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Letter to the Editor

Pathologic Features of Uterine Leiomyomas Following Uterine Artery Embolization

Burbank, Fred M.D.

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International Journal of Gynecological Pathology: October 2001 - Volume 20 - Issue 4 - p 407-409
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To the Editor:

I read with interest the recent work by McCluggage and associates (1). The observation by Ravina and coworkers that bilateral occlusion of the uterine arteries with embolic particles can effectively treat symptomatic leiomyomas is a remarkable discovery considering that it came at the end of the 20th Century (2–14). The safety and efficacy of uterine occlusion studies have been reproduced worldwide (15–34).

Important details of the procedure, however, are poorly understood. Although it is generally understood that most larger leiomyomas (those identified by imaging studies) die and then shrink after uterine artery embolization, the effect of the procedure on smaller leiomyomas (those only identified at the time of pathology) is less well understood. The article by McCluggage and associates has the potential to shed light on this area, but in the Material and Methods section, the authors state, “This procedure has been well described (4–12) and will not be detailed here.” Unfortunately, uterine artery occlusion with embolic particles is not practiced as a single, well-defined procedure. Three major variables exist that could influence whether or not smaller leiomyomas are killed at the time of embolization: the particle size, the particle type, and the completeness of occlusion of the uterine arteries at the conclusion of particle injection.

Gelfoam (an embolic agent that is metabolized over time) and PVA (an embolic agent that is not metabolized over time) are the most common embolic particle types. Different sizes of these agents are in common use. The completeness of occlusion of the uterine arteries is not generally reported in published series but published angiograms indicates that some angiographers completely stop antegrade flow in the uterine arteries bilaterally although others stop injecting embolic agents while antegrade flow is still present. For simplicity, I will refer to these styles as “complete occlusion” and “incomplete occlusion”(35). If there is no antegrade flow to the uterus from either uterine artery after embolization (blood throughout the uterus is clotted), it is conceivable that all, or nearly all, leiomyomas could die at the time of embolization. On the other hand, if antegrade flow is still present in either or both uterine arteries at the end of embolization and there are zones of myometrium that receive normal or near normal antegrade flow from the uterine arteries, it seems unlikely that leiomyomas that receive their blood supply from these perfused zones would die. Spies et al. (16,21) have published angiograms that indicate that they incompletely occlude the uterine arteries. A woman had a hysterectomy after incomplete uterine artery embolization by another group (36). Their Figure 2 showed persistent antegrade flow to the uterus as distal as the ascending uterine branch. Six leiomyomas were found in the surgical specimen ranging in size from 0.4 to 10.0 cm. Angiographically invisible small leiomyomas were described microscopically as “viable myomata with no hemorrhage, necrosis, or increased mitotic activity identified.” In contrast, the leiomyoma with occluded blood supply had undergone hyaline degeneration. It appears that when occlusion is not complete and antegrade flow to the uterus persists, all leiomyomas are not killed. Other angiographers completely stop antegrade flow in the uterine arteries bilaterally by embolization (15,37). When complete embolization was performed, pathology findings at hysterectomy 7 months later showed more than 20 leiomyomas in the surgical specimen, and microscopic analysis showed complete hyaline degeneration in all large leiomyomas and in many small ones (38). When occlusion is complete, leiomyoma tissue to the level of microscopic leiomyomas can be killed. Given such observations, it has been postulated that the procedure may eventually be performed to treat asymptomatic evolving myomata (6).

Table 2 might be more useful to your readership if each case were tabulated to indicate what sizes and types of particles were injected and whether or not occlusion of the uterine arteries was complete or incomplete. It would also be useful to know how many leiomyomas were observed per uterus, their size distribution, and the degree of necrosis of each leiomyoma. In patients 6–9 in Table 2 “smaller leiomyomas without necrosis” were reported. In the same patients “Extensive necrosis of leiomyoma....” was observed. Was “extensive necrosis” also observed in “smaller leiomyomas”? If so, how often and in which cases? Unfortunately, the devil is almost always in the details.

Can the authors provide these important additional details to their readership?

Sincerely,

Fred Burbank, M.D.

REFERENCES

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© 2001 Lippincott Williams & Wilkins, Inc.