Low Dose Intravenous Ertapenem for Hidradenitis Suppurativa

Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory disorder characterized by painful nodules, abscesses, sinus tract formation, and scarring, resulting in impaired quality of life. Patients with moderate to severe disease frequently require multimodal therapy, including systemic antibiotics, biologic agents, and procedural interventions [1]. Among intravenous antibiotics, ertapenem has emerged as a rescue therapy for severe refractory HS. Prior studies demonstrated clinical improvement with daily intravenous ertapenem, most commonly administered at 1 g daily for approximately 6 weeks, with some recent series reporting longer treatment durations [2]. Ertapenem therapy is associated with adverse effects including gastrointestinal symptoms, hypersensitivity reactions, hematologic abnormalities, rare neurologic effects such as seizures, and elevations in liver enzymes. Additionally, relapse after discontinuation is common in the absence of maintenance systemic therapy, and optimal dosing strategies remain undefined. We present a case of severe, refractory HS treated with low‐dose intravenous ertapenem following liver enzyme abnormalities that resolved with dose reduction while maintaining treatment efficacy.

A 46‐year‐old male presented with chronic, severe Hurley stage III HS involving the bilateral axillae, inguinal folds, and buttocks, with inflammatory nodules with ulceration, copious drainage, and extensive scarring. He had previously failed multiple systemic therapies, including sarecycline, doxycycline, secukinumab, and adalimumab. Intravenous ertapenem was initiated as rescue therapy at 1 g daily in combination with adalimumab, with marked clinical improvement. The patient developed asymptomatic elevations in liver enzymes, with peak laboratory values including alkaline phosphatase 152 U/L (reference range 9–122 U/L), aspartate aminotransferase 107 U/L (reference range 10–35 U/L), and alanine aminotransferase 135 U/L (reference range 9–59 U/L). Ertapenem was dose‐reduced to 500 mg daily and subsequently to 250 mg every other day, resulting in normalization of liver enzymes with maintained clinical improvement. After 16 weeks, ertapenem was discontinued per Yale pharmacy antimicrobial stewardship policy. The patient experienced good control of disease activity until recurrence at 6 months when reduced‐dose ertapenem (250 mg every other day) was re‐initiated as bridge therapy to bimekizumab for 12 weeks, with sustained improvement and no liver enzyme elevations.

This case demonstrates clinical improvement with low dose ertapenem in a patient with severe, refractory HS. Aminotransferase elevations necessitated dose reduction; however, clinical control was preserved at a reduced dose and again upon re‐challenge, suggesting that HS therapeutic benefit and safety with ertapenem may be achieved at a lower, less frequent dose.

Although HS is primarily considered an inflammatory follicular disorder, microbial dysbiosis is frequently identified in established disease and may contribute to ongoing inflammation. Microbiome studies of HS have demonstrated enrichment of anaerobic taxa, including Porphyromonas, Peptoniphilus, and Prevotella, alongside depletion of commensal organisms such as Cutibacterium [3, 4]. However, the precise role in disease pathogenesis is not entirely clear. In ertapenem‐treated HS cohorts, anaerobic species were not consistently abundant; some taxa, such as Prevotella, decreased early in treatment but re‐emerged during ongoing therapy [2]. Taken together, bacteria present in HS sinus tracts and lesional skin may act as secondary drivers of inflammation but their specific contribution needs further study. Ertapenem provides robust anaerobic coverage, and we suspect its antimicrobial activity may be maintained even at lower concentrations explaining the observed findings. While the therapeutic effect is most plausibly attributable to reduction in bacterial burden, additional mechanisms cannot be excluded. Ertapenem has been shown to bind acute‐phase proteins, including haptoglobin, fibrinogen, and Complement C4—molecules associated with HS severity—raising the possibility of immunomodulatory effects [5, 6]. However, any non‐antimicrobial effects remain speculative and require further investigation.

Funding

The authors have nothing to report.

Consent

The authors obtained consent from patients for their medical information to be published in print and online and with the understanding that this information may be publicly available. Patient consent forms were not provided to the journal but are retained by the authors.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.