SERUM URIC ACID LEVELS IN ORAL CANCER PATIENTS SEEN AT TERTIARY INSTITUTION IN NIGERIA


A.O. Lawal1, B. Kolude1 and B.F. Adeyemi1

Department of Oral Pathology, College of Medicine, University of Ibadan, Ibadan, Nigeria.

Abstract

Introduction: Toxicity by oxygen radicals has been considered as an important cause of cancer. It is proposed that the antioxidant properties of uric acid may act to prevent formation of oxygen radicals and thereby protect against
carcinogenesis. This study aims to assess the role of uric acid in the aetiology of oral cancer.

Materials and Methods: Thirty one oral cancer patients and thirty normal patients had serum uric acid measured using spectophotometer. The data obtained was analyzed using the Statistical Package for the Social Sciences, version 19.0 (SPSS19). Statistical significance was determined at P < 0.05.

Results: The mean serum uric acid level in oral cancer patients was 5.18 mg/dl (SD±1.96) while the mean was 7.09 mg/dl (SD±1.84) for the control group and this difference was statistically significant (p=0.000, t= -3.914, C.I. = – 2.885 to – 0.933). The risk of oral cancer was 3.98 times more in patients who had low serum uric acid.

Conclusion: This study showed that serum uric acid was lower in oral cancer patients compared with healthy volunteers and low serum uric acid was associated with increased risk of oral cancer development. However, further prospective cohort studies are suggested to better understand the role of serum uric acid in aetiology of oral cancer.

Correspondence:

Dr. A.O. Lawal
Department of Oral Pathology,
College of Medicine, University of Ibadan.
E-mail: toytoy219@yahoo.com
Tel: +2348055133964
Fax: +23422411768

Introduction

Toxicity by oxygen radicals has been suggested as an important cause of cancer, heart disease and aging.1 Oxygen radicals and other oxidants are toxic mainly because of their ability to initiate the chain reaction of lipid peroxidation. Lipid peroxidation in turn, generates reactive species such as radicals, hydro peroxides, aldehydes, and epoxides with the capability of causing cellular, DNA, and RNA injuries. 1

The protective systems against these injuries include enzymes, such as superoxide dismutase, the selenium containing glutathione peroxidase and antioxidants and radical scavengers; such as α -tocopherol and β -carotene in the lipid portion of the cell and glutathione and ascorbic acid in the aqueous phase.1 These protective mechanisms are now recognized as anti-carcinogenic and even having ability to increase life-span. 1

Uric acid is the final product of purine metabolism in humans, and its circulating concentrations are regulated by the balance in its production and excretion2. Uric acid is a known antioxidant, 1 and thus may prevent cancer by mopping up free radicals that may cause cellular and genetic injury. It is also said to help in stabilization of ascorbate in biological fluids3, and because its serum concentration is higher than that of ascorbate, it is thought to potentially have a higher antioxidant property than ascorbate. 3

Humans and other primates have higher serum urate and lower hepatic uricase levels compared to lower mammalian species.4 Ames et al.1 proposed that the uric acid may act to prevent formation of oxygen radicals and thereby protect against carcinogenesis. Only few studies have tested the association between uric acid and carcinogenesis with inconsistent results5, 6 , however, to the best of our knowledge, no study has examined the role of uric acid in the aetiology of oral cancer.

The aim of this study was to analyze the serum uric acid levels in oral cancer patients and compare them with those of normal patients in order to examine the possible role of uric acid in the aetiology of oral cancer.

MATERIALS AND METHODS
Thirty one histological confirmed oral cancer patients and thirty healthy volunteers were recruited from the Out-patient department of the Dental Centre University College Hospital Ibadan over an eighteen months period. Ethical clearance was obtained from the joint ethical committee of University of Ibadan and the University College Hospital. All patients were duly informed of the aim of the procedure and consented to participate in the study. Healthy volunteers under age 40 years and all those with known systemic diseases were excluded from the study (this is because things like alcohol, fructose containing sugars and purine containing foods may increase serum uric acid levels). Patients who previously had any form of radio therapy, chemo therapy or surgical interventions were excluded from the study.

10mls of intravenous blood was taken from all participants after an overnight fast. The blood was centrifuged at 3,000 rpm for 5 minutes and separated serum was aspirated into tubes and analyzed for uric acid with a DM520 spectrophotometer (Beckman USA).

The data obtained was analyzed using the Statistical Package for the Social Sciences, version 19.0 (SPSS19). Differences between the two groups were analyzed for statistical significance using the student t- test, odd ratio and logistic regression, where applicable. Statistical significance was determined at P < 0.05.