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Keywords
Acute psychosis, affective disorders, schizophrenia, tranquilizers, uric acid
Abstract
Background: The increasing number of latent and manifest hyperuricemia is important concerning differential diagnosis in neurological and psychiatric diseases. The pathological importance of hyperuricemia in these diseases is particularly unknown. Previous studies have shown that uric acid (UA) estimation in cerebrospinal fluid was made with neurological and psychiatric diseases. Monitoring serum UA levels, a relatively inexpensive and easily available test, may prove to be a useful adjunct in the assessment of certain indices of certain psychiatric illness. Tranquilizers like 1,4 - benzodiazepine (purinergic) are shown to decrease xanthine oxidase activity initially and may cause fluctuations in serum UA levels.
Objective: In the present study, an attempt was made to understand the effect of tranquilizers on serum UA levels in different psychiatric conditions.
Materials and Methods: A total of 40 cases (22 males and 18 females) of manic depressive psychosis and Schizophrenia who were undergoing treatment with different tranquilizers from the Psychiatric Hospital, Patna, India and 20 healthy controls (12 males and 8 females) not using any tranquilizers were included in the study.
Results: The serum UA levels were significantly elevated (P < 0.05) in these patients receiving treatment with tranquilizers. The levels of UA in male patients were significantly higher when compared with females and also over male controls (P < 0.01). In female patients UAs levels are raised but not significant (P > 0.05) over control females.
Conclusion: This preliminary study does indicate that serum UA levels do change with the administration of these drugs. Nature, gender, duration and the type of drugs used and their individual effects on different psychiatric disorders will be discussed.
Introduction
Uric acid (UA) is a constituent of the cell cytosol and also one of the soluble compounds in the blood, whose role in human physiology is controversial.® It is mainly synthesized from adenine- and guanine-based purines.® Humans lack uricase (urate oxidase) because of an acquired mutation in the urate oxidase gene, which makes the enzyme nonfunctional.® Thus, UA appears to be an end-product of the purine pathway, and circulating UA levels, which are dependent mainly on the nucleotide catabolism and cell turnover, are higher in humans.® According to Ames et al., inactivation of the urate oxidase gene,...