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Vasitis nodosa (a report of 7 cases).
Nodular thickenings of vasa deferentia in vasectomised males are most often due to stitch granulomas, sperm granulomas or simply due to fibrosis and chronic inflammation. However, in a few cases, there occurs a fusiform nodular thickening of the vas due to florid proliferation of the ductular epithelium, insinuating into the muscle coat and adventitia, and in the process resulting in extravasation of spermatozoa and consequent sperm granulomas.[11] In 1943. Benjamin et all recognised the true nature of this benign reactive proliferation, and termed it 'vasitis nodosa', to stress its close similarity to salpingitis isthmica nodosa. In the recent years, this entity has caught the pathologists' fancy mainly because the florid proliferation of the ductular element may be mistaken for a low grade adenocarcinoma or an adenomatoid tumour. Furthermore, 'benign neural invasion' by the proliferating ductules in vasitis nodosa is being recognised with increasing frequency.[6],[8],[12],[13] However, many pathologists are not familiar with this condition, and are likely to be alarmed by the profuse epithelial proliferation and the 'neural invasion'.
On screening all the lesions of vas deferens recorded in the surgical pathology files of our department for the last five years (1979-1983), we came across 5 cases of vasitis nodosa derived from five patients. During autopsies on male adults, scrotal sac was palpated routinely for nodular thickening of the vas, and 30 vas nodules were collected from 15 autopsies on adult male patients. Two of the nodules (derived from two patients) showed features of vasitis nodosa. These 7 cases form the basis of the present report. The paraffin blocks were cut and serial sections were stained routinely with haematoxylin and eosin. Elastic van-Gieson and Masson's trichrome stains were also used whenever necessary.
All the 5 cases collected from the surgical pathology files were young males, their ages ranging from 25 to 35 years. In all these cases, the vas nodules were excised during vasoplasty for recanalisation of the vas. Four of these patients had undergone vasectomy 3 to 10 years earlier before the present surgery, while in one case the exact duration since vasectomy was not known. Of the 15 cases where vas nodules were collected at autopsy, only two nodules (derived from 2 patients) showed features of vasitis nodosa, while all the other nodules showed mainly stitch granunomas and/or fibrosis. In these 15 cases, history regarding vasectomy was not known. Grossly, these 7 nodules were greyish white, soft to firm in consistency, and ranging from 0.5 to 1.5 cm in diameter. Histologically, all the seven cases showed varying degree of changes due to luminal obstruction and ductular proliferation with sperm granulomas. In two cases, the central lumen appeared dilated with irregular outpouching, and showed moderate ductal epithelial proliferation in continuity with the central lumen. In the other 5 cases, the central lumen appeared normal, lined by normal columnar epithelial cells. The one consistant feature in all the 7 cases was the ductular proliferation seen insinuating the muscle coat and adventitia [Fig. 1]. Many of the ductules were irregular and were stuffed with clumped up masses of spermatozoa with a few exfoliated epithelial cells. These ductules were lined by short columnar or cuboidal cells. Many of these columnar cells showed marked vacuolar change. Some of the ductules also showed marked atrophy of the lining epithelium [Fig. 2]. However, in none of these cases, was there any evidence of nuclear atypia or mitotic activity. Though the ductules were irregular in shape, most of these were separated from each other by at least a thin sling of smooth muscle. The ductules in the muscle coat and adventitia showed no obvious continuity with the central lumen of the vas. However, the presence of clumps of spermatozoa in the lumen of the proliferative ductules was evidence enough that there indeed was direct communication at some point proximal to obstruction. There was also varying degree of extravasation of spermatozoa in all these cases with many sperm granulomas in and around the muscle coat and adventitia. In one case, the proliferating ductules were very closely apposed to the nerve twigs in the adventitia with an occasional ductule in the perineural space. These ductules were lined by markedly atrophic or degenerated epithelium, and hence could not be differentiated from a capillary unequivocally. However, some of the nerve twigs in this case showed clumps of spermatozoa in the perneural space embracing the nerve element proving these channels as ductules (See [Fig. 1] on page 104B).
Vasitis nodosa is a benign, reactive proliferation of the ductular epithelium of the obstructed vas deferens, forming fusiform nodular thickening either following surgical or non-surgical trauma or infection. Understandably, most of the cases reported in the literature have been following vasectomy. Graham and O'Connor[7] in 1954 reported a case of "unusual vas deferens tumour in an infertility problem", which they considered to be a hyperplastic nodule. Obviously, these authors were not aware of the report by Benjamin el al[1] published in 1943, wherein the term 'vasitis nodosa' was first coined and its true nature identified. The recent interest in vasitis nodosa was triggered by Olson's[9] report of 3 cases in 1971; and since then many reports of this entity have been published,[4],[7],[10],[11],[13] stressing the fact that it can be mistaken by an unwary for a low grade adenocarcinoma or an adenomatoid tumour. This fear of a possible mistaken diagnosis of malignancy appears to be more real since Kovi and Agbata[8] in 1974 described benign neural invasion in a case of vasitis nodosa. Since then, many more reports have appeared demonstrating benign neural invasion by the proliferating ducts.[6],[10],[11],[13] Goldman et al6could demonstrate neural invasion in 3 of their 9 cases; while Zimmerman et al[13] reported nerve involvement in 3 of their 15 cases. Neural invasion in vasitis nodosa appears to be a fairly common feature. Till recently, neural invasion in a lesion with epithelial proliferation was taken as an evidence of malignancy. However, Taylor and Norris,[12] in 1967, reported 20 cases of peripheral nerve invasion in 1000 consecutive cases of florid fibrocystic disease of the breast. Several cases of 'neural invasion' have since been described in normal and hyperplastic prostate,[3] and in the pancreas with no evidence of tumour.[5] Neural invasion no more remains a firm ground for the diagnosis of malignancy in an equivocal situation. The exact mechanism of 'neural invasion' in a benign, reactive epithelial process is not known. It is probable that at least in vasitis nodosa, this occurs due to entrapment of epithelial elements by the regenerating nerve twigs following surgical or non-surgical trauma. This is difficult to prove since there are abundant nerve elements in the adventitia of the vas deferens and short of a well formed traumatic neuroma, regenerated excess nerve elements cannot be identified as such. Till to-date, however, traumatic neuroma has not been reported in association with 'benign neural invasion' either in vasitis nodosa or any other situation mentioned above. Essentially, vasitis nodosa represents the nature's attempt at re-establishing the communication in an obstructed lumen, and restore the reproductive capacity of the individual. Bunge[2] reported a case of bilateral spontaneous re-anastomosis of ductus deferens in a patient who had undergone bilateral vasectomy 6 years earlier. He could demonstrate sperm granulomas, which were responsible for the re-anastomosis, in one vas histologically examined.
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