Bing Lü

UConn Health

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Charles B. Eaton

Brown University

Jeffrey B. Driban

University of Massachusetts Chan Medical School

Grace H. Lo

Baylor College of Medicine

Timothy E. McAlindon

Tufts Medical Center

Jeffrey A. Sparks

Brigham and Women's Hospital

Karen H. Costenbader

Brigham and Women's Hospital

Daniel H. Solomon

Brigham and Women's Hospital

Lori Lyn Price

Tufts Medical Center

Elizabeth W. Karlson

Brigham and Women's Hospital

Mary F. Barbe

Temple University

Cooperative Institutions

Harvard University

233

Brigham and Women's Hospital

227

University of North Carolina at Chapel Hill

140

American College of Rheumatology

132

Emory University

127

Durham VA Medical Center

120

AID Atlanta

111

Convergence

104

Boston University

Massachusetts General Hospital

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Roles of Postdiagnosis Accumulation of Morbidities and Lifestyle Changes in Excess Total and Cause‐Specific Mortality Risk in Rheumatoid Arthritis

Arthritis Care & Research (2019)

Kazuki Yoshida Tzu‐Chieh Lin Melissa Y. Wei Susan Malspeis Su H. Chu

To elucidate how postdiagnosis multimorbidity and lifestyle changes contribute to the excess mortality of rheumatoid arthritis (RA).We performed a matched cohort study among women in the Nurses' Health Study (1976-2018). We identified women with incident RA and matched each by age and year to 10 non-RA comparators at the RA diagnosis index date. Specific causes of death were ascertained via death certificates and medical record review. Lifestyle and morbidity factors were reported biennially; 61 chronic conditions were combined into the Multimorbidity Weighted Index (MWI). After adjusting for baseline confounders, we used inverse probability weighting analysis to examine the mediating influence of postindex MWI scores and lifestyle factors on total, cardiovascular, and respiratory mortality, comparing women with RA to their matched comparators.We identified 1,007 patients with incident RA and matched them to 10,070 non-RA comparators. After adjusting for preindex confounders, we found that hazard ratios (HRs) and 95% confidence intervals (95% CIs) were higher for total mortality (HR 1.46 [95% CI 1.32, 1.62]), as well as cardiovascular (HR 1.54 [95% CI 1.22, 1.94]) and respiratory (HR 2.75 [95% CI 2.05, 3.71]) mortality in patients with RA compared to non-RA comparators. Adjusting for postindex lifestyle factors (physical activity, body mass index, diet, smoking) attenuated but did not substantially account for this excess RA mortality. After additional adjustment for postindex MWI scores, patients with RA had HRs of 1.18 (95% CI 1.05, 1.32) for total, 1.19 (95% CI 0.94, 1.51) for cardiovascular, and 1.93 (95% CI 1.42, 2.62) for respiratory mortality.We found that MWI scores substantially accounted for the excess total and cardiovascular mortality among women with RA. This finding underscores the importance of monitoring for the total disease burden as a whole in monitoring patients with RA.

10.1002/acr.24120

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Citations (42)

Hypercalcemia and severe osteoporosis in lactation associated with increasing parathyroid hormone-related protein: one case report

Zhonghua neifenmi daixie zazhi (2010)

Ping Gu Jian Wang Yanyan Wang Jiaqing Shao Hong Du

病例报告:患者女,29岁,因腰痛2个月,双下肢不能站立20余天,于2007年12月入院.患者于2007年9月正常顺产1足月男婴,母乳喂养,乳汁排泌量异常增多,约为2 500～3 000 ml/24 h.2007年10月中旬患者出现腰骶部疼痛,呈持续性、电击样疼痛,自行服用α-D_3(0.25 μg,每天1次)等药物及推拿等治疗,症状改善不明显,11月底出现腰骶部疼痛加重,伴活动受限,双下肢不能站立,自觉口干,多饮、多尿,偶感头晕,无明显头痛,无消瘦,无恶心呕吐,无腹痛便秘,无下肢浮肿,无肌肉萎缩、关节功能障碍等.12月来本院就诊,查腰椎磁共振示:胸12、腰4椎体改变,考虑压缩性骨折.血常规:白细胞5.6×10~9/L,红细胞3.52×10~12/L,血小板221×10~9/L;血生化检验示:血清钙3.4 mmol/L,磷1.22 mmol/L,碱性磷酸酶195U/L,总白蛋白69.2 g/L,白蛋白44.2 g/L,尿素氮8.4 mmol/L,肌酐44 μmol/L,尿酸281 μmol/L,遂以高钙血症,原发性甲状旁腺功能亢进?收住内分泌科。

Parathyroid hormone-related protein

10.3760/cma.j.issn.1000-6699.2010.02.026

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Composite quantitative knee structure metrics predict the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative

BMC Musculoskeletal Disorders (2020)

Matthew S. Harkey Julie E. Davis Lori Lyn Price Robert J. Ward James Mackay

Abstract Background We aimed to determine if composite structural measures of knee osteoarthritis (KOA) progression on magnetic resonance (MR) imaging can predict the radiographic onset of accelerated knee osteoarthritis. Methods We used data from a nested case-control study among participants from the Osteoarthritis Initiative without radiographic KOA at baseline. Participants were separated into three groups based on radiographic disease progression over 4 years: 1) accelerated (Kellgren-Lawrence grades [KL] 0/1 to 3/4), 2) typical (increase in KL, excluding accelerated osteoarthritis), or 3) no KOA (no change in KL). We assessed tibiofemoral cartilage damage (four regions: medial/lateral tibia/femur), bone marrow lesion (BML) volume (four regions: medial/lateral tibia/femur), and whole knee effusion-synovitis volume on 3 T MR images with semi-automated programs. We calculated two MR-based composite scores. Cumulative damage was the sum of standardized cartilage damage. Disease activity was the sum of standardized volumes of effusion-synovitis and BMLs. We focused on annual images from 2 years before to 2 years after radiographic onset (or a matched time for those without knee osteoarthritis). To determine between group differences in the composite metrics at all time points, we used generalized linear mixed models with group (3 levels) and time (up to 5 levels). For our prognostic analysis, we used multinomial logistic regression models to determine if one-year worsening in each composite metric change associated with future accelerated knee osteoarthritis (odds ratios [OR] based on units of 1 standard deviation of change). Results Prior to disease onset, the accelerated KOA group had greater average disease activity compared to the typical and no KOA groups and this persisted up to 2 years after disease onset. During a pre-radiographic disease period, the odds of developing accelerated KOA were greater in people with worsening disease activity [versus typical KOA OR (95% confidence interval [CI]): 1.58 (1.08 to 2.33); versus no KOA: 2.39 (1.55 to 3.71)] or cumulative damage [versus typical KOA: 1.69 (1.14 to 2.51); versus no KOA: 2.11 (1.41 to 3.16)]. Conclusions MR-based disease activity and cumulative damage metrics may be prognostic markers to help identify people at risk for accelerated onset and progression of knee osteoarthritis.

Sports medicine

10.1186/s12891-020-03338-7

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Citations (13)

Prospective association of periodontal disease with cardiovascular and all-cause mortality: NHANES III follow-up study

Atherosclerosis (2011)

Fayun Xu Bing Lü

National Death Index

Risk of mortality

10.1016/j.atherosclerosis.2011.07.091

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Citations (74)

Causal relationships between gut microbiota and hypothyroidism: a Mendelian randomization study

Endocrine (2023)

Zhaoxiang Wang Menghuan Wu Ying Pan Qianqian Wang Li Zhang

Mendelian Randomization

Mendelian inheritance

10.1007/s12020-023-03538-w

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Citations (6)

Dietary Patterns and Progression of Knee Osteoarthritis: Data from the Osteoarthritis Initiative

American Journal of Clinical Nutrition (2019)

Chang Xu Nathalie Marchand Jeffrey B. Driban Timothy E. McAlindon Charles B. Eaton

WOMAC

Quartile

Arthropathy

10.1093/ajcn/nqz333

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Citations (33)

Calcium Plus Vitamin D Supplementation and Joint Symptoms in Postmenopausal Women in the Women's Health Initiative Randomized Trial

Journal of the Academy of Nutrition and Dietetics (2013)

Rowan T. Chlebowski Mary Pettinger Karen Johnson Robert B. Wallace Catherine Womack

Women's Health Initiative

Joint pain

10.1016/j.jand.2013.06.007

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Citations (24)

Abstract 15621: History of Pregnancy Loss Predicts Coronary Heart Disease and Peripheral Vascular Disease in Post-Menopausal Women in the Women's Health Initiative (WHI)

Circulation (2011)

Donna R. Parker Bing Lü Megan Sands Charles B. Eaton

Background: Metabolic and hormonal changes that occur during pregnancy loss may contribute to the development of coronary heart disease (CHD) in adulthood. We prospectively evaluated a history of p...

Women's Health Initiative

Post menopausal

Cardiovascular Health

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The Cross-Sectional Relationship of Hemoglobin Levels and Functional Outcomes in Women with Self-Reported Osteoarthritis: Results from the Women's Health Initiative

Seminars in Arthritis and Rheumatism (2011)

Charles B. Eaton Marc C. Hochberg Annlouise Assaf Byron Cryer Bing Lü

Vitality

Cross-sectional study

SF-36

10.1016/j.semarthrit.2011.04.008

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Citations (7)

FRI0553 Obesity and The Risk of Systemic Lupus Erythematosus in The Nurses' Health Studies:

Annals of the Rheumatic Diseases (2016)

Sara K. Tedeschi Medha Barbhaiya Bing Lü Susan Malspeis Jeffrey A. Sparks

Background

Obesity in the U.S. has increased to an alarming extent over the past four decades. Obesity is related to risk of several autoimmune diseases, possibly via generation of adipokines and inflammatory cytokines. Prospective studies of obesity and systemic lupus erythematosus (SLE) risk are lacking however.

Objectives

To prospectively evaluate the association between obesity and SLE risk

Methods

We conducted a prospective cohort study of women in the U.S. Nurses9 Health Studies (NHS, 1976–2012, age 30–55 at baseline; NHSII, 1989–2013, age 25–42 at baseline). Incident SLE was confirmed by American College of Rheumatology 1997 criteria. Body mass index (BMI, kg/m²) was reported at baseline and on biennial questionnaires. Cumulative average BMI (18.5 to <25 [normal (ref)], 25 to <30 [overweight], ≥30 [obese]) was the primary exposure. Cox proportional hazards models estimated hazard ratios (HR) and 95% confidence intervals (CI) for SLE by cumulative average BMI category, adjusting for covariates (Table). Analyses were conducted in each cohort; results were meta-analyzed with a DerSimonian-Laird random effects model. Sensitivity analyses: 1) excluded women with cancer, and 2) started in 1988 (NHS)/1989 (NHSII) when obesity prevalence in the U.S. was most steeply increasing.

Results

We identified 154 SLE cases in NHS and 113 cases in NHSII. At baseline, obesity was present in 8.4% (NHS) and 11.8% (NHSII); mean age was 42.7 (SD 7.1) years (NHS) and 34.4 (SD 4.6) years (NHSII); 92% were White in each cohort. Obesity was significantly associated with SLE risk among women in NHSII, but not NHS (Table). In NHSII, a strong dose-dependent relationship between BMI and SLE risk was observed. After meta-analysis, obese women had a non-significantly elevated SLE risk compared to normal weight women (p trend 0.02). Results were similar in sensitivity analyses excluding women with cancer (HR 1.48, 95%CI 0.93–2.37, p trend 0.03). In analyses starting in 1988/1989, obese women had an increased SLE risk (meta-analyzed HR 1.76, 95%CI 1.19–2.58) compared to normal weight women (p trend <0.01).

Conclusions

Obesity was associated with a significant 88% increase in SLE risk in the younger cohort, NHSII, but did not significantly elevate SLE risk in NHS subjects. Meta-analysis revealed a non-significant 49% increased risk of SLE in obese women. We observed a stronger obesity-associated SLE risk when analyses started in 1988/1989 in both cohorts. The discrepant results between the cohorts are not fully understood and deserve further study.

Disclosure of Interest

None declared

Cumulative incidence

10.1136/annrheumdis-2016-eular.1977

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Citations (1)