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Topical cyclosporin as a novel treatment for pyoderma gangrenosa
P7018
P7048
Topical cyclosporin as a novel treatment for pyoderma gangrenosa Gabriel Urtea-Botero, MD, Gonzales Medical Group, San Antonio, TX, United States; Adelaide Hebert, MD, The University of Texas Medical School-Houston, Houston, TX, United States; Erik Maus, MD, The University of Texas Medical School-Houston, Houston, TX, United States
Ulcer dermatosis Ha Do, MD, MS, Indiana University, Dermatology Department, Indianapolis, IN, United States; Yongxue Yao, MD, PhD, Indiana University, Dermatology Department, Indianapolis, IN, United States An ulcer is clinically characterized by a loss of the epidermis and at least the papillary dermis. The cutaneous defect will leave some scarring when healed because of the destruction of the adnexal structures. We present 5 interesting cases of ulcer dermatosis with clinical photographs, histopathology photographs, and clinical pearls to highlight the vast etiologies that are often associated with ulcer formation in the pediatric population (aplasia cutis congenita and HSV-1 anogenital ulcer); the adult population (florid coumadin-induced ulcer); and the cancer patient population (deep fungal infection in a patient with myelofibrosis and paraneoplastic ulcer from thymoma).
A 56-year-old Hispanic woman with history of type II diabetes, hypertension, and hyperlipidemia presented with a painful right lower extremity ulcer of 3 months’ duration. The ulcer developed after minor trauma. On initial examination, the ulcer measured 6 cm 3 12 cm 3 1 cm initially but a week later, the ulcer had almost doubled in size. Wound cultures including anaerobes, AFG and fungi were also ordered. The patient underwent a series of serologic tests including aNCA, pANCA, RF, cryoglobulins, hepatitis panel, ANA among other. All results were negative except for the culture that demonstrated skin flora. The skin biopsy showed vascular stasis and focal neutrophilic vascular reaction. The pathology was interpreted as being consistent with the suspected diagnosis of pyoderma gangrenosum. The patient was started on prednisone 2 mg/kg/d but because of difficulty controlling hyperglycemia, the drug was discontinued after 2 weeks of therapy during which no improvement in ulcer size was seen. We proceded to treat with intralesional triamcinolone and topical tacrolimus with minimal response. She was started on nonmodified cyclosporine 50 mg PO bid and the ulcer slowly began to improve, but an increase in blood pressure led also to the discontinuation of the drug after 4 weeks. Based on her positive initial response, topical cyclosporine (Restasis 0.05%) was tried. About 1 cc of the medication was applied to the ulcer twice daily followed by the application of a petrolatum impregnated gauze and a light bandage. The ulcer that had been present for about 6 months before the use of topical cyclosporine healed in 8 weeks after institution of this drug. The ulcer remained closed at 12 weeks. Improvement of pain was also noticed once therapy was initiated with the drops. PG has no single therapeutic modality that is felt to be effective in all patients. The use of topical cyclosporin in dermatology has been questioned as it is believed that the molecule’s size is too large to penetrate the skin. This problem is not present in PG because the skin barrier is already broken because of the ulceration which allows the drug to come in contact with the target ulcer.
Commercial support: None identified.
Adelaide Hebert, MD has been a researcher, consultant and lecturer for Novartis.
P7120 Two cases of nicorandil-induced ulceration mimicking skin malignancy Ashish Sharma, MBBS, Solihull Hospital, Birmingham, United Kingdom; Jon Goulding, MBBS, Solihull Hospital, Birmingham, United Kingdom; Manjit Kaur, MBBS, Solihull Hospital, Birmingham, United Kingdom; Stephen Orpin, MBBS, Solihull Hospital, Birmingham, United Kingdom Nicorandil is a potassium channel activator used in the management of symptomatic ischemic heart disease. It is known to cause painful ulcerations, classically affecting the oral or perianal mucosa. We report 2 cases of nicorandil-induced ulceration, which are unusual in their anatomical location on the face. Patient 1 was an 88-yearold man with a 3-week history of a painful ulcer on his left temple. He was receiving 20 mg twice daily nicorandil for the previous 2 years. Examination revealed a 15-mm discoid, punched-out ulcer over the left temple with a purulent base and an erythematous rim. An incisional biopsy from the ulcer edge showed inflammatory change with no evidence of malignancy. After an unsuccessful trial of topical antibiotic therapy, the entire lesion was removed by curettage. Histology demonstrated a mixed suppurative and granulomatous inflammation with no neoplasia. After stopping his nicorandil therapy, the ulcer completely resolved in 4 weeks. Patient 2 was a 57-year-old woman with an 8-month history of a painful enlarging lump in the nose. She was taking nicorandil 20 mg twice daily for the previous 3 years. Examination revealed a 2- 3 1-cm well-defined ulcer with a raised pearlescent edge, on the left side columella extending onto the nasal septum. A biopsy demonstrated inflammatory features only, with no malignant change. After discontinuing her nicorandil medication, the lesion became asymptomatic within 4 weeks and resolved after 12 weeks. Nicorandil-induced ulceration is reported in patients aged 58 to 89 years, with both sexes affected equally. Ulceration begins between 2 weeks and 4 years after initiation of therapy, in a dose-dependent manner. Ulcers are characteristically painful, localized, extend into deeper tissues, and have little granulation tissue at the base. Histologic examination reveals fibrin deposition and a mixed inflammatory cell infiltrate, with one report of diffuse elastophagocytosis. After discontinuing medication, there is often significant improvement in pain and size after 4 weeks, with complete resolution after 3 to 6 months. Theories of pathogenesis include direct metabolite toxicity in secretions, vascular steal phenomenon, the accumulation of endogenous nicotinic acid, and the interference of neutrophil migration in wound healing. Cutaneous ulceration without mucosal involvement is rare, but a trial without nicorandil may allow enough improvement at 4-week review to make the diagnosis. Commercial support: None identified.
APRIL 2013
J AM ACAD DERMATOL
AB229
P7048
Topical cyclosporin as a novel treatment for pyoderma gangrenosa Gabriel Urtea-Botero, MD, Gonzales Medical Group, San Antonio, TX, United States; Adelaide Hebert, MD, The University of Texas Medical School-Houston, Houston, TX, United States; Erik Maus, MD, The University of Texas Medical School-Houston, Houston, TX, United States
Ulcer dermatosis Ha Do, MD, MS, Indiana University, Dermatology Department, Indianapolis, IN, United States; Yongxue Yao, MD, PhD, Indiana University, Dermatology Department, Indianapolis, IN, United States An ulcer is clinically characterized by a loss of the epidermis and at least the papillary dermis. The cutaneous defect will leave some scarring when healed because of the destruction of the adnexal structures. We present 5 interesting cases of ulcer dermatosis with clinical photographs, histopathology photographs, and clinical pearls to highlight the vast etiologies that are often associated with ulcer formation in the pediatric population (aplasia cutis congenita and HSV-1 anogenital ulcer); the adult population (florid coumadin-induced ulcer); and the cancer patient population (deep fungal infection in a patient with myelofibrosis and paraneoplastic ulcer from thymoma).
A 56-year-old Hispanic woman with history of type II diabetes, hypertension, and hyperlipidemia presented with a painful right lower extremity ulcer of 3 months’ duration. The ulcer developed after minor trauma. On initial examination, the ulcer measured 6 cm 3 12 cm 3 1 cm initially but a week later, the ulcer had almost doubled in size. Wound cultures including anaerobes, AFG and fungi were also ordered. The patient underwent a series of serologic tests including aNCA, pANCA, RF, cryoglobulins, hepatitis panel, ANA among other. All results were negative except for the culture that demonstrated skin flora. The skin biopsy showed vascular stasis and focal neutrophilic vascular reaction. The pathology was interpreted as being consistent with the suspected diagnosis of pyoderma gangrenosum. The patient was started on prednisone 2 mg/kg/d but because of difficulty controlling hyperglycemia, the drug was discontinued after 2 weeks of therapy during which no improvement in ulcer size was seen. We proceded to treat with intralesional triamcinolone and topical tacrolimus with minimal response. She was started on nonmodified cyclosporine 50 mg PO bid and the ulcer slowly began to improve, but an increase in blood pressure led also to the discontinuation of the drug after 4 weeks. Based on her positive initial response, topical cyclosporine (Restasis 0.05%) was tried. About 1 cc of the medication was applied to the ulcer twice daily followed by the application of a petrolatum impregnated gauze and a light bandage. The ulcer that had been present for about 6 months before the use of topical cyclosporine healed in 8 weeks after institution of this drug. The ulcer remained closed at 12 weeks. Improvement of pain was also noticed once therapy was initiated with the drops. PG has no single therapeutic modality that is felt to be effective in all patients. The use of topical cyclosporin in dermatology has been questioned as it is believed that the molecule’s size is too large to penetrate the skin. This problem is not present in PG because the skin barrier is already broken because of the ulceration which allows the drug to come in contact with the target ulcer.
Commercial support: None identified.
Adelaide Hebert, MD has been a researcher, consultant and lecturer for Novartis.
P7120 Two cases of nicorandil-induced ulceration mimicking skin malignancy Ashish Sharma, MBBS, Solihull Hospital, Birmingham, United Kingdom; Jon Goulding, MBBS, Solihull Hospital, Birmingham, United Kingdom; Manjit Kaur, MBBS, Solihull Hospital, Birmingham, United Kingdom; Stephen Orpin, MBBS, Solihull Hospital, Birmingham, United Kingdom Nicorandil is a potassium channel activator used in the management of symptomatic ischemic heart disease. It is known to cause painful ulcerations, classically affecting the oral or perianal mucosa. We report 2 cases of nicorandil-induced ulceration, which are unusual in their anatomical location on the face. Patient 1 was an 88-yearold man with a 3-week history of a painful ulcer on his left temple. He was receiving 20 mg twice daily nicorandil for the previous 2 years. Examination revealed a 15-mm discoid, punched-out ulcer over the left temple with a purulent base and an erythematous rim. An incisional biopsy from the ulcer edge showed inflammatory change with no evidence of malignancy. After an unsuccessful trial of topical antibiotic therapy, the entire lesion was removed by curettage. Histology demonstrated a mixed suppurative and granulomatous inflammation with no neoplasia. After stopping his nicorandil therapy, the ulcer completely resolved in 4 weeks. Patient 2 was a 57-year-old woman with an 8-month history of a painful enlarging lump in the nose. She was taking nicorandil 20 mg twice daily for the previous 3 years. Examination revealed a 2- 3 1-cm well-defined ulcer with a raised pearlescent edge, on the left side columella extending onto the nasal septum. A biopsy demonstrated inflammatory features only, with no malignant change. After discontinuing her nicorandil medication, the lesion became asymptomatic within 4 weeks and resolved after 12 weeks. Nicorandil-induced ulceration is reported in patients aged 58 to 89 years, with both sexes affected equally. Ulceration begins between 2 weeks and 4 years after initiation of therapy, in a dose-dependent manner. Ulcers are characteristically painful, localized, extend into deeper tissues, and have little granulation tissue at the base. Histologic examination reveals fibrin deposition and a mixed inflammatory cell infiltrate, with one report of diffuse elastophagocytosis. After discontinuing medication, there is often significant improvement in pain and size after 4 weeks, with complete resolution after 3 to 6 months. Theories of pathogenesis include direct metabolite toxicity in secretions, vascular steal phenomenon, the accumulation of endogenous nicotinic acid, and the interference of neutrophil migration in wound healing. Cutaneous ulceration without mucosal involvement is rare, but a trial without nicorandil may allow enough improvement at 4-week review to make the diagnosis. Commercial support: None identified.
APRIL 2013
J AM ACAD DERMATOL
AB229