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Year : 2005  |  Volume : 39  |  Issue : 2  |  Page : 117-120
Evaluation and assessment of the symptomatic uricaemia in vegetarian population

Department of Orthopaedics, MLN Medical College Allahabad, India

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Background: Hyperuricaemia has been reported to be in normal healthy population.
Method: Serum uric acid was estimated in 542 vegetarian healthy persons complaining of pain in the joint and in different musculoskeletal problems.
Results: Four hundred cases (73.80 %) were having uric acid level above 5 mg %. The mean uric acid level was found to be 6.16% + 3.08 percent. Increased uric acid level was not found to be associated with the age.
Conclusion: The rise in the uric acid does not merely indicate gout but derails the normal physiology in some musculoskeletal sites and produces symptoms. Its association with hypertriglyceridaemia and hypertension is also alarming .It is found also closely related to the high alcohol intake, diuretic drugs, hypothyroidism and obesity. Hyperuricaemia is more than what is as usually believed and needs investigation. The possible cause of the hyperuricaemia in normal healthy individuals is discussed.

Keywords: Serum uric acid; Pathophysiology; Assessments.

How to cite this article:
Srivastava D C, Gaur S C. Evaluation and assessment of the symptomatic uricaemia in vegetarian population. Indian J Orthop 2005;39:117-20

How to cite this URL:
Srivastava D C, Gaur S C. Evaluation and assessment of the symptomatic uricaemia in vegetarian population. Indian J Orthop [serial online] 2005 [cited 2020 Jan 22];39:117-20. Available from:

   Introduction Top

Hyperuricaemia as commonly seen in clinical practice does not represent a specific disease or is not an indication of therapy [1] . This laboratory finding is present in 2 % adult males in United States [2] , 17% of adult males in France [3] , 7% of adult males in Spain [4] and in India it is reported to be 0.2 to 2 % in adult male population increasing with age [5] .

Uric acid above 7 mg / dl is associated with increased risk of the gout and nephrolithiasis [6] . The lower urate level in the reproductive females is due to the effect of the estrogrenic compound on the tubular urate handling leading to the increased renal clearance of the urate [7] . Certain diseases related to hypoxia may cause hyperuricaemia by both the mechanism; overproduction and under excretion and in the vast majority of the cases under excretion is the main cause [8] .

The insulin resistance and hyperlipedaemia may decrease the excretion of the uric acid independent of the obesity and creatinine clearance by enhancing the sodium tubular reabsorption [9],[10],[11],[12],[13],[14] . The hyperuricemia is common in the insulin resistant patients and it may be the common factor that links the hypertension, hyperlipidaemia and hyperuricaemia [15].

Hypertensive patients with CHF and renal dysfunction are likely to have hyperuricaemia [16],[17],[18] . Malignant hypertension is associated with hyperuricaemia but it is not an independent predictor of hypertension [19],[20] . These finding have given stimulus to the epidemiological study of the uric acid in general population in USA and Europe. These studies largely but invariably supported the role of SUA as cardiac vascular disease risk factor [21],[22],[23],[24] .

Levine et al [25] in a prospective study of 2400 workers in The Chicago Industrial Heart Study, found SUA to be independently associated with increased mortality and morbidity in CVD patients . The first study done between 1970 and 1994 by the National Health and Nutritional Epidemiologic study in 14000 persons of US population found the baseline SUA is associated with CVD but this is only significant in women [26] . Banerjee et al [27] observed that the SUA concentration is below 7 mg / dl in 95 % unselected individuals in this part of the world.

We have done the study to explore the prevalence of the symtomatic uricaemia in healthy vegetarians with pain in joints and different musculoskeletal disorders.

   Material and methods Top

This retrospective study was done in 542 individuals who presented between 1990 and 2003 and had complaints of joint pains, low back pain, tennis elbow, Golfers elbow, retrocalcaneal bursitis, plantar fasciitis, bursitis anserina, intermetatarslgia, asymmetrical inter costal myalgia, pain at costochondral junction in the chest and generalized muscular pain.

There were 441 males and 101 females. The general physical examination was done. The account of the height and weight were kept systematically. Blood pressure was recorded regularly. Organomegalies and lymphadenopathy were ruled out clinically. Patients were also examined for possibility of the rheumatoid arthritis.

The individuals were investigated for serum uric acid, Rh factor, Hb, TLC, DLC, ESR, blood sugar, urea and creatinine and for the lipid profile specially the triglyceride. The uric acid was measured by the enzymatic method using Bayer's Autopak on RA- 50 analyzer .The symptomatic cases were followed for the period ranging from 6 month to 12 years.

Symptomatic cases with SUA level above 5 mg% were treated by allopurinol / colchicine (where there was no other apparent cause for the symptoms), and were followed for an average of 2.22 years ranging from 6 months to 11 years.

   Results Top

Average age was 38.62 + years ranging from 16 to 82 years. Average weight was 61.9 kg ranging from 42 kg to 91 kg. Average height was 161.1 cm ranging from 146 cm to 182.5 cm. Fasting blood sugar was above normal in 42 cases with an average of 132 mg %. The 71 % of the cases were over weight. Rh factor was positive in 31 cases mild to moderately. Serum urea and creatinine was with in the normal limit in all the cases.

Eighty percent of the cases who had the uric acid above the 7 mg / dl and 60.52 % cases who had serum uric acid above 5.5 mg % had the hypertriglyceridaemia. Mild to malignant hypertension was seen in 51 % of the cases who had above 9 mg / dl SUA (102 cases). ESR level was below 20 mm in 79.15% of the cases [Table - 1]. But the cases with above 9mg/dl SUA had the ESR level raised and ranged from 24 to 40 mm with an average of 28.88mm. This observation is seen quite uniformly .This finding gives the speculation that increased SUA level causes bone and soft tissue destruction.

Serum uric acid in 142 cases was less than 5 mg/dl (26.20%) where as the remaining 400 cases shows more than 5 mg/dl (73.80%). Mean SUA level was found to be 6.16% + 3.08. The 153 cases (18.11%) had the SUA level above the 7 mg/dl.

SUA level above 11 mg /dl was found in 5 cases and above 13 mg/dl was in 2 cases only. It indicates that the large number of the cases 247 (45.57%) fall in between the 5 to 7 mg /dl group [Table - 2].

We observed that above the age of 60 years there were only 33 cases and out of that the 23 (69.69%) cases in this category had the > 5 mg/dl SUA. Category with 40 to 60 years age had 161 cases and out of which 105 (65.21 %) cases had above 5 mg/dl SUA level. Cases in the category of 20 to 40 years of age were 285 and 79.29% (226 case) in this category had > 5.4 mg/dl of SUA and this represents the maximum number of the cases in all categories. In our series the age does not show the correlation of significance with the level of the SUA. This is contrary to the other reports which indicate that the higher age leads to the increase in the SUA level.

Fifty six cases of podagra and acute monoarticular synovitis with SUA average of 7.48 and 30 cases of synovitis knee with an average of 7.28, were the only two categories in which the serum uric acid level is high [Table - 3]. These 86 cases of the two categories when combined together showed an average of 7.31mg% (15.86%). Rest 458 cases (84.13%) of the different categories showed an average of 5.49 mg% + .205 and individually they shows an average ranging from 5.27 to 5.79. It means that 458 cases show very nearly an average of 5.5 mg % and if we consider it as disease related criteria for leveling the hyperuricaemia , this series indicates in Indian population the serum uric acid level of 5.5 mg % should be the parameter for hyperuricaemia. Cases averaging serum uric acid 5.5 mg% responded to the allopurinol treatment by complete relief in the symptoms and they were symptom free only when the serum uric acid level was maintained below 5 mg%.

   Discussion Top

Although the series is small, we have noticed most of the cases with complaints shown in [Table - 3] if there were no other apparent causative pathology after screening them by thorough clinical examination and biochemical tests for possible causes and they were associated with the SUA level nearing 5.5 mg%, they (96.2% cases) responded well to the allopurinol / colchicine treatment. They were symptom free only when the SUA level was maintained below 5 mg%. If we consider it a disease related criteria in our population the hyperuricaemia level should be 5.5 mg%.

Banerjee et al [27] have reported 5% prevalence of hyper­uricaemia with above 7 mg/dl level in Indian race, in randomly chosen individuals. Our series indicate that there is increase in the prevalence of the hyperuricaemia.

But the blind random trial in large number of people in population is required to establish the level of hyperuricaemia with these parameters.

Increase of free radicals facilitates the peroxidation of the low density lipoprotein in the arterial wall by the peroxynitrite and may play a role in the artherosclerosis [28] . Pathological role of SUA in producing the arthritis, by precipitated crystals interacting with the neutrophils in synovial fluid, is also well documented.

Probably the pollution, use of the pesticides and the chemical fertilizers in the food production (the contamination of the dietary materials) lead to the more break down of the nucleic acid and more production of the purine or it interferes with the process of purine conversion in to nucleoproteins or there is some interference in the secretion or reabsorption process.

As the hyperuricaemia seems to be an important factor in effecting the normal fitness of the man and it is also associated to the CVD, it requires the special attention. Our suggestion is that we should treat the associated causes like obesity, diabetes, hypertension and hyperlipidaemia.

Ultimately SUA seems to be one of the relative indictors of the body's metabolism, catabolism and salvage pathways and in other term an indicator of the good health and fitness. A good health education should be imparted to the community for proper and healthy dietary practices.

To conclude, in India the disease related upper limit of the hyperuricaemia should be 5.5mg%. It is often seen that the symptoms reappear in a treated symptom free cases if the purine reach diet is taken in last few days. ESR is high in hyperuricaemic cases with > 9 mg/dl SUA level.

   References Top

1.Ruilope LM, Garcia PJ. Hyperuricemia and renal function. Curr Hyper­tension Rep. Madrid. 2001; 25-30.  Back to cited text no. 1    
2.Hall AP, Barry PE, Dawber TR, Mc Namara PM. Epidemiology of gout and hyperuricemia : A long term population study. Am J Med. 1967; 42: 27-27.  Back to cited text no. 2    
3.Zalokar J, Lellouch J, Claude JR. serum urate and gout in 4663 young male workers. Semin Hop Pairs. 1981,57:664-68.  Back to cited text no. 3    
4.Noguera HE. Estudio epidemiologico de hiperuricemia gota espana. Face I Madrid: Saned. 1987; 8:19.  Back to cited text no. 4    
5.Smith C, Menon GN. Practical Rheumatology, ed 2000: pg. 337-356.  Back to cited text no. 5    
6.Campion EW, Glynn RJ, De Labry LO. Asymtomatic hyperuricemia. Risk and concequences in normative aging study. Am J Med. 1987; 82: 421-426.  Back to cited text no. 6    
7.Nichols A , Suiath ML, Scott JT. Effect of the oestrogen therapy on plasma and urine level of the uric acid. Br Med J. 1973; 1: 449-451.  Back to cited text no. 7    
8.Garcia PJ, Lopez JM et al. Renal handling of the uric acid in gout: impaired tubular transport of urate not dependent on serum urate level. Metabolism. 1986; 35: 1147-53.  Back to cited text no. 8    
9.Rathmann W, Funfhouser E, Dyer AR, Roseman JM. Relation of the hyperuricemia with various components of insulin resistant syndrome in young black and white adults. Ann Epidemiol. 1998; 8: 250-261.  Back to cited text no. 9    
10.Ficchini F, Chen YDI, Hollenback CB, et al. Relation between the resistant to insulin mediated glucose uptake, urinary uric acid clearance and plasma uric acid concentration. J Am Med Assoc. 1991; 266: 3008­3009.  Back to cited text no. 10    
11.Cappucio FD, Strazullo P, Farinaro E. Uric acid metabolism and tubular sodium handling : results from population based study. J Am Med Assoc. 1993; 270: 354-59.  Back to cited text no. 11    
12.Lee J, Sparrow D, Vokanos PS et al. Uric acid and coronary heart disease risk: evidence for a role of uric acid in obesity insulin resistant sysdrome. Am J Epidem. 1995; 142:288-294.  Back to cited text no. 12    
13.Kerntz AL. Insulin resistace. Br Med J. 1996; 313: 1385-89.  Back to cited text no. 13    
14.Mohan M, Halkin H, Karasik A, Lusky A. Elevated serum uric acid a facet of huperinsulinimia. Diabetologia. 1987; 30: 713-718.  Back to cited text no. 14    
15.Solomma VV, Tuomilehto J, et al. Hypertriglycerimia in different de­gree of glucose intolerance in finish population: based study. Diabetes Care. 1992; 15:657-65.  Back to cited text no. 15    
16.Cannon PJ, Simson WB, Demartini FE et al. Hyperuricemia in pri­mary and renal hypertension. N Engl J Med. 1966; 275; 457-65.  Back to cited text no. 16    
17.Levya F, Anker S, Swam JW et al. Serun uric acid as an index of impaired oxydative metabolism in chronic heart failure. Eur Heart J. 1997; 18:858-65.  Back to cited text no. 17    
18.Messerli FH, Frohlich ED, et al. Serum uric acid in essential hyperten­sion: an indication of the renal vascular involvement. Ann Intern Med. 1980; 93:817-827.  Back to cited text no. 18    
19.Iossa F, Farinaro E, Panica S et al. Serum uric acid and hypertension: the Olivetti heart study. J Hum Hypertens. 1994; 8:677-681.  Back to cited text no. 19    
20.Selbly IV, FriedhmanGD, Quesenberry CP et al. Precursors of es­sential hypertension: pulmonary function heart rate uric acid, serum cholesterol, and other serum chemistries . Am J Epidemiol. 1990; 131:1017-1027.  Back to cited text no. 20    
21.Moriarity JT, Folsom AR, et al. Serum uric acid and risk of coronary heart disease: atherosclerosis risk in communities study. Am J Epidemio.l 2000; 10:136-143.  Back to cited text no. 21    
22.Klein R, Klein BE, Cornoni JC et al. Serum uric acid: its relalation to the coronary heart disease risk factor and cardiovascular disease Evas country, Georgia. Arch Intern Med. 1973; 132: 401-410.  Back to cited text no. 22    
23.Bengtsson C, Lapidus L et al. Hyperuricemia risk of cardiovascular disease and over all death, 12 year of follow up of participants in the population study of women in Gotherberg Sweden. Acta Med Scand. 1988; 224; 549-555.  Back to cited text no. 23    
24.Lehto S, Ronnemaa T, et al. Predictors of the stroke in middle aged patients in non insulin dependent diabetes. Stroke. 1996; 27:63-68.  Back to cited text no. 24    
25.Levine W, Dyer AR, Shekelle RB et al. Serum uric acic and 11.5 year morbidity of middle aged women : findings of the Chicago Heart Asso­ciation Detection Project In Industry. J Clin Epidemiol. 1989; 42:257­267.  Back to cited text no. 25    
26.Freedom DS, Williamson DF et al. Relation of the serum uric acid to the morbidity and ischemic heart disease ; the NHANES I Epidemiologic follow up study. Am J Epidemiol. 1995; 141:637-644.  Back to cited text no. 26    
27.Banerjee B, Saha N. Blood uric acid level in India and Western adults and its seasional variation . 1967; 48:207-10.  Back to cited text no. 27    
28.Hoeschen RJ. Oxidative stress and cardiovascular diseases. Can J Cardiol. 1997;13:1021-25.  Back to cited text no. 28    

Correspondence Address:
D C Srivastava
Department of Orthopaedics, MLN Medical College Allahabad
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Source of Support: None, Conflict of Interest: None

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  [Table - 1], [Table - 2], [Table - 3]


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