scholarly journals Estimating the causal effect of adiposity on carpal tunnel syndrome: a Mendelian randomization study

2019 ◽  
Author(s):  
Iyas Daghlas ◽  
Nathan Varady
Keyword(s):  
Type 2 Diabetes ◽  
Body Mass Index ◽  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Abdominal Adiposity ◽  
Tunnel Syndrome

AbstractBackgroundWe aimed to examine evidence for a causal effect of overall and abdominal adiposity on carpal tunnel syndrome (CTS) using two-sample Mendelian randomization (MR).MethodsThe exposure included genetic instruments comprising independent variants associated with body mass index (BMI) (n=322,154), a proxy for overall adiposity, and waist-hip ratio adjusted for BMI (WHRadjBMI) (n=210,082), a proxy for abdominal adiposity. Associations of these variants with CTS were obtained from a genome-wide association study (GWAS) conducted in UK Biobank (12,312 CTS cases / 389,344 controls). Causal effects were estimated using inverse-variance weighted regression and conventional MR sensitivity analyses were conducted to assess for horizontal pleiotropy. In follow-up analyses we determined whether type 2 diabetes (T2D) or hyperlipidemia mediated the observed effects.ResultsA 1-standard deviation (SD, ∼4.7kg/m2) increase in genetically instrumented BMI increased the risk of CTS (OR 1.73, 95% CI 1.48-2.02, p=2.68e-12), with consistent effects across sensitivity analyses. This effect translates to an absolute increase of 17 CTS cases per 1000 person years amongst US working populations [95% CI 11.0-23.5]. Univariable MR was consistent with a causal effect of T2D (OR 1.08, 95% CI 1.03-1.11, p=5.20e-05), and the effect of BMI was partially attenuated (OR 1.53, 95% CI 1.38-1.68, p=2.85e-08) when controlling for T2D liability in multivariable MR. In contrast, no effect was observed of WHRadjBMI on CTS (OR 1.03, 95% CI 0.74-1.33, p=0.83).ConclusionThese data support a causal effect of overall adiposity on susceptibility to CTS that is only partially mediated through T2D, suggesting that efforts to reduce obesity may mitigate the population burden of CTS.Key messages- A one-standard deviation increase in body mass index, a proxy for overall adiposity, increased risk of carpal tunnel by 73%. In contrast, no effect of waist-to-hip ratio adjusted for BMI, a proxy for abdominal adiposity, was observed on risk of carpal tunnel syndrome.- The effects of BMI on carpal tunnel syndrome risk were partially attenuated when accounting for mediation through type 2 diabetes, suggesting that the majority of the causal effect operates independently of diabetes risk.- These data suggest that efforts to reduce rates of obesity could reduce the incidence of carpal tunnel syndrome.

scholarly journals Obesity, Type 2 Diabetes, and the Risk of Carpal Tunnel Syndrome: A Two-Sample Mendelian Randomization Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiarui Mi ◽  
Zhengye Liu
Keyword(s):  
Type 2 Diabetes ◽  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
The Body ◽  
Genome Wide Association Studies ◽  
Increased Risk ◽  
Tunnel Syndrome

Some previous observational studies have reported an increased risk of carpal tunnel syndrome (CTS) in patients with obesity or type 2 diabetes (T2D), which was however, not observed in some other studies. In this study we performed a two-sample Mendelian randomization to assess the causal effect of obesity, T2D on the risk of CTS. Single nucleotide polymorphisms associated with the body mass index (BMI) and T2D were extracted from genome-wide association studies. Summary-level results of CTS were available through FinnGen repository. Univariable Mendelian randomization (MR) with inverse-variance-weighted method indicated a positive correlation of BMI with CTS risk [odds ratio (OR) 1.66, 95% confidence interval (CI), 1.39–1.97]. Genetically proxied T2D also significantly increased the risk of CTS [OR 1.17, 95% CI (1.07–1.29)]. The causal effect of BMI and T2D on CTS remained consistent after adjusting for each other with multivariable MR. Our mediation analysis indicated that 34.4% of BMI’s effect of CTS was mediated by T2D. We also assessed the effects of several BMI and glycemic related traits on CTS. Waist circumference and arm fat-free mass were also causally associated with CTS. However, the associations disappeared after adjusting for the effect of BMI. Our findings indicate that obesity and T2D are independent risk factors of CTS.

Ultrasound-guided insulin injection for carpal tunnel syndrome in type 2 diabetes mellitus patients

2019 ◽  
Vol 38 (10) ◽  
pp. 2933-2940
Author(s):  
Shereen Refaat Kamel ◽  
Hanaa A. Sadek ◽  
Ahmed Hamed ◽  
Omima A. Sayed ◽  
Mona H. Mahmud ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Insulin Injection ◽  
Ultrasound Guided ◽  
Tunnel Syndrome

Effect of Treatment with an Aldosereductase Inhibitor on Symptomatic Carpal Tunnel Syndrome in Type 2 Diabetes

1995 ◽  
Vol 12 (12) ◽  
pp. 1097-1101 ◽  
Author(s):  
L. Monge ◽  
M. Mattei ◽  
F. Dani ◽  
A. Sciarretta ◽  
Q. Carta
Keyword(s):  
Type 2 Diabetes ◽  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Tunnel Syndrome ◽  
Effect Of Treatment

Ulcero-osteolytic lesions in a woman with type 2 diabetes and carpal tunnel syndrome: A case report and literature review

2016 ◽  
Vol 113 ◽  
pp. 204-207 ◽  
Author(s):  
Elisabetta L. Romeo ◽  
Marcello Previti ◽  
Annalisa Giandalia ◽  
Giuseppina T. Russo ◽  
Domenico Cucinotta
Keyword(s):  
Type 2 Diabetes ◽  
Case Report ◽  
Carpal Tunnel Syndrome ◽  
Literature Review ◽  
Carpal Tunnel ◽  
Osteolytic Lesions ◽  
Tunnel Syndrome

scholarly journals Sex Differences in the Risk of Coronary Heart Disease Associated With Type 2 Diabetes: A Mendelian Randomization Analysis

2020 ◽  
Author(s):  
Tricia M. Peters ◽  
Michael V. Holmes ◽  
J. Brent Richards ◽  
Tom Palmer ◽  
Vincenzo Forgetta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Genome Wide Association Study ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Chd Risk ◽  
Unit Increase

<b>Objective</b>: Observational studies have demonstrated that type 2 diabetes is a stronger risk factor for coronary heart disease (CHD) in women compared with men. However, it is not clear whether this reflects a sex differential in the causal effect of diabetes on CHD risk or results from sex-specific residual confounding. <p><b>Methods</b>: Using 270 single nucleotide polymorphisms (SNPs) for type 2 diabetes identified in a type 2 diabetes genome-wide association study, we performed a sex-stratified Mendelian randomization (MR) study of type 2 diabetes and CHD using individual participant data in UK Biobank (N=251,420 women and 212,049 men). Weighted-median, MR Egger, MR-PRESSO and radial MR from summary-level analyses were used for pleiotropy assessment. </p> <p><b>Results</b>: MR analyses showed that genetic risk of type 2 diabetes increased the odds of CHD for women (odds ratio [OR] 1.13, 95% confidence interval [CI] 1.08-1.18 per 1-log unit increase in odds of type 2 diabetes) and men (OR 1.21, 95% CI 1.17-1.26 per 1-log unit increase in odds of type 2 diabetes). Sensitivity analyses showed some evidence of directional pleiotropy, however, results were similar after correction for outlier SNPs.</p> <p><b>Conclusions</b>: This MR analysis supports a causal effect of genetic liability to type 2 diabetes on risk of CHD that is not stronger for women than men. Assuming a lack of bias, these findings suggest that the prevention and management of type 2 diabetes for CHD risk reduction is of equal priority in both sexes.</p>

scholarly journals Type 2 diabetes seems not to be a risk factor for the carpal tunnel syndrome: a case control study

2014 ◽  
Vol 15 (1) ◽  
Author(s):  
Steven H Hendriks ◽  
Peter R van Dijk ◽  
Klaas H Groenier ◽  
Peter Houpt ◽  
Henk JG Bilo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Risk Factor ◽  
Carpal Tunnel Syndrome ◽  
Carpal Tunnel ◽  
Case Control Study ◽  
Case Control ◽  
Tunnel Syndrome ◽  
Control Study

scholarly journals Sex Differences in the Risk of Coronary Heart Disease Associated With Type 2 Diabetes: A Mendelian Randomization Analysis

2020 ◽  
Author(s):  
Tricia M. Peters ◽  
Michael V. Holmes ◽  
J. Brent Richards ◽  
Tom Palmer ◽  
Vincenzo Forgetta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Genome Wide Association Study ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Chd Risk ◽  
Unit Increase

<b>Objective</b>: Observational studies have demonstrated that type 2 diabetes is a stronger risk factor for coronary heart disease (CHD) in women compared with men. However, it is not clear whether this reflects a sex differential in the causal effect of diabetes on CHD risk or results from sex-specific residual confounding. <p><b>Methods</b>: Using 270 single nucleotide polymorphisms (SNPs) for type 2 diabetes identified in a type 2 diabetes genome-wide association study, we performed a sex-stratified Mendelian randomization (MR) study of type 2 diabetes and CHD using individual participant data in UK Biobank (N=251,420 women and 212,049 men). Weighted-median, MR Egger, MR-PRESSO and radial MR from summary-level analyses were used for pleiotropy assessment. </p> <p><b>Results</b>: MR analyses showed that genetic risk of type 2 diabetes increased the odds of CHD for women (odds ratio [OR] 1.13, 95% confidence interval [CI] 1.08-1.18 per 1-log unit increase in odds of type 2 diabetes) and men (OR 1.21, 95% CI 1.17-1.26 per 1-log unit increase in odds of type 2 diabetes). Sensitivity analyses showed some evidence of directional pleiotropy, however, results were similar after correction for outlier SNPs.</p> <p><b>Conclusions</b>: This MR analysis supports a causal effect of genetic liability to type 2 diabetes on risk of CHD that is not stronger for women than men. Assuming a lack of bias, these findings suggest that the prevention and management of type 2 diabetes for CHD risk reduction is of equal priority in both sexes.</p>

scholarly journals Evaluation of glycemic traits in susceptibility to COVID-19 risk: a Mendelian randomization study

BMC Medicine ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shiu Lun Au Yeung ◽  
Jie V Zhao ◽  
C Mary Schooling
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Predisposition ◽  
Mendelian Randomization ◽  
Fasting Glucose ◽  
Association Studies ◽  
Sensitivity Analyses ◽  
Genome Wide Association Studies ◽  
Inverse Association ◽  
Wide Confidence Interval

Abstract Background Observational studies suggest poorer glycemic traits and type 2 diabetes associated with coronavirus disease 2019 (COVID-19) risk although these findings could be confounded by socioeconomic position. We conducted a two-sample Mendelian randomization to clarify their role in COVID-19 risk and specific COVID-19 phenotypes (hospitalized and severe cases). Method We identified genetic instruments for fasting glucose (n = 133,010), 2 h glucose (n = 42,854), glycated hemoglobin (n = 123,665), and type 2 diabetes (74,124 cases and 824,006 controls) from genome wide association studies and applied them to COVID-19 Host Genetics Initiative summary statistics (17,965 COVID-19 cases and 1,370,547 population controls). We used inverse variance weighting to obtain the causal estimates of glycemic traits and genetic predisposition to type 2 diabetes in COVID-19 risk. Sensitivity analyses included MR-Egger and weighted median method. Results We found genetic predisposition to type 2 diabetes was not associated with any COVID-19 phenotype (OR: 1.00 per unit increase in log odds of having diabetes, 95%CI 0.97 to 1.04 for overall COVID-19; OR: 1.02, 95%CI 0.95 to 1.09 for hospitalized COVID-19; and OR: 1.00, 95%CI 0.93 to 1.08 for severe COVID-19). There were no strong evidence for an association of glycemic traits in COVID-19 phenotypes, apart from a potential inverse association for fasting glucose albeit with wide confidence interval. Conclusion We provide some genetic evidence that poorer glycemic traits and predisposition to type 2 diabetes unlikely increase the risk of COVID-19. Although our study did not indicate glycemic traits increase severity of COVID-19, additional studies are needed to verify our findings.

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