Clinical features and risk factors for gout attacks during anti‐tuberculosis treatment: A case‐control study in South Korea

Abstract

Aim This study aimed to investigate the clinical features and risk factors of gout attacks during anti‐tuberculosis (TB) treatment in South Korea. Method We investigated the clinical characteristics of 49 patients who suffered from gout attacks while taking anti‐TB medications. Among them, 25 TB patients having newly developed gout attacks without prior history of gout were set to the gout group. Seventy‐five age‐ and sex‐matched TB patients without gout attacks during anti‐TB therapy were randomly selected as the control group. The demographics, clinical features, and laboratory findings between the two groups were compared to establish risk factors of gout attack during anti‐TB treatment. Results The gout patients had a mean age of 67.7 ± 13.2 years and 39 patients (79.6%) were male. Approximately half of the patients experienced an attack within 2 months of treatment initiation. The attacks typically involved lower extremity joints (87.8%). The serum uric acid (SUA) levels were significantly elevated at 2 and 6 months after starting anti‐TB medication compared with those at baseline. In the case‐control study, the factors associated with gout attack were higher body mass index (BMI), higher pre‐treatment SUA levels, dyslipidemia, and reduced renal function. In the multivariate model, higher BMI, chronic kidney disease (CKD), and pre‐treatment hyperuricemia (SUA ≥ 6.8 mg/dL) were independent risk factors of gout attack while taking anti‐TB medication. Conclusions Patients with high BMI, CKD, and pre‐treatment hyperuricemia are at a higher risk of gout attack during TB treatment.

Analysis of influencing factors on the plasma concentration of first-line anti-tuberculosis drugs-a single-center retrospective cohort study

“…Our study found that intravenous administration significantly increased plasma concentrations compared with oral administration, which may be attributed to the effect of food and the firstpass effect of the liver (21). A large number of previous studies have shown that anti-TB drugs can affect uric acid metabolism in humans, which could result in elevated blood uric acid (22)(23)(24). The mechanisms of the interaction between blood uric acid and anti-TB drug metabolism need to be further investigated.…”

Lowering and Raising Serum Urate Levels: Off-Label Effects of Commonly Used Medications

“…In one group of high-risk patients, the mean AE SD sU level was increased to 8.4AE3.1 mg/dL (P<.001) at 2 months from pretreatment levels of 5.5AE1.9 mg/dL. 100 Mean AE SD time from treatment initiation to gouty attack was 4.13AE4 months, and half of the attacks occurred during the first 2 months of treatment. 100 Anti-inflammatories and Immunosuppressives Low-Dose Aspirin.…”

“…100 Mean AE SD time from treatment initiation to gouty attack was 4.13AE4 months, and half of the attacks occurred during the first 2 months of treatment. 100 Anti-inflammatories and Immunosuppressives Low-Dose Aspirin. As noted previously herein, low doses of aspirin and other salicylates may raise sU levels by promoting renal UA reabsorption.…”

“…Similar to pyrazinamide, ethambutol was reported to reversibly increase sU by a mean of 3.2 mg/ dL after 1 month of therapy 72 and can precipitate gout flares, 99 with sU level returning to baseline after withdrawal of ethambutol. Overall, antitubercular treatment particularly results in increased risk of gout attacks in patients at higher risk for hyperuricemia, including those with higher body mass index, CKD, and higher baseline hyperuricemia, 100 and the effect on sU level can be dramatic, particularly when pyrazinamide and ethambutol are used together. In one group of high-risk patients, the mean AE SD sU level was increased to 8.4AE3.1 mg/dL (P<.001) at 2 months from pretreatment levels of 5.5AE1.9 mg/dL.…”

Host‐directed anti‐mycobacterial activity of colchicine, an anti‐gout drug, via strengthened host innate resistance reinforced by the IL‐1β/PGE2 axis

“…Hence, due to a paradigm shift in the TB treatment field towards HDTs by repurposing immunomodulatory drugs to combat TB (Fatima et al, 2021), novel treatment approaches focusing on host‐originated anti‐Mtb activities with FDA‐approved safe drugs have gained increased interest (Ramakrishnan et al, 2015). Based on the development of gout attacks while taking anti‐TB drugs (Ha et al, 2019) and recent evidence of employment of colchicine to improve outcomes of infectious diseases and other inflammatory diseases (Hariyanto et al, 2021; Vaidya et al, 2021), as well as its inconclusive roles in immunological actions on TB, to the best of our knowledge, we show here for the first time the positive effect of colchicine on controlling Mtb infection in macrophages and in vivo. Surprisingly, the underlying mechanism of colchicine, unlike its commonly reported role in the suppression of NLRP3 and IL‐1β secretion, is associated with enhancing the anti‐Mtb activities of macrophages through the reinforcement of IL‐1β signalling and high‐level PGE 2 production.…”