Abstract

ObjectiveThe aim of this study is to examine the clinical features of patients with Behçet’s disease (BD) in the presence or absence of latent tuberculosis infection (LTBI).MethodsThis was a retrospective study of 232 consecutive patients with active BD hospitalized between October 2012 and June 2017. LTBI was diagnosed based on the positive T-SPOT.TB assay, negative clinical, and imaging examinations.ResultsAmong the 232 patients, 68 (29.3%) had LTBI. The frequency, number, and scope of oral ulcers in the BD-LTBI group were significantly more serious than in the non-LTBI group (all P < 0.05). Genital ulcers and eye involvement in the LTBI group were significantly higher than in the non-LTBI group (both P < 0.01). No active TB was diagnosed during follow-up (median, 27.9 months; range, 3–58 months). The patients with LTBI had signs of liver damage compared with the non-LTBI group. In the LTBI group, the frequency of alanine transaminase >2.0, the upper limit of normal, was higher in the rifampicin subgroup compared with the non-rifampicin subgroup (P = 0.033).ConclusionPatients with BD and LTBI had worse clinical features than those with BD without LTBI. Rifampicin might be associated with the damage to liver in BD patients combined with latent TB.

Highlights

  • Behçet’s disease (BD) is a multisystem inflammatory disorder characterized by recurrent oral and genital ulcers, uveitis, and epididymitis, and with mucocutaneous, articular, gastrointestinal, neurologic, and vascular manifestations [1]

  • Environmental influences and genetic factors may play a role in the etiopathogenetic mechanisms that lead to the development of the disease, indicating the autoimmune and autoinflammatory nature of BD

  • All patients were diagnosed according to the international criteria for BD (ICBD) [22]; the 1990 version was used because it was the current version at the beginning of the study period

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Summary

Introduction

Behçet’s disease (BD) is a multisystem inflammatory disorder characterized by recurrent oral and genital ulcers, uveitis, and epididymitis, and with mucocutaneous, articular, gastrointestinal, neurologic, and vascular manifestations [1]. The etiopathological mechanisms of disease development in BD remain elusive, while genome-wide association studies showed human leukocyte antigen and non-human leukocyte antigen associations. Environmental influences and genetic factors may play a role in the etiopathogenetic mechanisms that lead to the development of the disease, indicating the autoimmune and autoinflammatory nature of BD. Its incidence is about 14 patients per 100,000 inhabitants in China [3]. Microbial infections such as oral anaerobes [4], herpesviruses, [5] and Mycobacterium tuberculosis (MTB) [6,7] are considered to be environmental triggers of BD. M. tuberculosis may trigger BD because of molecular mimicking, and vice versa, and the dysfunctional immune system in BD may increase the susceptibility to M. tuberculosis [6,7]

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