scholarly journals Modifiable and non-modifiable risk factors for obstetric anal sphincter injury in a Norwegian Region: A case-control study.

Author(s):  
Ragnhild Klokk ◽  
Kjersti Bakken ◽  
Trond Markestad ◽  
Mads Holten-Andersen

Objective To identify modifiable and non-modifiable risk factors for severe obstetric anal sphincter injury (OASI) following vaginal delivery. Design Retrospective case-control study. Setting Single center maternity clinic in South-Eastern Norway Population Women diagnosed with OASI following singleton vaginal birth after 30 weeks’ gestation (n = 421) and matched controls (n = 421) during 1990-2002. Methods Data were extracted retrospectively from an institutional birth registry. For each woman with OASI the first subsequent vaginal singleton delivery matched for parity was elected as control. Potential determinants for OASI were assessed by conditional logistic regression analyses. Main outcome measure OASI, defined as 3rd or 4th degree obstetric anal sphincter lesions. Results Among modifiable factors amniotomy was the strongest independent determinant for OASI in both primi- (adjusted odds ratio [aOR] 4.84; 95% CI 2.60–9.02) and multiparous (aOR 3.76; 95% CI 1.45–9.76) women, followed by augmentation with oxytocin (primiparous: aOR 1.63; 95% CI 1.08–2.46, multiparous: aOR 3.70; 95% CI 1.79–7.67). Vacuum extraction and forceps delivery were independently associated with OASI in primiparous women (vacuum: aOR 1.91; 95% CI 1.03–3.57, forceps: aOR 2.37; 95% CI 1.14–4.92), and episiotomy for OASI in multiparous women (aOR 2.64; 95% CI 1.36–5.14). Conclusions Amniotomy may be a hitherto unrecognized independent modifiable risk factor for OASI and should be further investigated for its potential role in preventive strategies for OASI. Funding Innlandet Hospital Trust research fund, grant number 150434. Keywords Obstetric anal sphincter injury; OASI; Birth; Birth injury; Modifiable risk factor; Amniotomy.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 973-973
Author(s):  
R. Gonzalez Mazario ◽  
J. J. Fragio-Gil ◽  
P. Martinez Calabuig ◽  
E. Grau García ◽  
M. De la Rubia Navarro ◽  
...  

Background:Cardiovascular disease (CV) is the most frequent cause of death in rheumatoid arthritis (RA) patients. It is well known that RA acts as an independent cardiovascular risk factor.Objectives:To assess the CV risk in RA patients using carotid ultrasonography (US) additionally to the traditional CV risk factors.Methods:A prospective transversal case control study was performed, including adult RA patients who fulfilled ACR/EULAR 2010 criteria and healthy controls matched according to CV risk factors. Population over 75 years old, patients with established CV disease and/or chronic kidney failure (from III stage) were excluded. The US evaluator was blinded to the case/control condition and evaluated the presence of plaques and the intima-media thickness. Statistical analysis was performed with R (3.6.1 version) and included a multivariate variance analysis (MANOVA) and a negative binomial regression adjusted by confounding factors (age, sex and CV risk factors).Results:A total of 200 cases and 111 healthy controls were included in the study. Demographical, clinical and US data are exposed in table 1. Not any difference was detected in terms of CV risk factors between the cases and controls. In both groups a relationship between age, BMI and high blood pressure was detected (p<0.001).Table 1.Table 2.RA basal characteristicsDisease duration (years)16,98 (11,38)Erosions (X-Ray of hands/feet)163 (81,5%)Seropositive (RF/anti-CCP)146 (73%)Extra-articular symptoms44 (22%)Intersticial difusse lung disease10 (5%)Rheumatoid nodules14 (7%)Prednisone use103 (51,5%)Median dose of Prednisone last year (mg)2,34 (2,84)sDMARDsMethotrexate104 (52%)Leflunomide29 (14,5%)Hydroxycloroquine9 (4,5%)bDMARDs89 (44,5%) TNFi41 (20,5%) Abatacept15 (7,5%) IL6i22 (11%) RTX11 (5,5%)JAKi26 (13%) Baricitinib11 (5,5%) Tofacitinib15 (7,5%)DAS 28-ESR3,1 (2,3, 3,9)SDAI7,85 (4,04, 13,41)HAQ0,88 (0,22, 1,5)RF (U/mL)51 (15, 164,25)Anti-CCP (U/mL)173 (22, 340)Patients showed higher intima-media (both right and left) thickness compared to controls (p<0.006). Moreover it was also related to the disease duration and DAS28 score (p<0.001). A higher plaque account was noted in cases(p<0.004) and it was also related to the disease duration (p<0.001).Conclusion:RA implies a higher CV risk. Traditional CV risk factors explains only partially the global risk. These findings support that RA acts as an independent cardiovascular risk factor.Disclosure of Interests:None declared


2019 ◽  
Vol 8 (5) ◽  
pp. 677-685
Author(s):  
Til Bahadur Basnet ◽  
Cheng Xu ◽  
Manthar Ali Mallah ◽  
Wiwik Indayati ◽  
Cheng Shi ◽  
...  

Abstract There are well-known traditional risk factors for coronary artery disease (CAD). Among them, smoking is one of the most prominent and modifiable risk factors. This study aims to determine the magnitude of smoking as a risk factor for CAD in the Nepalese population. A hospital-based age- and sex-matched case–control study was carried out with a total of 612 respondents. Bivariate analysis showed that the risk of developing CAD in ex-smokers and current smokers was higher (odds ratio (OR): 1.81 (confidence interval (CI): 1.21–2.7) and OR: 5.2 (CI: 3.4–7.97)), with p-values less than 0.004 and &lt;0.00001, respectively, compared to the risk in never smokers. From stratified socio-demographic, cardio-metabolic, behavioural and psychosocial risk factor analysis, smoking was found to be associated with CAD in almost all subgroups. In the subsequent multivariate analysis, adjustment for socio-demographic, cardio-metabolic and psychosocial risk factors showed a steady increase in risk. However, further adjustment for behavioural risk factors (alcohol use and physical activity) showed that the risk was attenuated by 59% in current smokers. After adjusting for the covariates, current smokers and ex-smokers had an increased risk of CAD (OR: 6.64, 95% CI: 3.64–12.12, p &lt; 0.00001; OR: 1.89, 95% CI: 1.08–3.31, p &lt; 0.012, respectively) compared with non-smokers. In conclusion, smoking was found to increase the risk of CAD in the Nepalese population.


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