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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 3  |  Page : 156-158

Serum uric acid levels in hypertensive patients with and without metabolic syndrome in the hills of Himachal Pradesh, India


1 Department of Medicine, Dr Rajendra Prasad Govt. Medical College, Tanda, Kangra, India
2 Department of Medicine, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
3 Department of Cardiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India

Date of Submission19-May-2014
Date of Decision20-Jul-2014
Date of Acceptance24-Jul-2014
Date of Web Publication19-Sep-2014

Correspondence Address:
Sujeet Raina
B 1 Type IV Qts, Dr. Rajendra Prasad Govt. Medical College, Tanda, Kangra 176 001, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2347-9906.141143

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  Abstract 

Introduction: The objective was to assess the prevalence of hyperuricemia among newly diagnosed hypertensive patients in a tertiary care hospital in the Northern hilly state of Himachal Pradesh, India. Materials and Methods: In all 118 newly diagnosed patients with hypertension above the age of 20 years were included. Uric acid (UA) was measured using enzymatic uricase method. Hyperuricemia was defined as serum urate level > 6.8 mg/dl. National Cholesterol Education Program-Adult Treatment Panel III criteria modified for Asian subjects, was used for defining metabolic syndrome (MS). Student's t-test for mean of continuous variables and Chi-square test for proportions were used for statistical significance. Results: The mean UA level among all the hypertensive subjects was 4.7 ± 1.0 mg/dl. The mean UA of patients with MS was 5.2 ± 1.3 mg/dl while in those without MS was 4.2 ± 0.7 mg/dl. The difference in mean UA in the two groups was statistically significant (P = 0.001). The prevalence of hyperuricemia was 5%, and all the patients were postmenopausal females among the MS group. Conclusion: In this study, cross-sectional associations between hypertension, MS and hyperuricemia were observed.

Keywords: Hyperuricemia, hypertension, metabolic syndrome, Western Himalayas


How to cite this article:
Raina S, Thakur S, Thakur S, Negi P C, Verma BS. Serum uric acid levels in hypertensive patients with and without metabolic syndrome in the hills of Himachal Pradesh, India. J Obes Metab Res 2014;1:156-8

How to cite this URL:
Raina S, Thakur S, Thakur S, Negi P C, Verma BS. Serum uric acid levels in hypertensive patients with and without metabolic syndrome in the hills of Himachal Pradesh, India. J Obes Metab Res [serial online] 2014 [cited 2019 Jun 25];1:156-8. Available from: http://www.jomrjournal.org/text.asp?2014/1/3/156/141143


  Introduction Top


Medicine is ever evolving with the rapid expansion of evidence-based knowledge, advancement in diagnostic and therapeutic options and by confronting debatable and emerging issues. Metabolic alteration like hyperuricemia is associated with metabolic syndrome (MS) and reflects defects in insulin action on the renal tubular reabsorption of uric acid (UA). Emerson has reviewed the evidence supporting inclusion of hyperuricemia as an intrinsic component of MS. [1] Hyperuricemia is defined as serum UA level > 6.8 mg/dl. This is the limit of the urate solubility at physiological temperature and pH. [2],[3] Over the past three decades, the prevalence of hypertension in adults has risen dramatically in India. The number of hypertensives, is estimated to be 213 million by 2025. [4] Although the etiology of hypertension is unclear in many patients, hyperuricemia is considered an independent risk factor for hypertension. Animal model studies suggest a two-phase mechanism for the development of hyperuricemic hypertension. The first phase of UA induced reversible vasoconstriction is followed by the second phase of vascular smooth-muscle cells proliferation and secondary arteriolosclerosis. The latter two-impair pressure natriuresis. No studies on estimation of serum UA levels in hypertensive patients from the native population living at moderate altitude of India have been done so far to the best of our knowledge. To assess the prevalence of hyperuricemia among newly diagnosed hypertensive patients, the present study was designed. The study was conducted in a tertiary care hospital located at a moderate altitude of 2200 m above mean sea level in the northern hilly state of Himachal Pradesh, India.


  Materials and methods Top


The study was conducted over a period of 1-year in the outdoor services of the Department of Internal Medicine and Cardiology in a tertiary care hospital. Newly diagnosed patients with hypertension based on JNC VII and above the age of 20 years were included in this cross-sectional study. Patients with secondary hypertension, secondary cause of obesity, any acute illness, pregnancy, steroidal medications or any medication likely to increase serum UA or plasma glucose, chronic renal failure and patients not willing to participate in the study were excluded. On the day of the presentation, each patient was subjected to a detailed history and clinical examination. Biochemical investigations were done in all patients on a venous sample after a minimum 8 h overnight fasting state. UA was measured using enzymatic uricase method. Hyperuricemia was defined as serum urate level > 6.8 mg/dl, that is, the limit of the urate solubility at physiological temperature and pH. [3] National Cholesterol Education Program-Adult Treatment Panel III criteria modified for Asian subjects, was used for estimating the prevalence of MS. [5] Student's t-test was used to compare the mean of the continuous variables. Chi-square test was used to compare proportions. The study was approved from college Ethics Committee.


  Results Top


In all 118 hypertensive patients who fulfilled the eligibility criteria, were included in the study. The prevalence of MS was 68.6%, and distribution among male was 58.1% and among female was 86.3%. The mean UA level among all the hypertensive subjects was 4.7 ± 1.0 mg/dl. The detailed clinical characters of hypertensive patients are shown in [Table 1]. The mean UA of patients with MS was 5.2 ± 1.3 mg/dl, while in those without MS was 4.2 ± 0.7 mg/dl. The difference in mean UA in the two groups was statistically significant (P = 0.001). The prevalence of hyperuricemia was 5%, and all the patients were postmenopausal females. All these patients fulfilled the criteria of having MS.
Table 1: Baseline characteristics of newly diagnosed hypertensive patients with and without MS


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  Discussion Top


Epidemiological transition in the prevalence of diseases is taking place worldwide and with regional variations. The shift is driven by nutritional, demographic, socioeconomic, industrialization, urbanization and associated changes in lifestyle. In developing countries, communicable diseases continue to be a major cause of death, but noncommunicable diseases related to inactivity and obesity are also on the rise and projected to increase substantially over the next two decades. [6]

High prevalence of MS in India falls in line with the rise in obesity. [7] Results of animal studies suggest that hyperuricemia might play a part in the development of MS. [8] Similarly, hypertension is increasing rapidly in most low and middle-income countries driven by diverse health transitions. [4] Over the last four decades, the mean serum UA levels among populations are increasing. Outcome conclusions from different studies found mean serum UA level of 4.9 mg/dl in 1965, 5.12 mg/dl in 1967, 6.14 in 2000 and 7.1 in 2004 across different populations. [9],[10],[11],[12]

Hyperuricemia is common in subjects living at high altitude and is associated with hypertension, proteinuria and erythrocytosis. The elevation in UA levels appears to be caused by increased urate generation secondary to hypoxia. In addition, a relative impairment in renal excretion also may play a role. [13] A high-altitude renal syndrome has been described. It includes polycythemia, hyperuricemia, systemic hypertension, and microalbuminuria. [14]

The mean serum UA level in our hypertensive population was 4.7 ± 1.0 mg/dl. It is lower in comparison to 6.0 ± 1.2 mg/dl found in a study conducted at a higher altitude of 4300 m and 6.1 ± 1.6 mg/dl as found in other study at an altitude of more than 3500 m. [13],[15]

The mean UA of patients with MS was 5.2 ± 1.3 mg/dl, while in those without MS was 4.2 ± 0.7 mg/dl. The prevalence of hyperuricemia was 5%, and all the patients were postmenopausal females.

Hyperuricemia is fairly common with the prevalence between 2.6% and 47.2% in various populations. [16] While studying the select nomad tribal population of Rajasthan, India the prevalence of hyperuricemia was found to be 13.5%. Hyperuricemia was more frequent in men (14.4%) than women (12.8%). [17]

Hyperuricemia is associated with an increased risk for incident hypertension, independent of traditional hypertension risk factors. In a systematic review and meta-analysis it was observed that overall risk for incident hypertension increased by 13%/1 mg/dl increase in serum UA level and the risk was more pronounced in younger individuals and in women. [18] Animal models data of pharmacologically induced hyperuricemia have linked UA as a predictor of hypertension which can be ameliorated by UA lowering drugs. Early hypertension is completely reversible with the urate reduction, but prolonged hyperuricemia results in irreversible sodium-sensitive hypertension which becomes independent of UA levels. The early hypertension is related to greater renal renin activity and reduction of circulating plasma nitric oxide leading to a phenotype of excessive vasoconstriction that can be reversed by reduction of UA or renin-angiotensin system blockade. The later irreversible hypertension is secondary to altered intrarenal vascular architecture and proliferation of vascular smooth-muscle cells. [19],[20] Elevated UA levels have been often found in children with primary hypertension. [21] A recent randomized trial has demonstrated a significant reduction of blood pressure and plasma renin activity with urate-lowering therapy in obese hypertensive adolescents. [22]


  Conclusion Top


This data expanded cross-sectional associations between hyperuricemia hypertension and metabolic. Whether this link is causal remains to be clarified further by future studies. It would be particularly important to design randomized trials and long-term incidence studies that determine the effect of urate-lowering therapy on the prevention or treatment of hypertension.

 
  References Top

1.Emmerson B. Hyperlipidaemia in hyperuricaemia and gout. Ann Rheum Dis 1998;57:509-10.  Back to cited text no. 1
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2.Grassi D, Ferri L, Desideri G, Di Giosia P, Cheli P, Del Pinto R, et al. Chronic hyperuricemia, uric acid deposit and cardiovascular risk. Curr Pharm Des 2013;19:2432-8.  Back to cited text no. 2
    
3.Neogi T. Clinical practice. Gout N Engl J Med 2011;364:443-52.  Back to cited text no. 3
    
4.Mohan S, Campbell N, Chockalingam A. Time to effectively address hypertension in India. Indian J Med Res 2013;137:627-31.  Back to cited text no. 4
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5.Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005;112:2735-52.  Back to cited text no. 5
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6.Gaziano TA, Gaziano TM. Epidemiology of cardiovascular disease. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18 th ed. New York: McGraw-Hill; 2012. p. 1811-6.  Back to cited text no. 6
    
7.Misra A, Khurrana L. Obesity and the metabolic syndrome in developing countries. J Clin Endocrinol Metab 2008;93 Suppl 1:s9-30.  Back to cited text no. 7
    
8.Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res (Hoboken) 2012;64:1431-46.  Back to cited text no. 8
    
9.Mikkelsen WM, Dodge HJ, Valkenburg H. The distribution of serum uric acid values in a population unselected as to gout or hyperuricemia: Tecumseh, Michigan 1959-1960. Am J Med 1965;39:242-51.  Back to cited text no. 9
    
10.Hall AP, Barry PE, Dawber TR, McNamara PM. Epidemiology of gout and hyperuricemia. A long-term population study. Am J Med 1967;42:27-37.  Back to cited text no. 10
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11.Lin KC, Lin HY, Chou P. Community based epidemiological study on hyperuricemia and gout in Kin-Hu, Kinmen. J Rheumatol 2000;27:1045-50.  Back to cited text no. 11
    
12.Yu KH, Luo SF, Tsai WP, Huang YY. Intermittent elevation of serum urate and 24-hour urinary uric acid excretion. Rheumatology (Oxford) 2004;43:1541-5.  Back to cited text no. 12
    
13.Jefferson JA, Escudero E, Hurtado ME, Kelly JP, Swenson ER, Wener MH, et al. Hyperuricemia, hypertension, and proteinuria associated with high-altitude polycythemia. Am J Kidney Dis 2002;39:1135-42.  Back to cited text no. 13
    
14.Arestegui AH, Fuquay R, Sirota J, Swenson ER, Schoene RB, Jefferson JA, et al. High altitude renal syndrome (HARS). J Am Soc Nephrol 2011;22:1963-8.  Back to cited text no. 14
    
15.Chen W, Liu Q, Wang H, Chen W, Johnson RJ, Dong X, et al. Prevalence and risk factors of chronic kidney disease: A population study in the Tibetan population. Nephrol Dial Transplant 2011;26:1592-9.  Back to cited text no. 15
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16.Wortmann RL. Gout and hyperuricemia. In: Firestein GS, Budd RC, Harris ED, McInnes IB, Ruddy S, Sergent JS, editors. Kelley's Textbook of Rheumatology. 8 th ed. Philadelphia: Saunders Elsevie; 2009. p. 1481-506.  Back to cited text no. 16
    
17.Sachdev B. Prevalence of hyperuricemia and its relation with metabolic syndrome in a select nomad tribal population of Rajasthan, India. Int J Health Sci Res 2012;2:25-32.  Back to cited text no. 17
    
18.Grayson PC, Kim SY, LaValley M, Choi HK. Hyperuricemia and incident hypertension: A systematic review and meta-analysis. Arthritis Care Res (Hoboken) 2011;63:102-10.  Back to cited text no. 18
    
19.Mazzali M, Hughes J, Kim YG, Jefferson JA, Kang DH, Gordon KL, et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001;38:1101-6.  Back to cited text no. 19
    
20.Mazzali M, Kanellis J, Han L, Feng L, Xia YY, Chen Q, et al. Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism. Am J Physiol Renal Physiol 2002;282:F991-7.  Back to cited text no. 20
    
21.Feig DI, Johnson RJ. Hyperuricemia in childhood primary hypertension. Hypertension 2003;42:247-52.  Back to cited text no. 21
    
22.Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: A randomized trial. JAMA 2008;300:924-32.  Back to cited text no. 22
    



 
 
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