The prevalence of hypothyroidism in gout
Patients to be started on allopurinol who had a measurement of TSH in the 6-month period prior to baseline evaluation were used for comparison. TSH levels and change in TSH levels at 12-month follow-up were compared between groups. Patients with abnormal TSH levels or previous thyroid disease or on amiodarone were not included for analysis. Eighty-eight patients treated with febuxostat and 87 with allopurinol were available for comparisons. Patients to be treated with febuxostat had higher urate levels and TSH levels, more severe gout, and poorer renal function, but were similar regarding other characteristics.
Hyperuricemia and gout in thyroid endocrine disorders
Even synthroid medicinenet if patients with recently diagnosed thyroid disease might have seen more often their physician, gouty arthritis is a very painful clinical condition and is most likely not diagnosed routinely or by chance. It is more likely that patients see their general practitioner because of acute joint pain than that they just wait for a follow-up consultation. It may be possible that patients who just started their treatment of hypothyroidism may be at greater risk of gout because a potential protective effect of thyroid hormone replacement therapy did not yet become active.
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Therefore, using data from a large cohort consisting of healthy individuals who underwent health screenings, this study aimed to estimate the risk of hyperuricaemia and gout in people with thyroid dysfunction (both hypothyroid and hyperthyroid status). First, the study only included people of European descent and cannot prove whether there are genetic differences between different ethnic groups, countries and regions. Second, MR fails to further explore the biological mechanisms of autoimmune hypothyroidism, autoimmune hyperthyroidism, thyroid nodules, and thyroid cancer and gout. Managing gout in hypothyroid patients requires a comprehensive approach that addresses both conditions simultaneously. In the case of hypothyroidism, hormone replacement therapy is the primary treatment.
- Finally, it’s important to stay well-hydrated by drinking adequate water each day to help flush out uric acid from the body.
- Since free T4 levels were all within the normal reference range even after the case group index date (that is, when the TSH level increased), the possibility of subclinical hypothyroidism (SCH) could be suspected38,39.
- Finally, all included populations were European, which reduced confounding bias.
Most laboratories report a normal TSH reference range of 0.4–0.5 mIU/L on the lower end and 4–5.5 mIU/L on the upper end of the range42,43. Primary hypothyroidism is manifested by elevated serum TSH with low serum FT4 levels. In SCH, although FT4 levels were within the normal reference range, there were elevations in TSH44.
Because nutritional changes are also a key component of treatment for gout, you may want to schedule a consult with one of Paloma’s registered nutritionists. As experts in healthy eating, our experienced nutritionists can help you make nutritional choices to support your overall health. Understanding the connection between these two conditions can lead to better management and treatment options for individuals experiencing symptoms related to both.
- Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.
- However, previous studies have reported high prevalence of hyperuricaemia in patients with both hypothyroidism 18 and hyperthyroidism 18, 19.
- The data for the description of the contributing study were obtained from the IEU OpenGWAS project.
They will also inquire about any risk factors or medical conditions that may increase the likelihood of developing gout. Gout and hypothyroidism may seem like unrelated health conditions, but they actually have a close relationship. Gout is a form of arthritis caused by the buildup of uric acid crystals in the joints.
- Due to the heterogeneity of the studies included, in order to further increase the reliability of the study, a subgroup analysis of age, area, and comorbidities in patients was performed.
- Medications included those that could affect TSH levels26,27,28,29,30,31,32,33,34 and medication used by gout patients, such as non-steroidal anti-inflammatories, acetaminophen, oxycodone, colchicine, and corticosteroids35,36 (Supplementary Table S3).
- These data included demographic information, medical diagnoses, prescriptions, referrals, laboratory test results, and clinical values.
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In this retrospective, observational study targeting a large cohort of Korean population groups in multiple centres, we performed an analysis of the association between allopurinol and increased TSH levels using the OMOP CDM. Gout is the most common form of inflammatory arthritis, caused by chronic elevation in serum uric acid levels above the saturation point of monosodium urate1. This leads to the deposition of monosodium urate crystals in the joints, tendons, and other tissues, triggering recurrent episodes of pronounced acute inflammation known as gout flares2. On the other hand, hypothyroidism is a condition characterized by an underactive thyroid gland. The thyroid hormones are crucial in regulating various bodily functions, including metabolism.
Dried Blood Spot Testing for Hypothyroidism
The crude prevalences of hyperuricaemia and gout were calculated for the euthyroid, hypothyroid, and hyperthyroid groups. Using the euthyroid group as reference, the differences in baseline characteristics were tested using the Student’s t test for continuous data and chi-square test for categorical data. Multinomial logistic regression was used to determine the factors affecting the risk of hyperuricaemia and gout. Multivariate relative risks (RRs) were adjusted for age, thyroid function status, the presence of low eGFR, and the number of metabolic syndrome components. All analyses were performed using IBM SPSS statistics software, version 19.0.
Confounding variables were selected by reviewing previous studies and expert consultations based on data available on the CDM network. We considered diseases and medications that could affect TSH levels as confounding variables and analysed the records for 6 months before selecting the case and control groups. This was a nested case–control study using distributed OMOP CDM databases loaded with data records from 19,200,973 patients based on electronic medical records (EMR) from seven hospitals. These data included demographic information, medical diagnoses, prescriptions, referrals, laboratory test results, and clinical values.
Details of medication prescriptions, including allopurinol were obtained (Supplementary Table S2). We selected the look-back period of allopurinol use for 6 months before the case–control index date and determined whether allopurinol was prescribed. Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.
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