Aesthetic surgery journal · 2025
Peripheral Nerve Injury After Deoxycholic Acid (ATX-101) Injection in an Experimental Rat Model.
СтатьяНазвание и аннотация: Перевод в очереди
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Chi David, Pinni Sai, Maloy Shea, Llaneras Noah, Hunter Daniel A, Wood Matthew D, Tenenbaum Marissa M, Mackinnon Susan E
Аннотация
BACKGROUND: Deoxycholic acid (ATX-101) is a drug administered by subcutaneous injection for local fat reduction. However, ATX-101 treatment has been reported to cause marginal mandibular nerve injury with noticeable functional deficits when targeting submental fat. As a cytolytic agent with some selectivity for adipocytes, ATX-101 may damage the lipid-rich myelin surrounding peripheral nerves.
OBJECTIVES: The aim of this study was to characterize nerve injury caused by ATX-101 injection in an experimental rat sciatic nerve model.
METHODS: Injuries to the sciatic nerve caused by intrafascicular and extrafascicular injections of ATX-101, and by lidocaine (positive control) and saline (negative control) injections, were compared. Nerves were harvested at a 2-week endpoint for histomorphometric analysis.
RESULTS: The cross-sectional area of nerve injury was significantly increased by ATX-101 injection. The damaged areas amounted to 75% ± 15% with intrafascicular ATX-101 (P < .001), 41% ± 21% with extrafascicular ATX-101 (P < .01), and 38% ± 20% with positive-control lidocaine (P < .01), compared with 7% ± 13% with negative-control saline. Demyelinating injury was a significant mechanism of injury in the affected nerve fibers compared with uninjured nerve fibers (P < .04), but there was no difference in the axon-to-myelin area ratio between the lidocaine and ATX-101 cohorts. After 2 weeks, Wallerian degeneration was evident with only small regenerating nerve fibers present in the ATX-101-injured groups compared with saline (average fiber width, 2.54 ± 0.26 μm vs 5.03 ± 0.44 μm, P < .001).
CONCLUSIONS: ATX-101 can cause extensive nerve injury in rats. The mechanism of action for ATX-101 does not preferentially target myelin more than other common neurotoxic agents. Appropriate knowledge of surgical anatomy and injection technique is necessary for any practitioners administering ATX-101 injections.
OBJECTIVES: The aim of this study was to characterize nerve injury caused by ATX-101 injection in an experimental rat sciatic nerve model.
METHODS: Injuries to the sciatic nerve caused by intrafascicular and extrafascicular injections of ATX-101, and by lidocaine (positive control) and saline (negative control) injections, were compared. Nerves were harvested at a 2-week endpoint for histomorphometric analysis.
RESULTS: The cross-sectional area of nerve injury was significantly increased by ATX-101 injection. The damaged areas amounted to 75% ± 15% with intrafascicular ATX-101 (P < .001), 41% ± 21% with extrafascicular ATX-101 (P < .01), and 38% ± 20% with positive-control lidocaine (P < .01), compared with 7% ± 13% with negative-control saline. Demyelinating injury was a significant mechanism of injury in the affected nerve fibers compared with uninjured nerve fibers (P < .04), but there was no difference in the axon-to-myelin area ratio between the lidocaine and ATX-101 cohorts. After 2 weeks, Wallerian degeneration was evident with only small regenerating nerve fibers present in the ATX-101-injured groups compared with saline (average fiber width, 2.54 ± 0.26 μm vs 5.03 ± 0.44 μm, P < .001).
CONCLUSIONS: ATX-101 can cause extensive nerve injury in rats. The mechanism of action for ATX-101 does not preferentially target myelin more than other common neurotoxic agents. Appropriate knowledge of surgical anatomy and injection technique is necessary for any practitioners administering ATX-101 injections.