The causal association between thyroid disease and gout: A Mendelian randomization study
During a physical examination, the doctor should assess the affected joint for tenderness, inflammation, and tophi (deposits of uric acid crystals). Gout symptoms typically include sudden and severe pain, swelling, redness, and tenderness in the joints, most commonly in the big toe. Gout attacks usually occur suddenly, often at night, and can last a few days or several weeks. Some individuals may experience recurring gout attacks, while others may have periods of remission with no symptoms.
Gout and Hypothyroidism
The mean FT4 level was within the normal reference range after the case group’s index date in all hospitals. The mean T4 level was within the normal reference range in all hospitals (Table 4). Mary Shomon is an internationally-recognized writer, award-winning patient advocate, synthroid overstimulation health coach, and activist, and the New York Times bestselling author of 15 books on health and wellness, including the Thyroid Diet Revolution and Living Well With Hypothyroidism. On social media, Mary empowers and informs a community of more than a quarter million patients who have thyroid and hormonal health challenges.
The association between thyroid disorders and incident gout: population-based case–control study
We were not able to disentangle effects of the underlying thyroid disorder from effects of thyroid hormone therapy on the risk of gout because hypo- and hyperthyroidism are treated with thyroid hormone replacement or suppression therapy. A further limitation was that GFR measurements were not available for all patients in the study. This is a common problem when dealing with laboratory values or biomarkers that are an important part of diagnostic assessments.
- The thyroid hormones are crucial in regulating various bodily functions, including metabolism.
- Gout and hypothyroidism may seem like unrelated health conditions, but they actually have a close relationship.
- A previous study showed that hyperthyroidism resulted in elevated levels of UA, but the increase was less than in hypothyroidism 31, which were similar to our results.
- Few data are available on the association between thyroid dysfunction anduric acid metabolism and the evidence is conflicting.
- In the case of hypothyroidism, hormone replacement therapy is the primary treatment.
An important note about allopurinol (Zyloprim)
Due to the lack of laboratory results, we could not consider the thyroid autoimmune reaction and iodine status as covariates in this study. Laboratory tests for a thyroid autoimmune reaction detect the presence and measure the number of specific thyroid autoantibodies in the blood. Therefore, if laboratory values are out of normal range in a patient who uses the allopurinol, we can suspect that allopurinol causes autoimmune diseases. Although the analyses accounted for a wide range of potential confounding variables, there is potential for residual confounding and indication biases in observational studies. Also a retrospective study, it is important to standardize and confirm the laboratory items using a laboratory study because the study is related to the reliability of the inspection items and results.
- We additionally adjusted the analyses for lifestyle factors (alcohol consumption and smoking status) and concomitant diseases such as hypertension, congestive heart failure, ischemic heart disease, and renal impairment.
- Therefore, prospective longitudinal studies are needed to further confirm these results.
- Thyroid diseases include both hypo and hyperthyroidism with types of overt and subclinical 30.The relationship between overt thyroid dysfunction (hyperthyroidism and hypothyroidism) and UA has received considerable attention.
Therefore, a further study that reflects these considerations is required. The first stage involved screening titles and abstracts to identify and exclude irrelevant articles. All full-text versions of studies that were potentially relevant were then screened in relation to the inclusion criteria. Two researchers independently searched and screened the literature and collected and cross-checked the relevant data. If the results were inconsistent, those would be discussed together or judged by a third senior researcher.
Continuous follow-up is necessary, even if no specific clinical symptoms appear immediately. This study analyzed data from individuals who participated in health screening programs at Chang Gung Memorial Hospital in northern Taiwan (2000–2010). Participants were categorized as having euthyroid, hypothyroid, or hyperthyroid status according to their thyroid-stimulating hormone (TSH) levels. Multinomial logistic regression models were used to calculate the odds ratios (95% CI) for hyperuricaemia and gout in participants with thyroid dysfunction compared to euthyroid participants.
In a first sensitivity analysis, we excluded patients with a history of renal impairment, congestive heart failure, or hypertension prior to the index date. In a second sensitivity analysis, we stratified the study population by the presence or absence of these comorbidities. Although the association between hypo- and hyperthyroidism and kidney function has been described in the literature, the risk of clinically manifest gout in association with hypo- or hyperthyroidism has not been comprehensively examined. Additionally, the association between use of thyroid hormone replacement or suppression therapy and gout has not yet been studied. We therefore assessed the risk of developing incident gout in association with hypo- or hyperthyroidism and thyroid hormone replacement or suppression therapy, respectively. From 2000 to 2010, a total of 87,813 people were enrolled in our study.
As a result, uric acid levels in the blood increase, increasing the risk of gout development. In conclusion, this study provided a systemic analysis of the association between subclinical thyroid dysfunctions. Moreover, as most of the included studies are from China, our results may be more applicable to Chinese subjects. One of the limitations of our study is the lack of a brief description of the purine content of foods with known effects on thyroid function. Inclusion and exclusion criteria for included studies are given in Table S2 in Supplementary Materials.
Medical records are converted into standardised data in a common format and used as secondary data sources through the distributed research network. Gout is typically diagnosed using a combination of medical history, physical examination, and laboratory tests. The doctor will ask about the symptoms experienced by the patient, such as sudden and intense joint pain, swelling, and redness.
Residual confounding by indication by CKD and congestive heart failure which are causally linked to development of hyperuricemia, cannot be excluded in the present study despite every effort to minimize such a bias. We adjusted for use of drugs indicated for treatment of these comorbidities, and we stratified our analyses by the most important chronic comorbidities, namely arterial hypertension, congestive heart failure, and renal impairment. Few data are available on the association between thyroid dysfunction anduric acid metabolism and the evidence is conflicting. The correlation between TSH and serum uric acid levels was weak 16, 17. However, previous studies have reported high prevalence of hyperuricaemia in patients with both hypothyroidism 18 and hyperthyroidism 18, 19.