INTRODUCTION
Pressure injuries are exceedingly common lesions which cause a great deal of morbidity, especially in the elderly.1 Treatment is mostly supportive, with avoidance of pressure on the injury being the mainstay of therapy. Other measures, such as topical ointments and oral antibiotics to treat bacterial colonization are sometimes used.2 Nevertheless, no adequate therapies exist, and pressure injuries remain a great unmet need. We previously developed a topical proteasome inhibitor, ACU-D1 (Pentaerythritol tetrakis (3-(3,5-di-tert-butyl-4-hydroxyphenyl)propionate)), which was tested in a phase 2A clinical trial in rosacea (NCT03064438).3 In this case report, we demonstrate the efficacy of ACU-D1 in an elderly patient who did not respond to other supportive therapies. This proof of principle case report suggests the need for larger studies to evaluate the efficacy of ACU-D1 in pressure injuries.
CASE REPORT
The patient is an 80-year-old male with a history of type 2 diabetes (treated with Dulaglutide, Levemir U-100 insulin, and metformin), and hypertension (treated with amlodipine and metoprolol succinate). His past dermatologic history is notable for tinea pedis and squamous cell carcinoma. He presented with a stage II pressure injury (partial thickness loss of dermis) on his right gluteal region (Figure 1A). The wound was cleaned initially with hydrogen peroxide. Supportive therapy was then initiated with mupirocin ointment, moist dressing with pressure-offloading bandages, as well as further instructions to avoid pressure on the site. After one month, there was no improvement with pain or healing. The patient elected to try
topical 10% ACU-D1 cream on the pressure injury, applied once daily, which led to rapid reduction of pain and re-epithelialization of the injury (Figure 1B).
DISCUSSION
Pressure injuries are common causes of morbidity in the elderly. The exact etiology is unknown, but is hypothesized to result from compromised small vessels that vascularize the buttocks. In addition, an inflammatory component has been noted, and lesions are commonly colonized by polymicrobial flora, which leads to fibrin lysis and inhibition of re-epithelialization.4,5 Conservative measures (especially decreased pressure on the wound area), debridement, and both topical and oral antibiotic therapy, are the cornerstones of current pressure injury
