Research reportHigh serum uric acid level in adolescent depressive patients
Introduction
With an estimated prevalence of 4–5% of the world׳s population, mid to late adolescence depressive disorder is a serious mental illness that impacts society as it endangers physical and mental health (Costello et al., 2006). By the year 2020, depression is projected to reach second place as a global burden of disease for all ages and both sexes (WHO, 2012). Additionally, depressive disorder is a mental illness that has a high recurrence rate and its pathological mechanisms are still unclear. In regards to neurochemistry, the most widely accepted hypothesis of depression is a lack of monoamine neurotransmitter with an emphasis placed on the neurotransmitter 5-HT (Mahar et al., 2014).
Uric acid (UA) is the end-product of purine metabolism in the human body. There are two sources of purine: (1) endogeneity, a nucleic acid degradation which accounts for about 80% of the total amount of UA, and (2) exogeneity, a diet high in purine which accounts for about 20%. Research has shown that approximately 90% of patients with depression have differing levels of anxiety symptoms (Gaynes et al., 2007), with 40–50% of the patients having at least one kind of anxiety disorder comorbid with their depression (Howland et al., 2009, Rush et al., 2005). Patients with anxiety present with a hyperfunctioning of the HPA axis (Westberg et al., 1991, Pardon et al., 2003). Recent theories of depression have focused on biological factors such as HPA axis dysfunction related with chronic stress response and the theory that chronic stress response is the pathogenesis of depression (Mahar et al., 2014). The HPA axis affects the activity of cells, which further affects the metabolism of these cells and results in cell degradation. In addition, stress response not only influences the activity of the neurotransmitter 5-HT but also affects the metabolic pathway of monoamine neurotransmitters, which results in degradation (Lupien et al., 2009). Therefore, depression may be closely related with SUA.
Adulthood depression often develops from depression that has had its onset during adolescence (Birmaher et al., 2004). Because of this correlation, research on adolescent depression should do more to reflect early developmental mechanisms. Currently, there is a lack of relevant data as doctors often overlook key biochemical indexes and hormone levels when researching adolescent depression. The evaluation of such biochemical indexes and hormone levels can facilitate the early diagnosis and monitoring treatment process of adolescent depression (Chaudhari et al., 2010). Considering the deficit in research on biochemical and hormone levels, our research attempts to explore the pathological mechanisms of depression from the perspective of clinical biochemical index.
Section snippets
Subjects
The case group consisted of 152 mid-moderate depressed patients, all in their first hospitalizations in China Young Mental Development Base, General Hospital of Beijing Military Region. All patients were male, from all parts of China, with ages ranging from 13 to 25 years old (average age was 17.95±3.18). The criteria of inclusion consisted of (1) meeting the diagnostic criteria of depression as referenced in the Diagnostic and Statistical Manual of Mental Disorders Volume 4 (DSM-4), (2)
The SUA level of the research subjects
The SUA level was significantly higher than the control group (t=8.92, p<0.001) (see Table 1). There were 75 high SUA cases in the case group, amounting to 49.34% of the total group. The cases with higher than 400 μmol/L amounted to 69.5%. There were only 6 high SUA cases in the control group, accounting for 3.95%. The difference was of statistical significance (χ2=80.13, P<0.001).
Depression and anxiety levels of the research subjects
The 152 cases in the case group scored 15.58±5.32 on the HAMD-17, which was of a significant positive correlation
Discussion
This research is the first to discover that high levels of SUA exist among adolescent depressed patients. There are three possible causes that lead to having high SUA levels: (1) increased oxygenolysis of nucleic acid, (2) ingestion of a high-purine diet, and (3) the decreased excretion of urine acid. The level of blood urea nitrogen and creatinine among the case study group appeared within a normal range. The patients maintained a normal diet and did not present with disorders of the immune
Role of fundings
None.
Conflicts of interests
The authors declared no competing financial interests.
Acknowledgment
None.
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