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<p>This article reports a case of significant procalcitonin (PCT) elevation induced by tigecycline use. This finding provides clinicians with new insights into the potential adverse effects of tigecycline and highlights the importance of monitoring PCT levels during tigecycline therapy. The patient was a 76-year-old woman with a medical history of gastric cancer surgery and hypertension. She was admitted due to the fracture of internal fixation following corrective surgery for scoliosis. During hospitalization, she underwent removal of the scoliosis fixation rod and replacement with a titanium rod. Postoperatively, the patient experienced poor wound healing, and bacterial culture of the wound secretions revealed <i>Escherichia coli</i> (CRE). During tigecycline treatment for the infection, the patient’s PCT levels rose from 0.628&#xa0;ng/mL to a peak of 5.944&#xa0;ng/mL, despite absent fever or worsening infection. C-reactive protein (CRP), another inflammatory marker, remained stable (9.89–10.71&#xa0;mg/L) during this period. After discontinuation of tigecycline, the PCT levels gradually decreased to 0.574&#xa0;ng/mL; however, they increased to 2.017&#xa0;ng/mL again upon re-administration of tigecycline. While the exact mechanism is unclear, we hypothesize&#xa0;that&#xa0;tigecycline may affect hepatic enzyme systems involved in PCT metabolism or upregulate PCT synthesis pathways, given the drug’s hepatic metabolism and PCT’s liver-derived production. This case highlights that tigecycline may cause PCT elevation, a rare adverse reaction. This finding reminds clinicians to consider drug-related factors when interpreting PCT results to avoid misjudging infection status. Additionally, this case underscores the critical role of clinical pharmacists in monitoring and managing adverse drug reactions.</p>

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Case report: tigecycline-induced procalcitonin elevation

  • 期刊论文

  • 发表日期：

    2025年8月6日

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  • Benben Zhu,
  • Ting Yang,
  • Dongsheng Wang

摘要

This article reports a case of significant procalcitonin (PCT) elevation induced by tigecycline use. This finding provides clinicians with new insights into the potential adverse effects of tigecycline and highlights the importance of monitoring PCT levels during tigecycline therapy. The patient was a 76-year-old woman with a medical history of gastric cancer surgery and hypertension. She was admitted due to the fracture of internal fixation following corrective surgery for scoliosis. During hospitalization, she underwent removal of the scoliosis fixation rod and replacement with a titanium rod. Postoperatively, the patient experienced poor wound healing, and bacterial culture of the wound secretions revealed Escherichia coli (CRE). During tigecycline treatment for the infection, the patient’s PCT levels rose from 0.628 ng/mL to a peak of 5.944 ng/mL, despite absent fever or worsening infection. C-reactive protein (CRP), another inflammatory marker, remained stable (9.89–10.71 mg/L) during this period. After discontinuation of tigecycline, the PCT levels gradually decreased to 0.574 ng/mL; however, they increased to 2.017 ng/mL again upon re-administration of tigecycline. While the exact mechanism is unclear, we hypothesize that tigecycline may affect hepatic enzyme systems involved in PCT metabolism or upregulate PCT synthesis pathways, given the drug’s hepatic metabolism and PCT’s liver-derived production. This case highlights that tigecycline may cause PCT elevation, a rare adverse reaction. This finding reminds clinicians to consider drug-related factors when interpreting PCT results to avoid misjudging infection status. Additionally, this case underscores the critical role of clinical pharmacists in monitoring and managing adverse drug reactions.