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<p>A 74-year-old man was referred to our hospital with persistent fever and fatigue. He had been receiving Golimumab for rheumatoid arthritis for 15&#xa0;months. At the time of GLM initiation, latent tuberculosis (TB) was suspected, and Isoniazid was prophylactically administered for 8&#xa0;months. Fifteen months after Golimumab initiation, he developed the symptoms. Reactivation of latent TB was suspected, however, chest and abdominal CT revealed no abnormal findings, and acid-fast bacillus smear and PCR tests from sputum, urine, blood, and gastric juice samples were negative for TB. Given that blood tests showed elevated hepatobiliary enzymes, miliary TB was suspected, and liver biopsy was performed, revealing caseous necrosis. Therefore, he was diagnosed with reactivation of latent TB caused by INH-resistant <i>Mycobacterium tuberculosis</i>. Following the treatment of rifampicin, ethambutol, levofloxacin, and streptomycin, the fever quickly resolved, and hepatobiliary enzyme levels were normalized. Culture of the liver biopsy tissue for acid-fast bacilli yielded INH-sensitive <i>Mycobacterium tuberculosis</i>. Although very rare, our case underscores that careful observation for reactivation of latent TB is important for patients receiving TNFα inhibitors even after appropriate prophylactic treatment for latent TB. Liver biopsy should be considered, when elevated liver enzymes are observed in suspected cases of miliary TB.</p>

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A case of miliary tuberculosis after prophylactic therapy for latent tuberculosis

  • 期刊论文

  • 发表日期：

    2026年6月1日

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  • Hirotaka Kashima,
  • Taro Ueo,
  • Akihisa Fukuda,
  • Hiroshi Seno

摘要

A 74-year-old man was referred to our hospital with persistent fever and fatigue. He had been receiving Golimumab for rheumatoid arthritis for 15 months. At the time of GLM initiation, latent tuberculosis (TB) was suspected, and Isoniazid was prophylactically administered for 8 months. Fifteen months after Golimumab initiation, he developed the symptoms. Reactivation of latent TB was suspected, however, chest and abdominal CT revealed no abnormal findings, and acid-fast bacillus smear and PCR tests from sputum, urine, blood, and gastric juice samples were negative for TB. Given that blood tests showed elevated hepatobiliary enzymes, miliary TB was suspected, and liver biopsy was performed, revealing caseous necrosis. Therefore, he was diagnosed with reactivation of latent TB caused by INH-resistant Mycobacterium tuberculosis. Following the treatment of rifampicin, ethambutol, levofloxacin, and streptomycin, the fever quickly resolved, and hepatobiliary enzyme levels were normalized. Culture of the liver biopsy tissue for acid-fast bacilli yielded INH-sensitive Mycobacterium tuberculosis. Although very rare, our case underscores that careful observation for reactivation of latent TB is important for patients receiving TNFα inhibitors even after appropriate prophylactic treatment for latent TB. Liver biopsy should be considered, when elevated liver enzymes are observed in suspected cases of miliary TB.