Postoperative endometrial cancer with electronic brachytherapy (Axxent)
ForPostop endometrial cancer, FIGO IA to IVA, adjuvant VBT ± pelvic EBRT
TL;DRAxxent eBT vs replanned Ir-192 HDR: bladder D2cc 63.8% vs 70.1%, rectum 61.2% vs 68.4% of prescription; one G2 acute toxicity in 94 pts.
The prescription copied Ir-192 doses onto a 26 keV source with no RBE adjustment, so the OAR %PD reductions are physical-dose figures and the higher V150/V200 sits at the mucosa. Low acute mucositis at 25 Gy/5 fx and 15 Gy/3 fx is reassuring, but vaginal stenosis and late effects are untested here.
In postop endometrial pts needing vaginal cuff brachytherapy at a centre with no HDR afterloader, this supports eBT as feasible on acute toxicity; it does not inform late vaginal toxicity or cuff control vs Ir-192 HDR.
Ir-192 prescriptions were applied to a 26 keV source without RBE correction (cited RBE 1.29 to 1.85 at 5 mm), so the bladder and rectal %PD reductions are physical dose and the mucosa carries higher V150/V200. Acute toxicity at 25 Gy/5 fx and 15 Gy/3 fx was low; late vaginal effects remain untested.
11 details
Single-centre series of 94 pts treated with Axxent eBT, Sept 2015 to Oct 2017. Each eBT plan was replanned a posteriori for Ir-192 and Co-60 (282 plans); toxicity scored by RTOG. Mean follow-up 14 mo (4 to 25).
Postoperative endometrial cancer, mean age 65.9 (33 to 84), FIGO IA through IVA. 33 pts (35%) received chemo before RT.
eBT alone 25 Gy/5 fx (n=37, stage IA plus seven IB1) or pelvic EBRT 23 × 2 Gy then eBT 15 Gy/3 fx (n=57), twice weekly. Dose prescribed at 5 mm from a 2.5 to 3.5 cm cylinder; 50 kVp source, TG-43 planning, no RBE correction.
Only one G2 acute event. At 1 month, vaginal G1 5.3%, rectal G1 1.1%, urinary G1 2.1%, no G2.
PORTEC-2 established vaginal brachytherapy as adjuvant RT for high-intermediate risk disease using conventional HDR; this series does not test eBT against that clinical benchmark. A cited multicentre eBT series reported bladder V50% 11.5 ± 9.7% and rectum 17.4 ± 10.9%, in the same range as here.
Higher V150/V200 places hotter dose at the vaginal mucosa, where late stenosis would show and 14 mo cannot capture it. TG-43 without heterogeneity correction may misstate low-energy dose in tissue.
The OAR advantage comes from rapid dose fall-off at low energy, the same property that concentrates dose near the applicator surface. Whether uncorrected RBE translates into more late mucosal toxicity, or whether RBE-based de-escalation would cost control, remains open.
| OAR parameter | Axxent eBT | Ir-192 HDR |
|---|---|---|
| Bladder D2cc (%PD) | 63.8% | 70.1% |
| Bladder V50% | 7.2% | 12.7% |
| Bladder V35% | 15.2% | 28.2% |
| Rectum D2cc (%PD) | 61.2% | 68.4% |
| Rectum V50% | 7.9% | 14.3% |
| Rectum V35% | 16.7% | 32% |
Single-centre uncontrolled series, 14 mo mean f/u; HDR comparison is replanning, not a treated arm; no late toxicity or local control data at meaningful follow-up.
- Late vaginal mucosal toxicity with uncorrected RBE
- Vaginal cuff control vs Ir-192 HDR at longer follow-up
- Should eBT prescriptions be RBE-adjusted?
📚 Sources · 📄 1 paper
Abstract
The longer read
The question this series answers is narrower than its conclusion suggests. It shows that a 50 kVp electronic source, run with the same prescription and cylinder geometry as a conventional afterloader, delivers less physical dose to bladder and rectum and produces very little acute toxicity in 94 women. That is useful to know, but it is a planning result plus an uncontrolled toxicity audit, and the comparator never treated anyone. The Ir-192 and Co-60 plans were computed retrospectively on the same CT datasets, so the comparison isolates source physics and nothing else. That makes the dosimetric difference clean and the clinical difference unmeasured.
The central issue a radiation oncologist should weigh is radiobiology. The authors prescribed eBT without correcting for relative biological effectiveness, despite a mean beam energy of 26 keV against 355 keV for Ir-192, and they cite RBE estimates of 1.29 to 1.85 relative to Ir-192 at 5 mm. Read one way, that means the bladder and rectal reductions they report in percent of prescription are understated as biological sparing for those organs at depth, and work by Rava et al. cited in the paper points in that direction for BED3. Read the other way, the vaginal mucosa sits closest to the source, where V150 and V200 were already higher with eBT, and the same RBE logic implies a biologically hotter surface dose. Acute mucositis was low, but mucosal late effects such as stenosis and telangiectasia are the toxicities that would express that excess, and they cannot appear within a mean 14 months.
The absence of recurrence carries limited weight. Only 31 pts had reached 12 months, and vaginal cuff recurrence after adjuvant brachytherapy is uncommon enough that a series this size and duration could not distinguish eBT from HDR even if a real deficit existed. The authors themselves note that dose de-escalation for RBE could compromise control, citing a skin series where reduced dosing lowered tumour control, which frames the trade-off honestly: the prescription choice here leans toward control at a possible mucosal cost.
Against the context of PORTEC-2, which established vaginal brachytherapy as adjuvant therapy for high-intermediate risk disease with conventional sources, eBT is being offered as a substitute delivery device rather than a new treatment. The case for it is logistical: no shielded vault, no isotope exchange, portability. For a department without an afterloader, the acute safety data make eBT a defensible choice. For a department with one, this paper gives no clinical reason to switch, and the calculation method (TG-43, no heterogeneity correction) adds uncertainty to the low-energy dose estimates themselves. What would change the read is multi-year follow-up with formal late vaginal toxicity scoring and cuff recurrence rates, ideally against a contemporaneous HDR cohort.