Acneiform eruptions caused by an epidermal growth factor receptor-tyrosine kinase inhibitor ZD 1839 1

Acneiform eruptions caused by an epidermal growth factor receptor-tyrosine kinase inhibitor ZD 1839 1

P153 P155 CAROTENEMIA ASSOCIATED WITH INCREASED CONSUMPTION OF GREEN BEANS Tanya A. Sale, MD, University of Wisconsin-Madison, Madison, WI, United S...

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CAROTENEMIA ASSOCIATED WITH INCREASED CONSUMPTION OF GREEN BEANS Tanya A. Sale, MD, University of Wisconsin-Madison, Madison, WI, United States, Erik Stratman, MD, Marshfield Clinic, Marshfield, WI, United States Carotenemia is a condition characterized by yellow discoloration of the skin and elevated blood carotene levels. Excessive and prolonged ingestion of carotene-rich, yellow or orange colored foods such as carrots and winter squash is the most common cause, but it may also more rarely be associated with consumption of other foods as well as with hypothyroidism, diabetes mellitus, anorexia nervosa, liver disease, or kidney disease. Awareness of carotenemia can help the provider avoid confusion with jaundice and avoid unnecessary worry and costly workup. We describe carotenemia in an 8-month-old Caucasian female secondary to increased consumption of commercial infant food green beans.

ACNEIFORM ERUPTIONS CAUSED BY AN EPIDERMAL GROWTH FACTOR RECEPTOR-TYROSINE KINASE INHIBITOR ZD 1839 Gavin A Wong, MBChB, Division of Dermatology, Toronto, ON, Canada, Simon Nigen, MD, Division of Dermatology, Toronto, ON, Canada, Scott Walsh, MD, Division of Dermatology, Toronto, ON, Canada, Neil Shear, MD, Division of Dermatology, Toronto, ON, Canada ZD1839 is a selective inhibitor of the epidermal growth factor receptor-tyrosine kinase enzyme (EGFR-TK). EGFR-TK has been identified in many tumor types and can stimulate tumor proliferation mechanisms when activated. Studies of ZD1839, in a number of tumor types, have shown promising results.1 Adverse cutaneous reactions have been reported.1,2 We present 2 patients with acneiform eruptions due to ZD 1839. Case 1: A 66-year-old man developed a rash 8 days after commencing ZD1839 for prostate cancer. He was on no other medication. Clinical examination revealed numerous erythematous papules and pustules, distributed on his face, upper chest and upper back. Skin biopsy showed an inflammatory folliculitis with a large collection of neutrophils in a hair follicle opening, focal rupture of the follicular epithelium and a mixed perifollicular inflammatory infiltrate. He was treated with 0.1% betamethasone cream to the trunk and 1% hydrocortisone cream to the face. This controlled the rash and he continued Iressa treatment. Case 2: A 73-year-old man developed a rash 14 days after commencing ZD1839 500mg for prostate cancer. His other medication included metformin and glyburide. Examination revealed an acneiform eruption over his chest, back, beard area and scalp. Biopsy showed a perivascular lymphocytic infiltrate in the dermis with a few dilated vessels. No hair follicle was present in this biopsy specimen. He was treated with clindamycin 2% in hydrocortisone 2.5% lotion twice daily with good response. The patient decided to discontinue Iressa treatment. The mechanism by which EGFR-TK inhibition causes a follicular eruption is unknown. Effects on keratinocyte differentiation and on hair cycle control are suggested.2 Cutaneous reactions in patients on Iressa tend to be mild and do not necessitate treatment discontinuation.1 In summary, 2 patients with acneiform eruptions due to ZD1839 are presented. Clinical studies of this drug are ongoing and therefore dermatologists should be aware of the skin reactions associated with its use. References 1. LoRusso PM. Phase I studies of ZD1839 in patients with common solid tumors. Semin Oncol 2003;30(1 Suppl 1):21-9. 2. Van Doorn R, Kirtschig G, Scheffer E, et al. Follicular and epidermal alterations in patients treated with ZD183, an inhibitor of the epidermal growth factor receptor. Br J Dermatol 2002;147:598-601.

Disclosure not available at press time.

Disclosure not available at press time.

P156 P154 TAZAROTENE 0.05% CREAM FOR THE TREATMENT OF KERATOSIS PILARIS Melissa A. Bogle, MD, The University of Texas at Houston, Houston, TX, United States, Asra Ali, MD, The University of Texas at Houston, Houston, TX, United States, Holly Bartel, BS Background: Keratosis pilaris is an autosomal-dominant condition presenting with follicular hyperkeratosis, particularly on the posterior upper arms, anterior thighs, cheeks, buttocks, and trunk. Keratosis pilaris is known to have a high number of cellular retinoic acid binding proteins. Objective: A randomized, placebo-controlled, double blind prospective study to determine the effectiveness of tazarotene 0.05% cream for the treatment of keratosis pilaris on the posterior arms. Methods: Thirty-three patients of any gender or skin type, age 12-70, with greater than 20 hyperkeratotic red papules on the posterior upper arms were instructed to apply a vehicle cream daily to one arm and tazarotene 0.05% cream daily to the other arm as determined by randomization. Subjects were assessed at three monthly visits for itching, roughness, and redness by the clinician and by themselves in a survey format. The number of hyperkeratotic red papules were also evaluated by the investigators at each visit. Results: Tazarotene 0.05% cream improves the pruritus, erythema, and roughness of keratosis pilaris on the posterior arms significantly better than placebo. Conclusion: Tazarotene 0.05% cream is an effective and well tolerated agent for the treatment of keratosis pilaris on the posterior arms. Disclosure not available at press time. Allergan supplied medication, placebo, and parking fees for each patient.

MARCH 2004

PUZZLING POST-SURGICAL PAPULES AND PLAQUES Shannon Heck, MD, Eastern Virginia Medical School, Norfolk, VA, United States, Frederick Quarles, MD, Eastern Virginia Medical School, Norfolk, VA, United States, Antoinette Hood, MD, Eastern Virginia Medical School, Norfolk, VA, United States A 65-year-old man with a history of diabetes mellitus and coronary artery disease was referred for evaluation of symptomatic skin lesions confined to surgical scars on his left arm and right thigh, where veins had been harvested for cardiac bypass surgery several years earlier. The lesions developed shortly after his cardiac surgery and persisted for 3 years despite aggressive topical and systemic therapies. He had no prior history of skin disease. On examination, within surgical scars on his upper and lower extremities, there were erythematous to tan, indurated plaques with coalescent papules forming an annular border. His sternal surgical scar was uninvolved; the remainder of his cutaneous examination was within normal limits. Biopsy specimens from the annular border showed broad horizontal zones of altered collagen in the mid and deep reticular dermis surrounded by a peripheral palisading mononuclear cell infiltrate with occasional multinucleated cells, and a patchy perivascular lymphoplasmocytic infiltrate. These changes were interpreted as being entirely consistent with necrobiosis lipoidica. Necrobiosis lipoidica is a well-documented clinical entity of unknown pathogenesis that occurs most commonly in diabetic individuals. The disorder has a curious predilection for areas of trauma such as the anterior lower legs. In reviewing the literature, we found only two other reports of necrobiosis lipoidica presenting in surgical scars, and only one patient like ours, in which this was the sole manifestation of the disease. We present this case for its uniqueness, and for interest. The authors have no conflicts of interest to disclose.

J AM ACAD DERMATOL

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