the case of mono DR (12.09%), poly DR (4.19%) MDR (0.547%). As a risk factor, DM has a significant association with DR-TB, mono drug-resistant, and pyrazinamide-resistant TB (P-value <0.05). The MDR and PDR separately do not show any significant association with DM, but for further analysis, it shows a significant association with DM when we combined.  Conclusion: Our study identified diabetes mellitus as a risk factor for developing DR-TB. Better management of DM and TB infection caring programs among DM patients might improve TB control and prevent DR-TB development in KSA.


2017 ◽  
Vol 35 (2) ◽  
pp. 78-84 ◽  
Author(s):  
Sebastian Yu ◽  
Hung-Pin Tu ◽  
Chu-Ling Yu ◽  
Chih-Hung Lee ◽  
Chien-Hui Hong

2020 ◽  
Vol 183 (4) ◽  
pp. 776-778 ◽  
Author(s):  
I.A. Vallerand ◽  
R.T. Lewinson ◽  
L.M. Parsons ◽  
M.W. Lowerison ◽  
S.B. Patten ◽  
...  

2020 ◽  
Vol 7 (5) ◽  
pp. 541-548
Author(s):  
Lisa R Rogers ◽  
Quinn T Ostrom ◽  
Julia Schroer ◽  
Jaime Vengoechea ◽  
Li Li ◽  
...  

Abstract Background Metabolic syndrome is identified as a risk factor for the development of several systemic cancers, but its frequency among patients with glioblastoma and its association with clinical outcomes have yet to be determined. The aim of this study was to investigate metabolic syndrome as a risk factor for and affecting survival in glioblastoma patients. Methods A retrospective cohort study, consisting of patients with diagnoses at a single institution between 2007 and 2013, was conducted. Clinical records were reviewed, and clinical and laboratory data pertaining to 5 metabolic criteria were extrapolated. Overall survival was determined by time from initial surgical diagnosis to date of death or last follow-up. Results The frequency of metabolic syndrome among patients diagnosed with glioblastoma was slightly greater than the frequency of metabolic syndrome among the general population. Within a subset of patients (n = 91) receiving the full schedule of concurrent radiation and temozolomide and adjuvant temozolomide, median overall survival was significantly shorter for patients with metabolic syndrome compared with those without. In addition, the presence of all 5 elements of the metabolic syndrome resulted in significantly decreased median survival in these patients. Conclusions We identified the metabolic syndrome at a slightly higher frequency in patients with diagnosed glioblastoma compared with the general population. In addition, metabolic syndrome with each of its individual components is associated with an overall worse prognosis in patients receiving the standard schedule of radiation and temozolomide after adjustment for age.


Neurology ◽  
2014 ◽  
Vol 83 (2) ◽  
pp. e27-e33 ◽  
Author(s):  
J. Breuer ◽  
M. Pacou ◽  
A. Gautier ◽  
M. M. Brown

Sign in / Sign up

Export Citation Format

Share Document