scholarly journals Serum uric acid increases after smoking cessation (Longitudinal study)

2006 ◽  
Vol 30 (2) ◽  
pp. 217-223
Author(s):  
Shoichi Mizuno ◽  
Masako Tomita ◽  
Takashi Murayama
2018 ◽  
Vol 11 (6) ◽  
pp. 431-439 ◽  
Author(s):  
Fang Cheng ◽  
Xin Yin ◽  
Wenhou Duan ◽  
Runze Ye ◽  
Yakun Zhu ◽  
...  

Bone ◽  
2013 ◽  
Vol 52 (1) ◽  
pp. 400-406 ◽  
Author(s):  
Joanna Makovey ◽  
Monique Macara ◽  
Jian Sheng Chen ◽  
Christopher S. Hayward ◽  
Lyn March ◽  
...  

2005 ◽  
Vol 56 (2) ◽  
pp. 83-88 ◽  
Author(s):  
Mirei Uetani ◽  
Yasushi Suwazono ◽  
Etsuko Kobayashi ◽  
Takeya Inaba ◽  
Mitsuhiro Oishi ◽  
...  

2015 ◽  
Vol 28 (8) ◽  
pp. 966-970 ◽  
Author(s):  
Cristina Pellegrino Baena ◽  
Paulo Andrade Lotufo ◽  
José Geraldo Mill ◽  
Roberto de Sa Cunha ◽  
Isabela J Benseñor

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wenqiang Zhang ◽  
Rongsheng Luan

Abstract Background Short-term starvation has been related to hyperuricemia. However, little is known about the long-term effect of early-life exposure to famine on hyperuricemia risk in adulthood. Methods The analysis included 2383 participants from the China Health and Retirement Longitudinal Study in 2015. Hyperuricemia was diagnosed as serum uric acid ≥7 mg/dL in men and serum uric acid ≥6 mg/dL in women. Famine exposure subgroups were defined as unexposed (born between October 1, 1962, and September 30, 1964), fetal-exposed (born between October 1, 1959, and September 30, 1961), and early-childhood exposed (born between October 1, 1956, and September 1, 1958). The association between early-life famine exposure and hyperuricemia risk was assessed using multivariate logistic regression. Results The prevalence of hyperuricemia in the unexposed, fetal-exposed, and early-childhood exposed participants was 10.7, 14.1, 11.1%, respectively. Compared with unexposed and early-childhood exposed participants combined as an age-balanced control, fetal-exposed participants showed an increased risk of hyperuricemia in adulthood (OR = 1.41; 95% CI: 1.06–1.88), after adjusting for gender, marital status, famine severity, residence, smoking, drinking, BMI, hypertension, and diabetes. The famine effect on hyperuricemia was accentuated by overweight or obesity (P for interaction = 0.042). Compared with unexposed and BMI < 24 kg/m2 participants, the OR (95%CI) of hyperuricemia was 3.66 (2.13–6.30) for fetal-exposed and overweight/obesity participants. However, combined unexposed and early-childhood exposed participants as an age-balanced control, the interaction of famine exposure and BMI was not statistically significant (P for interaction = 0.054). Conclusion Famine exposure in the fetal stage was associated with an increased risk of hyperuricemia in adulthood.


Rheumatology ◽  
2021 ◽  
Author(s):  
Dong Jin Go ◽  
Dong Hyun Kim ◽  
Jie Young Kim ◽  
Ali Guermazi ◽  
Michel Daoud Crema ◽  
...  

Abstract Objectives Emerging evidence suggests a potential link between OA and gout; however, the association between serum uric acid (UA) itself and knee OA remains uncertain due to a lack of longitudinal studies. Here, we investigated the association between serum UA and knee OA according to cartilage status in elderly community residents without gout. Methods In this longitudinal study, participants without a history of gout were recruited from among the Korean cohort of the Hallym Aging Study (n = 296 for radiography study and n = 223 for MRI study). Weight-bearing knee radiographs and 1.5-T MRI scans, along with blood collection for analysis of serum UA, were performed at baseline and after 3 years. The severity and structural progression of knee OA were evaluated using the Kellgren–Lawrence grading system and the Whole-Organ MRI Score (WORMS) cartilage scoring method. Multivariable logistic regression analysis was conducted using generalized estimating equation (GEE) models. Results Serum UA levels were not associated with radiographic progression after adjusting for age, sex and BMI. There was no significant association between serum UA and tibiofemoral cartilage loss on MRI. However, baseline serum UA levels were negatively associated with patellofemoral cartilage loss over 3 years (adjusted odd ratio 0.70 per 1 mg/dl increase, 95% CI: 0.49, 0.98). Conclusion In this population-based cohort, serum UA was not a risk factor for knee OA progression. Further large-scale longitudinal studies in other populations are needed to validate the effects of UA on cartilage damage.


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