Does androgen insufficiency cause lacrimal gland inflammation and aqueous tear deficiency?

PURPOSE. The current investigators have shown that androgen treatment suppr esses inflammation and stimulates the function of lacrimal glands in mouse models of Sjogren's syndrome. Recently, others have hypothesized that andro gen insufficiency induces an autoimmune process in lacrimal tissue, leading to inflammation, a Sjogren's syndrome-like pathology, and aqueous tear def iciency. The purpose of the present study was to test this hypothesis. METHODS. Lacrimal glands were obtained from adult testicular feminized (Tfm ) and control mice; castrated rats, guinea pigs, and rabbits; and castrated rats without anterior or whole pituitary glands and were processed for his tology and image analysis. Tear volumes were measured in mice, in patients taking antiandrogen medications, and in age-matched human control subjects. RESULTS. Tfm mice, which are completely resistant to classical androgen act ion, did not have increased lymphocyte infiltration in their lacrimal gland s or decreased tear volumes. No inflammation was evident in lacrimal tissue s of male or female rats, guinea pigs, or rabbits 12 to 31 days after castr ation, no inflammation existed in rat lacrimal glands 15 to 31 days after o rchiectomy and pituitary removal, and no aqueous tear deficiency was appare nt in patients receiving antiandrogen therapy. CONCLUSIONS. Androgen deficiency may promote the progression of Sjogren's s yndrome and its associated lacrimal gland inflammation, meibomian gland dys function, and severe dry eye. However, androgen insufficiency alone does no t cause lacrimal gland inflammation, a Sjogren's syndrome-like pathology in lacrimal tissue, or aqueous tear deficiency in nonautoimmune animals and h umans.