similar improvement in ocular symptoms compared with an oral antihistamine (loratadine) in patients with SAR (Table 1). 5 Overall, the reduction in ocular symptom scores was less than 46% but similar to the effects on ocular symptoms by other intranasal steroids. To date, prospective comparative data on the ocular safety of triamcinolone acetonide aqueous nasal spray are not available. Al- though insufficient evidence exists to support an association be- tween INS and the development of cataracts and/or glaucoma at licensed doses, periodic monitoring is warranted in patients with a high predisposition to either condition. These data may further the argument for a class effect of INS in the treatment of the ocular symptoms associated with AR because triamcinolone acetonide and other INS in these studies demonstrate a potential positive impact on ocular allergy symptoms. 6,7 It would appear that to maximize the impact of INS use of the drugs should be started before the patient’s allergy season. Given the established efficacy of INS in reducing nasal symptoms, such a treatment approach in patients with AR may reduce the need for multiple medications, potentially resulting in increased adherence and im- proved patient outcomes. LEONARD BIELORY, MD, MS* GEORGE GEORGES, MD† GARY GROSS, MD‡ *Asthma & Allergy Research Center UMDNJ-New Jersey Medical School Newark, New Jersey †sanofi-aventis US Inc. Bridgewater, New Jersey ‡Dallas Allergy & Asthma Center Dallas, Texas bielory@umdnj.edu ACKNOWLEDGMENTS The authors thank Medicus International for their editorial assis- tance. 1. Settipane G, Korenblat PE, Winder J, et al. Triamcinolone acetonide aqueous nasal spray in patients with seasonal ragweed allergic rhinitis: a placebo-controlled, double-blind study. Clin Ther. 1995;17:252–263. 2. Lumry W, Hampel F, LaForce C, Kiechel F, el-Akkad T, Murray JJ. A comparison of once-daily triamcinolone acetonide aqueous and twice-daily beclomethasone dipropionate aqueous nasal sprays in the treatment of seasonal allergic rhinitis. Allergy Asthma Proc. 2003;24:203–210. 3. Gross G, Jacobs RL, Woodworth TH, Georges GC, Lim JC. Comparative efficacy, safety, and effect on quality of life of triamcinolone acetonide and fluticasone propionate aqueous nasal sprays in patients with fall seasonal allergic rhinitis. Ann Allergy Asthma Immunol. 2002;89:56 – 62. 4. Berger WE, Kaiser H, Gawchik SM, et al. Triamcinolone acetonide aqueous nasal spray and fluticasone propionate are equally effective for relief of nasal symptoms in patients with seasonal allergic rhinitis. Otolaryngol Head Neck Surg. 2003;129: 16 –23. 5. Schoenwetter W, Lim J. Comparison of intranasal triamcinolone acetonide with oral loratadine for the treatment of patients with seasonal allergic rhinitis. Clin Ther. 1995;17:479 – 492. 6. Weber RW. Ocular impact of intranasal corticosteroid therapy: all that surprising? Ann Allergy Asthma Immunol. 2008;100:193. 7. Bielory L. Intranasal corticosteroids reduce ocular symptoms of allergic rhinitis as a class effect. J Allergy Clin Immunol. 2008;121:538 –539. CHRONIC URTICARIA CAUSED BY FOLIC ACID A 72-year-old woman presented with an 8-month history of daily urticaria and occasional facial angioedema. She received antihista- mines but was free of hives only for a few hours each day. Four years ago, she was diagnosed as having autoimmune hemolytic anemia/thrombocytopenia (Evans syndrome) and was treated with prednisone. Because of the adverse effects of the treatment, her therapy was changed to azathioprine, 50 mg/d, 3 years ago, and folic acid, 400 g/d, 2 years ago. She had no history of intake of non- steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, or other medications and no previous drug reactions. No wheals, dermographism, organomegaly, or lymphadenopathy were present on physical examination. Laboratory data showed a hemoglobin level of 13.7 g/dL (reference range, 12–16 g/dL); he- matocrit, 39.9% (reference range, 37%– 47%); platelets, 203  10 3 /L (reference range, 150 – 450  10 3 /L); and leukocytes, 3.5  10 3 /L (reference range, 6 –19  10 3 /L). Polyclonal hyper- gammaglobulinemia was detected. The levels of analytes were as follows: serum globulin, 4.80 g/dL (reference range, 1.5–3.0 g/dL); -globulins, 28.2% (reference range, 10%–19%); IgG, 3,729 mg/dL (reference range, 1,000 –2,100 mg/dL); IgA, 525 mg/dL (reference range, 100 –500 mg/dL); and IgM, 273 mg/dL (reference range, 44 –290 mg/dL). The results of antibody tests directed against hep- atitis B and C, nuclear, thyroglobulin, thyroid peroxidase, DNA, mitochondrial, and lupus anticoagulant antigens were negative. We suspected that folic acid was the possible cause of the urticaria, and its use was discontinued. Azathioprine therapy was maintained. A few days later, the urticaria disappeared. One month after discontinuation of folic acid use, prick and intradermal tests were performed with folic acid, 1 and 5 mg/mL, while the patient was using azathioprine and after the patient stopped using azathioprine for a week. The results were negative. Histamine phosphate, 10 mg/mL, used as a positive control pro- duced a 5-mm papule with a 7-mm flare in the prick test and a 12-mm papule with a 15-mm flare in the intradermal test. The results of single-blind oral challenge tests with increasing doses of folic acid, 1 mg/mL, administered at 30-minute intervals (0.25, 0.50, and 1 mL) were positive. Ten minutes after the 1-mL dose, the patient developed red pruriginous wheals. Generalized urticaria, facial and lingual edema, and bilateral conjunctival congestion were observed 2 hours later. The patient’s arterial blood pressure and pulse re- mained stable. The results of the oral challenges were negative, with placebo and folic acid excipients. Folic acid specific IgE testing was performed using the enzyme-linked immunosorbent assay method, 1 with some modifications. The result was negative. Histamine release tests were not performed. Three weeks after the folic acid challenge, a single-blind paren- teral challenge test with folinic acid, 50 mg/5 mL, was performed. One hour after the 5-mL intramuscular dose, the patient developed a red pruriginous macule (10  8 cm) over her torso. There were no reactions at the site of injection (left arm). We believed that if we increased the folinic acid dose, the patient would have had an unnecessary generalized reaction. The patient was advised to dis- continue folic acid treatment. Six months later, she remained free of urticaria. Hypersensitivity reactions to folic acid are extremely unusual; to our knowledge, only 7 cases have been reported in the literature. 2–8 In this study, the relationship between chronic urticaria and folic acid has been strongly suggested through the discontinued use of the drug and the resulting permanent control of the urticarial symptoms. This was additionally confirmed through the positive oral challenge test result. The negative skin test and enzyme-linked immunosorbent assay results suggest a non–IgE-mediated condition evolving in our patient. Folinic acid also produced a positive reaction after the parenteral challenge test. Clinical and immunological cross-reactiv- ity was previously described by Dykewicz et al. 4 Contrary to the Disclosures: Authors have nothing to disclose. VOLUME 103, JULY, 2009 81