Decidual vasculopathic-like lesion in endometrial ablation.

To the Editor.--I read with interest the article by Fadare et al (1) concerning the histology of radio-frequency endometrial ablation, especially after reviewing a recent endometrial curettage specimen in our institution from a woman with a prior hydrothermal ablation for menorrhagia. An interesting histologic finding among the endometrial and myometrial necrosis was a profile of a vessel containing lesion that appeared similar to the fibrinoid necrosis and atherosis seen in maternal decidual vasculopathy in pregnancy (Figure). Perhaps the similarity in appearance is more than casual if we consider such a lesion final common pathway of more than one cause for vascular thrombosis. The pathophysiology of vascular damage in maternal decidual vasculopathy is unknown, but the 2 key findings in the involved vessels in this lesion are well described: (1) atherosis appears to be histiocytic phagocytosis of damaged endothelial cells of the spiral arteries, and (2) the dense pink fibrinoid necrosis may be some amalgam of the coagulation cascade proteins and intermediate filaments. These lesions are thought to cause the infarctions often seen in the placentas of women with preeclampsia. Oxidative stress leading to maternal endothelial damage early in embryogenesis may play a role in producing maternal decidual vasculopathy. (2) Underlying genetic maternal thrombophilic conditions existing in some women makes them predisposed to the development of vasculopathy. (3) Since we find similar lesions in both pregnancy and iatrogenically damaged endometrium, it can be suggested that oxidative damage and thermal ablation have similar effects on spiral arteries. It would be interesting to reexamine the endometrial specimens examined by Fadare et al1 to see whether a similar histology is seen in the vessels of radio-frequency -ablated endometrium.

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(1.) Fadare O, Qin L, Martel M, Tavassolli FA. Pathology of the NovaSure (radio-frequency) impedance-controlled endometrial ablation system. Arch Pathol Lab Med. 2005;129:1175-1178.

(2.) Dekker GA, Sibai BM. Etiology and pathogenesis of preeclampsia: current concepts. Am J Obstet Gynecol. 1998;179:1359-1375.

(3.) Kupferminc MJ, Eldor A, Steinman N, et al. Increased frequency of genetic thrombophilia in women with complications of pregnancy. N Engl J Med. 1999;340:9-13.

The authors have no relevant financial interest in the products or companies described in this article.

PHILIP J. KATZMAN, MD

Department of Pathology and

Laboratory Medicine

University of Rochester

Medical Center

Rochester, NY 14642

In Reply.--We thank Dr Katzman for the interest in our report. He reports a focal decidual vasculopathy-like change in an endometrial curettage specimen from a woman who had previously undergone an ablation procedure, and he inquired about the presence of such a lesion in the case we reported. Our case was reviewed in detail, and no such lesion was identified. Rather, as stated and illustrated in our report, the vascular changes were limited to ectatic and thrombotic vessels with varying levels of organization in the hyalinized band/myometrial interface. However, the author's hypothesis that "oxidative damage and thermal ablation have similar effects on spiral arteries" is an intriguing one, and the absence of the decidual vasculopathylike change in our patient may be related to the relatively long duration (38 days) between the endometrial ablation and hysterectomy. These issues are certainly worthy of further study.

The authors have no relevant financial interest in the products or companies described in this article.

OLUWOLE FADARE, MD

Department of Pathology

Wilford Hall Medical Center

Lackland Air Force Base 

San Antonio, TX 78236

FATTANEH A. TAVASSOLI, MD

Women's Health Program

Department of Pathology

Yale University School of

Medicine

New Haven, CT 06510