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We aimed to study the influence of smoking habits, exposure to passive smoking and snuff use on disease progression, cognitive performance and quality of life in patients with multiple sclerosis (MS).MethodPatients from two population-based case–control studies were categorised based on tobacco exposure at diagnosis and were followed up to 15 years post diagnosis through the Swedish MS registry (n=9089) regarding changes in Expanded Disability Status Scale (EDSS), Multiple Sclerosis Impact Scale 29 and Symbol Digit Modalities Test. We used linear mixed models to analyse long-term changes, and Cox regression models with 95% CI using 24-week confirmed disability worsening, reaching EDSS 3 and EDSS 4, respectively, physical and psychological worsening and cognitive disability worsening as end points. The influence of smoking cessation post diagnosis was also investigated.ResultsCompared with non-smokers, current smokers had a faster EDSS progression (βcurrent smoking×time=0.03, 95% CI 0.02 to 0.04). A faster EDSS progression was also associated with passive smoking (βcurrent passive smoking×time=0.04, 95% CI 0.03 to 0.06). Smoke exposure negatively impacted all secondary outcomes. Those who continued smoking had worse outcomes than those who stopped smoking post diagnosis. Snuff users had a more favourable EDSS progression, compared with never users.ConclusionsOur findings indicate that both smoking and passive smoking have a negative influence on MS and that smoking cessation post diagnosis may be an important secondary preventive measure. Snuff use was associated with slower disease progression, suggesting that nicotine replacement therapy could be an attractive way to increase the chance of quitting smoking among patients with MS.

Multiple sclerosis (MS) is a major, immune-mediated, demyelinating disease and the major cause of non-traumatic disability in young adults. Susceptibility to disease is controlled by a variety of interacting features that include genetic and notably environmental factors. One of these risk factors appears to be the occurrence of traumatic brain injury. In a follow-on to previous analysis of head injury-induced risk factors for MS, analysis of Swedish Registry data of MS and matched controls demonstrates enhanced susceptibility to MS, notably when stratified for the presence of HLA-DRB1*15.01, absence of HLA-A*02.01 and occurrence of smoking, which are known risk factors, the risk of MS increases to OR 65.4 (95% CI 8.35 to 512). This can be mechanistically supported by a number of routes whereby brain injury can lead to expression of autoantigenic targets, or damage-related release of neuroantigens that could generate a novel autoantigenic response in draining lymph nodes following glymphatic/meningeal lymphatic drainage. These may be different from other mechanisms that are relevant to susceptibility due to human leucocyte antigen expression and smoking.

Background Smoking and obesity interact to exacerbate the risk of hypertension, diabetes, and cardiovascular disease, but their potential synergistic effects on outcomes in multiple sclerosis (MS) have not been well studied. We aimed to study whether smoking and obesity interact to affect disease progression and cognitive function in patients with MS. Methods Incident cases from the population‐based case–control study Epidemiological Investigation of MS (EIMS) were categorized by smoking and obesity status at diagnosis and followed up to 15 years postdiagnosis through the Swedish MS registry (n = 3336). Cox regression was used to analyze outcomes, including clinical disease worsening (CDW), progression to Expanded Disability Status Scale (EDSS) levels 3 and 4, physical worsening as measured by a 7.5‐point increase in the MS Impact Scale (MSIS) physical score, and cognitive decline, defined as an 8‐point or greater reduction on the Symbol Digit Modalities Test (SDMT). Interaction effects on the additive scale were assessed by combining dichotomous variables for smoking (nonsmoker = 0, smoker = 1) and obesity (nonobese = 0, obese = 1), yielding four categories: 0/0 (reference category), 0/1, 1/0, and 1/1. Results Additive interactions between smoking and obesity were identified for CDW (attributable proportion due to interaction [AP] 0.18, 95% CI 0.03–0.30), progression to EDSS 4 (AP 0.18, 95% CI 0.08–0.26), MSIS‐Physical score worsening (AP 0.32, 95% CI 0.21–0.42), and cognitive decline (AP 0.27, 95% CI 0.19–0.35). Conclusions Smoking and obesity appear to synergistically worsen MS progression and cognitive functioning, with the observed additive interactions across most outcomes suggesting that these factors partly share common biological pathways contributing to disease progression.

ObjectiveTo determine how the perception of families elicited after reading progress note social commentary differs by patient race.Study designWe retrospectively performed content analysis of social commentary in physician progress notes for neonatal intensive care unit patients hospitalized from 2018–2019. Neonatologists blinded to patient race rated how commentary impacted their perception of the patient’s family on a 5-point Likert scale. Frequency of negative ratings was compared across reported race using chi-squared tests.ResultsWe reviewed charts of 460 neonates. In total, 225 (49%) contained social commentary beyond parents’ names. Twelve neonatologists rated how commentaries impacted their perception of the patient’s family; 79%, 18%, and 3% were rated neutrally, negatively, and positively, respectively. Frequency of negative ratings was significantly greater among American Indian/Alaska Native than other patients (35% vs. 22%, p < 0.001).ConclusionsPhysician documentation of social commentary in patient notes may reflect and perpetuate implicit biases that contribute to race-based healthcare disparities.

Smoking is one of the most established risk factors for multiple sclerosis (MS). The aim of this study was to investigate how age at smoking debut, duration, intensity and cumulative dose of smoking, and smoking cessation influence the association between smoking and MS risk. In two Swedish population-based case-control studies (7,883 cases, 9,264 controls), subjects with different smoking habits were compared regarding MS risk, by calculating odds ratios with 95 % confidence intervals. We observed a clear dose response association between cumulative dose of smoking and MS risk (p value for trend <10⁻³⁵). Both duration and intensity of smoking contributed independently to the increased risk of MS. However, the detrimental effect of smoking abates a decade after smoking cessation regardless of the cumulative dose of smoking. Age at smoking debut did not affect the association between smoking and MS. Smoking increases the risk of MS in a dose response manner. However, in contrary to several other risk factors for MS that seem to affect the risk only if the exposure takes place during a specific period in life, smoking affects MS risk regardless of age at exposure, and the detrimental effect slowly abates after smoking cessation.

Background and purpose Higher latitude has been associated with increased occurrence of multiple sclerosis (MS) and with more severe disease. The aim was to study the impact of sun exposure habits on MS disease progression and health‐related quality of life. Methods Patients from a population‐based case–control study were categorized based on sun exposure habits at diagnosis and were followed up to 15 years post‐diagnosis through the Swedish MS registry (n = 3314) with regard to changes in Expanded Disability Status Scale (EDSS). Linear mixed models were used to analyse long‐term changes, while Cox regression models, with 95% confidence intervals, were used to investigate outcomes, including 24‐week confirmed diasability worsening, EDSS3, EDSS4, and physical worsening as measured by the physical component of the Multiple Sclerosis Impact Scale 29. Results Compared to average sun exposure (median value), low exposure to sunlight was associated with faster EDSS progression, increased risk of confirmed disability worsening (hazard ratio [HR] 1.48, 95% CI 1.21–1.81), increased risk of reaching EDSS 3 (HR 1.35, 95% CI 1.02–1.79), EDSS 4 (HR 1.47, 95% CI 1.01–2.20) and self‐reported physical worsening (HR 1.27, 95% CI 1.00–1.62). Significant trends revealed a lower risk of unfavourable outcomes with increasing sun exposure. Conclusions Very low levels of sun exposure are associated with worse disease progression and health‐related quality of life in patients with MS.

BackgroundLarge register-based studies have reported an association between head trauma and increased risk of multiple sclerosis (MS). We aimed to investigate possible interactions between head trauma and MS-associated HLA genes in relation to MS risk.MethodsWe used a Swedish population-based case-control study (2807 incident cases, 5950 matched controls with HLA genotypes available for 2057 cases, 2887 controls). Subjects with and without a history of self-reported head trauma were compared regarding MS risk, by calculating ORs with 95% CIs using logistic regression models. Additive interaction between head trauma, HLA-DRB1*1501 and absence of HLA-A*0201, was assessed by calculating the attributable proportion (AP) due to interaction.ResultsA history of head trauma was associated with a 30% increased risk of subsequently developing MS (OR 1.34, 95% CI 1.17 to 1.53), with a trend showing increased risk of MS with increasing number of head impacts (p=0.03). We observed synergistic effects between recent head trauma and HLA-DRB1*15:01 as well as absence of HLA*02:01 in relation to MS risk (each AP 0.40, 95% CI 0.1 to 0.7). Recent head trauma in individuals with both genetic risk factors rendered an 18-fold increased risk of MS, compared with those with neither the genetic risk factors nor a history of head trauma (OR 17.7, 95% CI 7.13 to 44.1).ConclusionsOur findings align with previous observations of a dose-dependent association between head trauma and increased risk of MS and add a novel aspect of this association by revealing synergistic effects between recent head trauma and MS-associated HLA genes.

IntroductionSmoking has consistently been associated with increased risk of developing rheumatoid arthritis (RA). The aim of this study was to estimate the influence of passive smoking on the risk of developing anti-cyclic citrullinated peptide antibodies (ACPA)-positive and ACPA-negative RA.MethodsA population-based case–control study using incident cases of RA was performed in Sweden, and the study population in this report was restricted to include never-smokers (589 cases, 1764 controls). The incidence of RA among never-smokers who had been exposed to passive smoking was compared with that of never-smokers who had never been exposed, by calculating the OR with a 95% CI employing logistic regression.ResultsNo association was observed between exposure to passive smoking and RA risk (OR 1.0, 95% CI 0.8 to 1.2 for ACPA-positive RA, and OR 0.9, 95% CI 0.7 to 1.2, for ACPA-negative RA). No suggestion of a trend between duration of passive smoking and RA risk was observed.DiscussionsNo association was observed between exposure to passive smoking and RA risk, which may be explained by a threshold below which no association between smoke exposure and RA occurs.

ObjectiveIt has been debated whether the different clinical disease courses in multiple sclerosis (MS) are the consequence of different pathogenic mechanisms, with distinct risk factors, or if all MS clinical phenotypes are variations of similar underlying disease mechanisms. We aimed to study environmental risk factors and their interactions with human leucocyte antigen DRB1*15:01 with regards to relapsing-onset and progressive-onset MS.MethodsWe used two Swedish population-based case–control studies, including 7520 relapsing-onset cases, 540 progressive-onset cases and 11 386 controls matched by age, sex and residential area. Logistic regression was used to estimate ORs with 95% CIs for associations between the different MS phenotypes and a number of environmental and lifestyle factors. Interaction between the DRB1*15:01 allele and environmental risk factors was evaluated on the additive scale.ResultsAll environmental and lifestyle factors associated with risk of developing MS apply to both relapsing-onset and progressive-onset disease. Smoking, obesity and Epstein-Barr virus nuclear antigen-1 (EBNA-1) antibody levels were associated with increased risk of both MS phenotypes, whereas snuff use, alcohol consumption and sun exposure were associated with reduced risk. Additive interactions between DRB1*15:01 and smoking, obesity, EBNA-1 antibody levels and sun exposure, respectively, occurred to increase MS risk regardless of the clinical phenotype.InterpretationOur finding that the same environmental and lifestyle factors affect both relapsing-onset and progressive-onset MS supports the notion that the different clinical phenotypes share common underlying disease mechanisms.

BackgroundBenign multiple sclerosis (MS), characterised by minimal disability despite long disease duration, remains poorly understood in terms of its determinants and prognostic implications. While lifestyle factors have been implicated in modifying disease progression, their role in distinguishing benign and non-benign MS remains unclear.MethodsWe conducted a comparative analysis of patients with benign (n=2040) and non-benign MS (n=4283) using data from Swedish nationwide case-control studies with long-term follow-up. Logistic regression models were used to analyse associations between a history of infectious mononucleosis (IM) and lifestyle factors (smoking, body mass index, fish consumption and sun exposure habits) and the likelihood of benign MS. Additionally, Cox regression was used to follow patients with benign MS from the 15-year mark onward, identifying factors associated with the transition to non-benign MS over time.ResultsThe odds of having benign MS were reduced in association with a history of IM (OR 0.54, 95% CI 0.45 to 0.65), adolescent overweight and obesity (OR 0.69, 95% CI 0.56 to 0.85 and 0.46, 95% CI 0.32 to 0.66, respectively) and infrequent fish consumption (OR 0.72, 95% CI 0.60 to 0.88). Similar associations were observed for the risk of transitioning from benign to non-benign MS over time.ConclusionsA history of IM and modifiable lifestyle factors significantly influence the probability of a benign disease course in MS. These findings underscore the potential for targeted lifestyle interventions to improve MS outcomes. Further research is needed to elucidate the mechanisms by which a past IM infection can continue to influence MS progression long after the initial infection.