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<p>We report the case of a 64-year-old woman who developed malignant and treatment-resistant arterial hypertension (HT) following the introduction of rifampicin for spondylodiscitis. Her previously stable blood pressure (BP) deteriorated rapidly despite extensive antihypertensive therapy. The utilisation of pharmaceutical agents that demonstrated minimal or no interaction with rifampicin has yielded only partial control over HT. Furthermore, biological settings provided evidence of pseudohyperaldosteronism. A comprehensive workup ruled out other secondary causes of HT. BP normalized progressively after rifampicin withdrawal, without additional therapeutic intervention. This temporal combination supports a causative role of rifampicin, potentially through mechanisms beyond drug interactions. We discuss hypotheses including corticosterone-driven pseudohyperaldosteronism resulting from cytochrome P450 induction, and pregnane X receptor agonism as contributors to HT. This case highlights the importance of recognizing rifampicin as a potential inducer of severe HT, even in patients receiving adjusted antihypertensive regimens, and suggests a pathophysiological mechanism that may extend beyond pharmacokinetic interferences.</p>

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Malignant hypertension and pseudohyperaldosteronism associated with rifampicin therapy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月16日

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  • Alexandre Szedleski,
  • Cédric Ilbert,
  • Véronique Goncette,
  • Laurent Vroonen,
  • Justine Huart

摘要

We report the case of a 64-year-old woman who developed malignant and treatment-resistant arterial hypertension (HT) following the introduction of rifampicin for spondylodiscitis. Her previously stable blood pressure (BP) deteriorated rapidly despite extensive antihypertensive therapy. The utilisation of pharmaceutical agents that demonstrated minimal or no interaction with rifampicin has yielded only partial control over HT. Furthermore, biological settings provided evidence of pseudohyperaldosteronism. A comprehensive workup ruled out other secondary causes of HT. BP normalized progressively after rifampicin withdrawal, without additional therapeutic intervention. This temporal combination supports a causative role of rifampicin, potentially through mechanisms beyond drug interactions. We discuss hypotheses including corticosterone-driven pseudohyperaldosteronism resulting from cytochrome P450 induction, and pregnane X receptor agonism as contributors to HT. This case highlights the importance of recognizing rifampicin as a potential inducer of severe HT, even in patients receiving adjusted antihypertensive regimens, and suggests a pathophysiological mechanism that may extend beyond pharmacokinetic interferences.