Vol. 115, No.1
lyon the scalp and face, in 17 recently reported cases only one case involving the eyelid or ocular adnexa was described.i" Despite its locally aggressive growth, tricholemmal carcinoma does not appear to metastasize. Local tumor recurrence can occur. Management of tricholemmal carcinoma should include complete surgical excision with histologically documented tumor-free margins, followed by regular clinical examinations. Tricholemmal carcinoma should be considered in the differential diagnosis of eyelid tumors with the appearance of squamous cell carcinoma or keratoacanthoma.
Fig. 2 (Dailey, Helm, and Goldberg). Histologic appearance of tricholemmal carcinoma. Top, The tumor is composed of a mixture of pale and clear cells that resemble the outer root sheath of hair follicles (hematoxylin and eosin, x 500). Bottom, The tumor extends in a lobular arrangement from the epidermis into the upper dermis (hematoxylin and eosin, x 50).
Iy, several mitotic figures were noted. The
tumor appeared to be centered around hair follicles, and it partially spared the interfollicular epithelium. Pagetoid cells were seen within the epidermis. Tricholemmal carcinomas are histologically characterized by a follicular-oriented epidermal tumor composed of clear or pale cells that resemble the external root sheath of hair follicles. The tumor may focally involve the interfollicular epidermis, and pagetoid cells may be present. The histologic differential diagnosis includes Bowen's disease (squamous cell carcinoma in situ), clear cell basal cell carcinoma, or sebaceous carcinoma. In these three neoplasms, the histologic findings are not centered around hair follicles. In clear cell basal cell carcinoma, pagetoid cells and involvement of the upper layers of the epidermis should not be present. Sebaceous carcinoma can be excluded by the lack of sebaceous differentiation. Tricholemmal carcinoma typically occurs on the sun-exposed, hair-bearing skin of elderly individuals. Although occurring most common-
1. Wick, M. R., and Swanson, P. E.: Cutaneous Adnexal Tumors, A Guide to Pathologic Diagnosis. Chicago, American Society of Clinical Pathologists, 1991, p. 125. 2. Swanson, P. E., Marrogi, A. J., Williams, D. J., Cherwitz, D. L., and Wick, M. R.: Tricholemmal carcinoma. Clinicopathologic study of 10 cases. J. Cutan. Pathol. 19:103, 1992. 3. Boscaino, A., Terracciano, L. M., Donofrio, V., Ferrara, G., and DeRosa, G.: Tricholemmal carcinoma. A study of seven cases. J. Cutan. Pathol. 19:94, 1992. 4. Lee, J. Y., Tang, C. K., and Leung, Y. S.: Clear cell carcinoma of the skin. A tricholemmal carcinoma? J. Cutan. Pathol. 16:31, 1989.
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Meibomian Gland Function and Giant Papillary Conjunctivitis EDITOR: In the article "Meibomian gland function and giant papillary conjunctivitis," by W. D. Mathers and M. Billborough (Am. J. Ophthal-
AMERICAN JOURNAL OF OPHTHALMOLOGY
mol. 114:188, August 1992), the authors hypothesized " ... that meibomian gland dysfunction would cause increased ocular irritation and lead to an increased likelihood of giant papillary conjunctivitis." We believe, however, that the meibomian gland dysfunction could be viewed as a sequela rather than the cause of giant papillary conjunctivitis. There is considerable evidence that giant papillary conjunctivitis is caused by an im~uno logically mediated response, coupled with contact lens-induced mechanical disturbances. Chronic giant papillary conjunctivitis can lead to immunologically mediated thickening of the lower and upper tarsal conjunctivae. Conjunctival mast cells and a type-1 hypersensitivity reaction playa key role in giant papillary conjunctivitis. Henriquez, Kenyon, and Allansmith! found that 30% of conjunctival mast cells are in a state of degranulation in giant papillary conjunctivitis. Furtherm~re, by i~ munohistochemical and electronmicroscopic techniques, we demonstrated that the majority of mast cells in giant papillary conjunctivitis are of the connective tissue type on the basis of their neutral protease content.v' We also found increased levels of tryptase, a mast cell specific product and mar~er i~ tear sa~ples obtained from patients with giant papillary conjunctivitis. However, tryptase lev~l~ were not detected in patients with blepharitis an? other nonallergic ocular inflammatory conditions. We believe that in conjunction with infrared meibomian gland photography tryptase assays can be used to evaluate the .association between blepharitis and giant papillary conjunctivitis.
SALIM I. BUTRUS, M.D. ANDREW I. RABINOWITZ, M.D.
3. Butrus, S. I., Ochsner, K. I., Abelson, M. B., and Schwartz, L. B.: The level of tryptase in human tears. An indicator of activation of conjunctival mast cells. Ophthalmology 97:1678, 1990.
Drs. Butrus and Rabinowitz have suggested that meibomian gland dysfunction may be a sequela of giant papillary conjunctivitis rather than the reverse. Inasmuch as we do not know the cause of meibomian gland dysfunction, speculation regarding possible causes is appropriate. We believe that meibomian gland dysfunction may occur as a phenomenon of hyperkeratinization, which occludes the or~fice and ducts of the meibomian glands leading to inspissation and gland degeneration. Inflammation of the eyelid margin may be one factor that causes or accelerates this hyperkeratinization process, and giant papillary conjunctivitis with inflammation of the conjunctiva could therefore contribute to the induction of meibomian gland dysfunction. Meibomian gland dysfunction appears, however, to be a process present during most of one'.s ad~lt. l.if~. Conversely, giant papillary conjunctivitis IS ~ rel.atively short-term phenomenon, and the likelihood that an inflammatory process of the conjunctiva of such a short dur~tion w?~ld be a significant cause of this chronic condition of the eyelid margin seems unlikely. Other causes of inflammation of the eyelid margin such as toxins from bacterial flora are more likely candidates. Meibomian duct hyperkeratinization may even be an abnormal response to a normal level of inflammatory stimulus. None of this reasoning negates the relationship we proposed that meibomia~ gland ?ysfunction creates added inflammation, WhICh contributes to giant papillary conjunctivitis.
W. D. MATHERS, M.D.
Iowa City, Iowa
References 1. Henriquez, A. S., Kenyon, K. R., and AlIansmith, M. R.: Mast cell ultrastructure. Comparison in contact lens-associated giant papillary conjunctivitis and vernal conjunctivitis. Arch. Ophthalmol. 99: 1266, 1981. 2. Butrus, S. I., Laby, D. M., Zacharia, J. S., Abelson, M. B., Craig, S. S., and Schwartz, L. B.: Electronmicroscopic analysis of conjunctival mast cells in GPc. ARVO abstracts. Supplement to Invest. Ophthalmol. Vis. Sci. Philadelphia, J. B. Lippincott, 1992, p.851.
M. BILLBOROUGH, M.D.
West Reading, Pennsylvania
Meibomian Gland Function and Giant Papillary Conjunctivitis EDITOR:
In the article, "Meibomian gland function and giant papillary conjunctivitis," by W. D.