Study of the incidence of hyperuricemia in young males' population with rapid entry into the plateau of 4 500m
doi: 10.2478/fzm-2022-0005
-
Abstract:
Objective To study the incidence and risk factors of hyperuricemia in young males who rapid entered into the plateau of 4 500 m. Methods The study contained 390 males aged 18-35 years (21.6 ± 2.5 years), who rapidly entered the plateau with an altitude of 4 500 m. According to their basic level of uric acid (UA), they were divided into two groups, high uric acid (HUA) group and normal uric acid (NUA) group. The characteristics and physiological index, such as the body weight and the height, of them were recorded. For the test of the biochemical indicators, the venous blood samples were collected at the altitude of 4 500 m in the morning. The count of blood cells, blood urea nitrogen (BUN), serum creatinine (SCR), lactate dehydrogenase (LDH), total bilirubin (TBIL), direct bilirubin (DBIL) and indirect bilirubin (IDBIL) were compared between the two groups. Results The incidence of hyperuricemia was 65.1% (254/390) at 4 500 m. At the altitude of 4 500 m, the mean hemoglobin concentration (MCHC) of red blood cells in the HUA group was significantly lower than that in the NUA group. Hemoglobin (HGB), mean red blood cell volume (MCV), TBIL, IDBIL, BUN, SCR and LDH in the HUA group were significantly higher than those in the NUA group, though without statistically significant differences in the other variables. Meanwhile, multivariate analysis showed at the altitude of 4 500 m, the risk of HUA increased by 0.982, 1.038 and 1.045 times when MCHC decreased by one unit and TBIL and SCR increased by one unit, respectively. Conclusion The incidence of hyperuricemia was high of 65.1% rush entry into the plateau of young male. Decreased MCHC and elevated TBIL and SCR were independent risk factors for hyperuricemia when rapid enter into 4 500 m. -
Key words:
- rapid entry /
- the plateau /
- hyperuricemia /
- renal function
-
Table 1. Clinical characteristics (at altitude of 4 500 m) of the objectives
Variables HUA group(n=254) NUA group(n=136) Z value P value BMI 21.47(20.36, 23.06) 21.63(20.24, 22.88) -0.102 0.919 RBC 5.58(5.49, 5.89) 5.76(5.5, 5.93) -1.286 0.185 HGB 161(157, 175) 171(162, 176) -2.073 0.021* HCT 52(49.6, 55.48) 54.0(51.23, 56.12) -1.971 0.041* MCV 94.9(91.28, 99.43) 93.38(87.66, 98.01) -2.961 0.009* MCH 29.46(28.75, 30.47) 30(29.21, 31.04) -0.861 0.407 MCHC 309(302.45, 323.15) 323.4(303.5, 336.4) -4.127 < 0.001* PLT 221.5(191.75, 253) 222(192, 253.5) -0.168 0.891 PDW 16.8(14.865, 18.6) 16.41(14.7, 18.9) -0.149 0.799 MPV 12.2(11.3, 13.4) 12.6(11.03, 13.5) -0.296 0.734 PCT 0.28(0.24, 0.32) 0.27(0.24, 0.33) -0.306 0.695 TBIL 14.96(11.08, 19.96) 11.93(9.04, 17.33) -4.318 < 0.001* DBIL 3.88(2.76, 5.89) 3.76(2.62, 5.01) -1.974 0.056 IDBIL 10(6.46, 14.37) 7.57(5.51, 11.63) -3.780 < 0.001* BUN 6.6(5.84, 7.7) 5.4(4.16, 6.28) -6.665 < 0.001* SCR 100.54(82.34, 116.37) 74.2(68.3, 82.4) -9.163 < 0.001* LDH 232(181.57, 276.5) 185.2(142.35, 229) -4.399 < 0.001* * P < 0.05.
BMI: Body Mass Index; RBC: Red Blood Cell; HGB: Hemoglobin; HCT: Hematocrit; MCV: Mean Corpusular Volume;
MCH: Mean Corpusular Hemoglobin; MCHC: Mean Corpusular Hemoglobin Concerntration; PLT: Platelet; PDW: Platelet Distribution Width; MPV: Mean Platelet Volume; PCT: plateletocrit; TBIL: Total Bilirubin; DBIL: Direct Bilirubin; IDBIL: Indirect Bilirubin; BUN: Blood Urea Nitrogen; SCR: Serum Creatinine; LDH: Lactic Dehydrogenase.Table 2. Logistic Regression analysis (4 500 m)
Regression coefficient Standard error Wald statistics P value OR value MCHC -0.017 0.009 5.329 0.025 0.987 TBIL 0.034 0.019 4.565 0.036 1.041 SCR 0.045 0.005 55.728 < 0.001 1.039 MCHC: Mean Corpusular Hemoglobin Concerntration;
TBIL: Total Bilirubin; SCR: Serum Creatinine -
[1] Multidisciplinary Expert Task Force on Hyperuricemia and Related Diseases. Chinese multidisciplinary expert consensus on the diagnosis and treatment of hyperuricemia and related diseases. Chin Med J (Engl), 2017; 130(20): 2473-2488. doi: 10.4103/0366-6999.216416 [2] Evans P L, Prior J A, Belcher J, et al. Obesity, hypertension and diuretic use as risk factors for incident gout: a systematic review and meta-analysis of cohort studies. Arthritis Res Ther, 2018; 20(1): 136. doi: 10.1186/s13075-018-1612-1 [3] Thottam G E, Krasnokutsky S, Pillinger M H. Gout and metabolic syndrome: a tangled web. Curr Rheumatol Rep, 2017; 19(10): 60. doi: 10.1007/s11926-017-0688-y [4] Kuo C F, Yu K H, Luo S F, et al. Gout and risk of non-alcoholic fatty liver disease. Scand J Rheumatol, 2010; 39(6): 466-471. doi: 10.3109/03009741003742797 [5] Roughley M J, Belcher J, Mallen C D, et al. Gout and risk of chronic kidney disease and nephrolithiasis: meta-analysis of observational studies. Arthritis Res Ther, 2015; 17(1): 90. doi: 10.1186/s13075-015-0610-9 [6] Abeles A M, Pillinger M H. Gout and cardiovascular disease: crystallized confusion. Curr Opin Rheumatol, 2019; 31(2): 118-124. doi: 10.1097/BOR.0000000000000585 [7] Tung Y C, Lee S S, Tsai W C, et al. Association between gout and incident type 2 diabetes mellitus: a retrospective cohort study. Am J Med, 2016; 129(11): 1219. e17-1219. e25. [8] Pontremoli R. The role of urate-lowering treatment on cardiovascular and renal disease: evidence from CARES, FAST, ALL-HEART, and FEATHER studies. Curr Med Res Opin, 2017; 33(Sup3): 27-32. doi: 10.1080/03007995.2017.1378523 [9] Qin T, Zhou X, Wang J, et al. Hyperuricemia and the prognosis of hypertensive patients: a systematic review and meta-analysis. J Clin Hypertens (Greenwich), 2016; 18(12): 1268-1278. doi: 10.1111/jch.12855 [10] Rafiullah M, Siddiqui K, Al-Rubeaan K. Association between serum uric acid levels and metabolic markers in patients with type 2 diabetes from a community with high diabetes prevalence. Int J Clin Pract, 2020; 74(4): e13466. [11] Nielsen S M, Bartels E M, Henriksen M, et al. Weight loss for overweight and obese individuals with gout: a systematic review of longitudinal studies. Ann Rheum Dis, 2017; 76(11): 1870-1882. . doi: 10.1136/annrheumdis-2017-211472 [12] Li P, Huang J, Tian H J, et al. Regulation of bone marrow hematopoietic stem cell is involved in high-altitude erythrocytosis. Exp Hematol, 2011; 39(1): 37-46. doi: 10.1016/j.exphem.2010.10.006 [13] Glantzounis G K, Tsimoyiannis E C, Kappas A M, et al. Uric acid and oxidative stress. Curr Pharm Des, 2005; 11(32): 4145-4151. doi: 10.2174/138161205774913255 [14] Ullah M M, Basile D P. Role of renal hypoxia in the progression from acute kidney injury to chronic kidney disease. Semin Nephrol, 2019; 39(6): 567-580. doi: 10.1016/j.semnephrol.2019.10.006 [15] D'Alessandro A, Xia Y. Erythrocyte adaptive metabolic reprogramming under physiological and pathological hypoxia. Curr Opin Hematol, 2020; 27(3): 155-162. doi: 10.1097/MOH.0000000000000574 [16] Harada M, Fujii K, Yamada Y, et al. Relationship between serum uric acid level and vascular injury markers in hemodialysis patients. Int Urol Nephrol, 2020; 52(8): 1581-1591. doi: 10.1007/s11255-020-02531-w [17] Li P, Huang J, Tian H J, et al. Regulation of bone marrow hematopoietic stem cell is involved in high-altitude erythrocytosis. Exp Hematol, 2011; 39(1): 37-46. doi: 10.1016/j.exphem.2010.10.006 [18] Tzounakas V L, Karadimas D G, Anastasiadi A T, et al. Donor-specific individuality of red blood cell performance during storage is partly a function of serum uric acid levels. Transfusion, 2018; 58(1): 34-40. doi: 10.1111/trf.14379 [19] Mohanty J G, Nagababu E, Rifkind J M. Red blood cell oxidative stress impairs oxygen delivery and induces red blood cell aging. Front Physiol, 2014; 5: 84. [20] Neimark E, LeLeiko N S. Antioxidant effect of bilirubin and pediatric nonalcoholic fatty liver disease. Pediatrics, 2009; 124(6): e1240-e1241. doi: 10.1542/peds.2009-2487 [21] Song K, Zhang Y, Ga Q, et al. High-altitude chronic hypoxia ameliorates obesity-induced non-alcoholic fatty liver disease in mice by regulating mitochondrial and AMPK signaling. Life Sci, 2020; 252: 117633. doi: 10.1016/j.lfs.2020.117633
计量
- 文章访问数: 240
- HTML全文浏览量: 164
- PDF下载量: 14
- 被引次数: 0