Our continually developing society has resulted in increased incidence of atopic dermatitis, characterized by itchiness; eczematous lesions; and dry, thickening skin with an increased number of markings.¹ Atopic dermatitis is also associated with lens opacity; approximately 20% of patients with atopic dermatitis have a cataract.² Recently, atopic cataracts started developing more frequently in younger people who are still professionally active and need good visual acuity. Thus, the scale of the problem is growing, and atopic cataracts are becoming a public health problem.^3-5

Approximately 25% to 40% of adults with atopic dermatitis also have ophthalmic problems,⁶ such as deplumation, staphylococcal marginal blepharitis, chronic keratitis, or atopic cataract. The problem has become more significant, and disease onset is now observed in younger patients. The peak disease occurrence is between the ages of 30 and 50 years; however, in some instances, atopic dermatitis may affect children and adolescents. Chen described the case of a 16-year-old boy who had to undergo surgery to remove a cataract resulting from the aggravation of atopic dermatitis.⁷ In this case, the lens was removed and an IOL was implanted with good restoration of visual acuity in both eyes.

Ophthalmic surgery should be planned and performed preferably in symptom-free intervals between bouts of allergy. The allergist in charge should be consulted regarding preoperative assessment and management because he knows the patient's symptoms, including the severity. If such cooperation is impossible, the patient's antiallergy medication should be administered. In cases where surgery is performed during a bout of allergy symptoms, both local and systemic steroids must be used.

ALLERGIC PROCESS
Cataracta allergica, or cataracta dermatogens, is a type of presenile cataract associated with atopic dermatitis; it is usually bilateral and can be characterized by rapid progression.⁶ Concomitant occurrence of cataract and dermatitis atopica was described at the beginning of the 20th century;² however, the association was unaccounted for. In fact, the etiology of allergic cataract has not been fully elucidated until recently.^2,6 We now know that the allergic process itself causes the cataract, with allergy as the probable initiating factor. Other contributing factors include steroid therapy and immune response to lens proteins, such as albuminoid and crystalline.^6,8

The allergic process associated with atopic lesions stimulates enhanced production of the stress response protein (srp60) within the mitochondrial membrane of the lens epithelium. As a result, the number of mitochondria increases in the opacified lens epithelium. T-cells (ie, lymphocytes that play a central role in cell-mediated immunity) recognize srp60 as an antigen, and therefore, they attack the cells producing it, causing chronic inflammation of autoimmune origin. Because the crystalline lens is an avascular tissue, the T-cells do not directly recognize srp60. Its expression is probably an effect of the activity of humoral substances, such as cytokines, that occur in the aqueous humor of patients with atopic cataract. Thus, srp60 acts as an autoantigen, resulting in the development of the atopic cataract.⁵

In this way, the T-cells initially attack the lens capsule; an anterior subcapsular cataract subsequently develops, at an early stage (Figures 1 and 2), with characteristic discoid opacity and folding of the anterior capsule. However, as the disease progresses, other forms of cataract can be observed, including posterior subcapsular, mixed, and mature.

In the early stages, the ubiquitin-proteasome complex,⁹ which destroys abnormal proteins accumulated during the atopic inflammation in the epithelial cells of the lens,^10,11 assumes great importance. The advent of modern immunohistochemical techniques allowed identification of protein gene product (PGP) 9.5 within the epithelial cells. PGP 9.5 is a neurospecific marker whose enzymatic activity causes protein deubiquitination. When produced, it acts as a protective mechanism against cytotoxic agents present in abnormal stress-generated proteins.¹⁰

Allergy therapies can also cause cataract formation, including the now widely used steroid therapy. Steroids disturb the blood-aqueous barrier and cause protein accumulation in the lens, leading to secondary changes in lens transparency. Cataract incidence was increased in patients on systemic steroid therapy compared with those receiving steroids via inhalation or nasally.¹²

In the course of steroid therapy, opacity first develops in the posterior part of the lens (Figure 3). It is believed that the inflammatory process continues to the anterior aqueous humor, which causes posterior capsular opacification, and then quickly progresses to form a posterior subcapsular cataract. Patients with this disease pattern are more likely to develop retinal detachment following cataract surgery.¹³ As a result of chronic inflammation of the ciliary body, the epithelium in the proximity of the ora serrata is fragile and easily breakable; retinal lesions may resemble those accompanying traumatic events.

Surgical removal of the mature cataract caused by chronic allergic inflammation is associated with increased frequency of retinal complications. Approximately 5% of patients operated on for atopic cataract develop retinal complications as a result of surgical trauma.^13,14

TREATMENT OPTIONS
Patients with allergic cataract can undergo standard phacoemulsification; however, the pupil may be too small or may not properly dilate. Anterior capsular and mature allergic cataracts may require use of the capsulorrhexis technique because the capsule may be hard or fibrotic.

The postoperative course may be similar to that of a nonallergic patient; however, a greater incidence of inflammation or endophthalmitis has been observed. This may be because of an inflammatory response to the implant or the material of the ophthalmic viscosurgical device (OVD). Thus, attention should be paid to meticulously remove the OVD. Allergy to drugs, dressing materials, or even the procedure itself may also develop. Patients with a history of contact allergy may develop a sterile inflammatory response to the implant.

These patients more often demonstrate posterior capsular opacity and vitreous body opacities, even proliferative, which may contract and pull on the retina. This may even result in retinal detachment.

Phaco with IOL implantation, local and systemic prophylaxis with antiallergy medication, and local and systemic steroids are the best options to treat patients with atopic cataract. I work in a specialist center and perform many difficult medical cases. We perform approximately 120 to 150 surgical procedures per week, including six to 10 patients with allergic cataract (ie, 5% of patients yearly). Detailed statistical data on allergic cataract have not been documented.

Developments in our society have undoubtedly resulted in increased incidence of atopic dermatitis concomitant with atopic keratoconjunctivitis (AKC). AKC is considered the most serious and threatening form of allergic eye disease because its complications may lead to blindness.3 Asthma, inflammation of nasal mucosa, migraine, and urticaria are among other symptoms of atopy often present in AKC patients.⁷ Following is my treatment protocol for patients with atopic cataracts.

Prior to surgery, providone-iodine should be used, according to standards set forth by the European Society of Cataract and Refractive Surgeons (ESCRS). Upon completion of the procedure, a prophylactic subconjunctival injection of cefuroxime plus steroid should be given. Additionally, the local administration of levofloxacin or ofloxacine for approximately 7 days and an obligatorily topical steroid should be used for a minimum of 4 weeks.

After surgery, pupil dilation depends on the condition of the eye. Steroids should generally be administered; however, the length of use should depend on the condition of the eye after surgery. It would be best if the degree of the anterior chamber flare were monitored in every patient and treatment modified accordingly.

Ewa Mrukwa-Kominek, MD, PhD, is an Assistant Professor in the Department of Ophthalmology, Medical University of Silesia, Katowice, Poland. Professor Mrukwa-Kominek is a member of the CRST Europe Editorial Board. She states that she has no financial interest in the products or companies mentioned. She may be reached at tel: +48 601528850; e-mail: emrowka@poczta.onet.pl or mrukwa@okulistyka.katowice.pl.

1. Krafchik BR. Atopic Dermatitis. Emedicine Web site. Available at: http://emedicine.medscape.com/article/1049085-overview. Accessed January 21, 2009.
2. Strzalka A, Przepiorkowski R. Cataract in an atopic dermatitis patient: case report and review of literature. Klin Oczna. 2006;108:10-12.
3. Beare N. Cataract surgery in latex allergy patients. Eye. 2004;18:791-792. [Author reply, 2004;18:845-846.]
4. Burtus S, Portela R. Ocular allergy: diagnosis and treatment. Ophthalmol Clin N Am. 2005;18:485-492.
5. Ishicura R, Kato S, Nagata M, Tamai A, Ohama E. Expression of stress-response protein 60 in lens epithelial cells in atopic cataract. Jpn J Ophthalmol. 1999;43:89-96.
6. McGill JI, Holgate ST, Church MK, Anderson DF, Bacon A. Allergic eye disease mechanisms. Br J Ophthalmol. 1998;82:1203-1214.
7. Chen CC, Huang JL, Yang KD, Chen HJ. Atopic cataracts in a child with atopic dermatitis: a case report and review of the literature. Asian Pac J Allergy Immunol. 2000;18:69-71.
8. Fagerholm P, Palmquist BM, Philipson B. Atopic cataract: changes in the epithelium and subcapsular cortex. Graefe's Arch Clin Exp Ophthalmol. 1984;221:149-152.
9. Nakajima J, Mekada A, Nakamura J, Nishida Y, Tokunaga Y. Expression of protein gene product 9.5 in the interior lens epithelial cells of atopic cataracts. J Cataract Refract Surg. 2002;28:2035-2039.
10. Yoki N, Hirano S, Okamoto S, Matsumoto Y, Yoki K, Ikeda T, Kinoshita S, Katoh N, Yasuno H. Assosiation of eosinophil granule major basic protein with atopic cataract. Am J Ophthalmol. 1996;122:825-834.
11. Yokoi K, Yokoi N, Kinoshita S. Impairement of ocular surface epithelium barrier function in patients with atopic dermatitis. Br J Ophthalmol. 1998;82:797-800.
12. Derby L, Maier WC. Risk of cataract among users of intranasal corticosteroids. J Allergy Clin Immunol. 2000;105(5):912-916.
13. Takahashi M, Suzuma K, Inaba I, Ogura Y, Yoneda K, Okamoto H. Retinal detachement associated with atopic dermatitis. Br J Ophthalmol. 1996;80:54-63.
14. Sevel D, Weinberg EG, Niekerk CH. Lenticular complications of long-term steroid therapy in children with asthma and eczema. J Allergy Clin Immunol. 1977;60:215-217.