Introduction Acute gouty arthritis (AGA) is characterized by the accumulation of pro‐inflammatory factors. This research aimed to examine the regulation of long non‐coding RNA HOXA distal transcript antisense RNA (HOTTIP) in AGA on inflammation and its potential mechanisms. Methods Serum levels of HOTTIP in AGA patients were examined by reverse‐transcription quantitative polymerase chain reaction. The receiver operating characteristic curve was performed in the diagnosis of AGA patients. Monosodium urate (MSU) stimulation of THP‐1‐derived macrophages was used to establish an in vitro AGA model. Enzyme‐linked immunosorbent assay was carried out to assess the levels of pro‐inflammatory cytokines. Pearson correlation was applied to examine the correlation. RNA immunoprecipitation assay and dual‐luciferase reporter assay were employed to identify the targeting relationship between miR‐101‐3p and HOTTIP or bromodomain‐containing 4 (BRD4). Results HOTTIP and BRD4 were statistically overexpressed in AGA patients compared with controls, while miR‐101‐3p was reduced (P < 0.05). Serum HOTTIP can significantly distinguish AGA patients from healthy controls. HOTTIP bound with miR‐101‐3p then augmented BRD4 via a competing endogenous RNA mechanism. Additionally, HOTTIP levels were elevated in a dose‐dependent manner by MSU (P < 0.05). Weakened HOTTIP significantly inhibited MSU‐induced release of pro‐inflammatory factors interleukin (IL)‐1β, IL‐8, and transforming growth factor‐α in macrophages (P < 0.05), but this inhibition was reversed by silencing miR‐101‐3p (P < 0.05). Conclusion In short, HOTTIP contributes to inflammation via miR‐101‐3p/BRD4 axis, and serves as a new diagnostic biomarker. This study offers a renewed perspective on the diagnosis and treatment of AGA.

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