痛风性关节炎与单纯性高尿酸血症临床指标的比较

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Abstract Objective To investigate the difference of clinical indicators between patients with gout arthritis and those with simple hyperuricemia.Methods The clinical data of 151 patients with hyperuricemia treated in Hubei Provincial Corps Hospital of Chinese People's Armed Police Force between January 2011 and October 2017 was retrospectively analyzed.Forty-three of these patients were assigned the gout arthritis group(GA)and the rest to the simple hyperuricemia group(SHUA). The difference in age, sex, body mass index (BMI), smoking, alcohol consumption, rates of abnormal blood pressure, blood pressure (BP), fasting plasma glucose (FPG), rates of abnormal blood glucose, triglyceride (TG), cholesterol (CHOL), high-density lipoprotein (HDL), low density lipoprotein (LDL), serum creatinine (CR), serum uric acid (UA) ,left ventricular shortening rate (LVFS),and left ventricular ejection fraction (LVEF)was compared between the two groups.Results 1. There was no significant difference between the two groups in age, smoking history, drinking history or body mass index (P<0.05). However, the proportion of males was higher in the GA group, and the difference was significant(P=0.01).2. Compared with the SHUA group, rates of abnormal blood glucose levels,fasting glucose levels,rates of abnormal blood pressure,systolic blood pressure and the level of triglyceride in the GA group were significantly lower(P<0.05). while the diastolic blood pressure levels, cholesterol, high-density lipoprotein, and low density lipoprotein were not significantly different between the two groups(P>0.05). 3. The serum creatinine level of the GA group was significantly higher than that in the SHUA group, and the difference was significant(P=0.001). 4. The serum uric acid level in GA group was not significantly different from that in SHUA group(P=0.399). 5. In terms of the left ventricular shortening rate(LVFS), the GA group was significantly higher than the SHUA group (P=0.024), but there was no significant difference between the two groups in the left ventricular ejection fraction (P=0.059).Conclusions The clinical indicators of gout arthritis (GA)patients are better than those of patients with simple hyperuricemia(SHUA)alone in hyperuricemia.

Key words： simple hyperuricemia hyperuricemia clinical indicator gout gout arthritis

Received: 20 October 2017

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	PAN Dezhang
	WANG Yong
	WANG Meijun

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PAN Dezhang,WANG Yong,WANG Meijun. Comparison of clinical indicators between patients with gout arthritis and those with simple hyperuricemia[J]. Med. J. Chin. Peop. Armed Poli. Forc., 2018, 29(3): 236-239.

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http://journal08.magtechjournal.com/Jwk_wjyx/EN/ OR http://journal08.magtechjournal.com/Jwk_wjyx/EN/Y2018/V29/I3/236

[1]	Liu H, Zhang X M, Wang Y L, et al. Prevalence of hyperuricemia among Chinese adults: a national cross-sectional survey using multistage, stratified sampling[J]. J Nephrol,2014, 27(6): 653-658.
[2]	王淑芳,冯丽珍,宋梅,等. 驻呼和浩特市男性新兵高尿酸血症与痛风的流行病学调查[J]. 武警医学, 2016, 27(1): 5-7.
[3]	Zhu Y,Pandya B J,Choi H K. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008[J]. Arthritis Rheum,2011,63(10):3136-3141.
[4]	Merriman T R. An update on the genetic architecture of hyperuricemia and gout[J]. Arthritis Res Ther, 2015, 17(1): 98.
[5]	Merriman T R, Choi H K, Dalbeth N. The genetic basis of gout [J].Rheum Dis Clin North Am, 2014, 40(2):279-290.
[6]	Dalbeth N, Merriman T R, Stamp L K. Gout [J]. Lancet, 2016, 388(10055): 2039-2052.
[7]	MacFarlane L A,Kim S C, et al. Gout: a review of nonmodifiable and modifiable risk factors [J]. Rheum Dis Clin North Am, 2014, 40(4):581-604.
[8]	Lam N N,Kim S J,Prasad G V, et al. Gout after living kidney donation: a matched cohort study [J]. Am J Kidney Dis, 2015, 65(6): 925-932.
[9]	Jing J,Kielstein J T, Schultheiss U T,et al. Prevalence and correlates of gout in a large cohort of patients with chronic kidney disease: the German Chronic Kidney Disease(GCKD) study [J]. Nephrol Dial Transplant, 2015, 30(4): 613-621.
[10]	Ragab G, Elshahaly M, Bardin T,et al. Gout: an old disease in new perspective- a review[J]. J Adv Res, 2017,8(5):495.
[11]	Davies M J, Trujillo A, Vijapurkar U, et al. Effect of canagliflozin on serum uric acid in patients with type 2 diabetes mellitus [J]. Diabetes Obes Meta, 2015, 17(4): 426-429.
[12]	Katsiki N,Papanas N,Fonseca V A,et al. Uric acid and diabetes: is there a link?[J]. Curr Pharm Des, 2013,19(27):4930-4937.
[13]	Nakanishi N, Suzuki K, Kawashimo H, et al. Serum uric acid: correlation with biological, clinical and behavioral factors in Japanese men[J]. Am J Epidemiol,1999,9(2):99-106.
[14]	Chen J H,Pan W H,Hsu C C,et al.Impact of obesity and hypertriglyceridemia on gout development with or without hyperuricemia: a prospective study [J]. Arthritis Care Res, 2013, 65(1):133-140.
[15]	周慧,刘振,李长贵,等. 痛风与单纯性高尿酸血症人群高脂血症的对比分析[J]. 现代生物医学进展, 2017, 17(17): 3278-3281.
[16]	MandalA K, Mount D B. The molecular physiology of uric acid homeostasis [J]. Annu Rev Physiol, 2015, 77: 323-345.

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