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Cytarabine induced palmar–plantar erythrodysesthesia mimicking cellulitis
Cytarabine induced palmareplantar erythrodysesthesia mimicking cellulitis
(Poster reference number 5388)
Zachary Zinn, MD, West Virginia University, Morgantown, WV, United States; Rodney Kovach, MD, West Virginia University, Morgantown, WV, United States Palmareplantar erythrodysethesia, also known as handefoot syndrome and chemotherapy-induced acral erythema, is a relatively common reaction to cytotoxic drugs, especially cytarabine. The classic clinical description is well demarcated tender erythematous plaques of the palms and soles beginning days to weeks after administration of the offending drug. Here we present a case of palmareplantar erythrodysethesia induced by cytarabine that initially mimicked cellulitis. Biopsy was consistent with cytotoxic changes secondary to chemotherapy. The cytotoxic reaction eventually resolved upon withdrawal of cytarabine. Commercial support: None identified.
Drug reaction with eosinophilia and systemic symptoms (DRESS): A retrospective analysis of 21 cases in a tertiary teaching hospital in Hong Kong
(Poster reference number 5215)
Johnny Chun-yin Chan, MBBS, The University of Hong Kong, Hong Kong, Hong Kong; Chi Keung Yeung, MBBS, The University of Hong Kong, Hong Kong, Hong Kong Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) is an acute, distinct and severe idiosyncratic reaction with a mortality of 8% to 10%. Owing to the rarity of the syndrome, large-scale studies are limited. Important data including the pattern of etiological agents, clinical and biochemical features and prognosis are lacking. Objective: To investigate the demographic data, clinical and biochemical characteristics, causative agents, treatment, and outcome of cases of DRESS in Hong Kong. Methods: A single center retrospective study on 21 cases of DRESS from February 2007 to February 2011. Medical records, clinical photographs, and sequential laboratory data were reviewed. An attempt was made to identify any correlation among the clinical pattern and specific causative agents. Main outcome measures: Clinical and biochemical pattern for specific drugs, treatment outcome and prognosis of DRESS. Results: Age of onset ranged from 14 to 77. No sex predilection was observed. The most common offending drug was allopurinol (28.6%), followed by phenobarbitone and trimethoprim-sulfamethoxazole. Mean latency period was 21.6 days. Exanthematous eruption was the most common cutaneous manifestation. Fever, hepatitis and eosinophilia were present in all cases. Renal impairment was observed in 7 patients (33.3%). Allopurinol-induced DRESS was associated with a higher frequency of preexisting renal insufficiency (P ¼ .02) and increased risk of renal involvement as part of the syndrome (P ¼.002). Lichenoid dermatitis was the most common histopathologic feature. Systemic corticosteroid was commenced in 15 cases (71.4%). The average initial dose was 54.6 mg/day (0.95 mg/kg/day). The mean duration of corticosteroid use was 33 weeks. Steroid-sparing agents were used in 7 cases. Two cases in the case series developed autoimmune thyroiditis and one case developed bronchiolitis obliterans organizing pneumonia on subsequent followups. The overall mortality was 4.8%. Prolonged erythroderma were observed in 2 cases induced by trimethoprim-sulfamethoxazole. Conclusion: DRESS is a form of severe cutaneous adverse reaction and associated with a variety of clinical and biochemical features. Allopurinol is a common causative agent of DRESS and its use in patients with pre-existing renal insufficiency should be cautiously monitored. Commercial support: None identified.
Diffuse truncal skin induration and ulcerations due to pentazocineinduced calcinosis cutis
(Poster reference number 5685)
Galina Y. Stetsenko, MD, University of Washington, Seattle, WA, United States; Julia Shlyankevich, University of Washington, Seattle, WA, United States; Roy M. Colven, MD, University of Washington, Seattle, WA, United States Pentazocine is a potent analgesic developed in 1967 as a ‘‘nonaddicting narcotic.’’ Subsequent abuse of this medication was recognized. We present a case of an 82year-old woman with a 7-month history of woody induration of the abdomen, back, and buttocks with nonpainful nonhealing ulcers. Her medical history included hypothyroidism and breast carcinoma status postmastectomy, in remission. Physical examination revealed confluent rock-hard induration of skin and subcutis extending from abdomen and midback to upper posterior thighs. Several 1-3 cm draining ulcers with granulation tissue and yellow-white mineral deposits present at ulcer bases were noted on thighs and back. Laboratory studies including calcium, phosphate and parathyroid hormone levels were normal. Biopsy of left lower back ulcer showed scattered dermal densely calcified nodules. No bone formation, significant inflammation, necrosis or calcium deposits associated with or around blood vessels were present. Clinical differential diagnosis for diffuse skin and soft tissue calcification includes dystrophic calcification from autoimmune connective tissue diseases, trauma, infections, genetic disorders, metastatic calcification from renal disease, cancer-related hypercalcemia, granulomatous disease or hyperparathyroidism. History of narcotics and alcohol abuse was initially denied, but was later confirmed by patient’s son. The patient injected pentazocine subcutaneously, supplied by her husband, an anesthesiologist. History of pentazocine abuse, absence of systemic diseases, and normal laboratory evaluation were supportive of the diagnosis of pentazocine-induced calcinosis cutis. Ulcers were treated with wet to dry dressings, serial debridement and skin grafts. Patient healed well; however, 7 years later she developed a similar ulcer in the vicinity of the graft site. She was planned to undergo wound care, debridement, and another skin graft, but was lost to follow-up. Pentazocine is a well-known drug of abuse among health care professionals. It can be tested for in urine by gas chromatography and mass spectrometry. Pentazocine use causes granulomatous inflammation, dystrophic calcification, and scleroderma-like changes of skin at injection sites. The mechanism of sclerodermatous changes is not known. Truncal distribution of lesions is common, as it serves to hide injection sites. Recognition of this presentation of pentazocine-induced skin ulcers is important for diagnostic considerations and avoidance of a misdiagnosis. Commercial support: None identified.
APRIL 2012
HenocheSch€ onlein purpura associated with solid-organ malignancies: A report of 3 cases from Mayo Clinic and literature review
(Poster reference number 4828)
Joshua Podjasek, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; David Wada, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; David Wetter, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; Mark Pittelkow, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States Adult HenocheSch€ onlein purpura is rarely associated with solid-organ malignancies. We describe the cases of 3 adult patients with HenocheSch€ onlein purpura diagnosed within 3 months of the diagnosis of associated solid-organ malignancies, including pulmonary, prostate, and renal carcinomas. Two patients had complete remission with a combination of immunosuppressive therapies and treatment of the associated malignancy. The third patient had partial remission with immunosuppressive therapies but never received treatment of the associated malignancy and did not achieve complete remission before his death 10 months after diagnosis of HenocheSch€ onlein purpura. Our cases suggest that HenocheSch€ onlein purpura associated with solid-organ malignancies may be resistant to immunosuppressive therapies without treatment of the associated malignancy. Therefore, evaluation for solid-organ malignancies should be considered in adult patients without an identifiable cause of HenocheSch€ onlein purpura, especially if the disease is not self-limited or does not respond appropriately to treatment. Commercial support: None identified.
J AM ACAD DERMATOL
AB129
(Poster reference number 5388)
Zachary Zinn, MD, West Virginia University, Morgantown, WV, United States; Rodney Kovach, MD, West Virginia University, Morgantown, WV, United States Palmareplantar erythrodysethesia, also known as handefoot syndrome and chemotherapy-induced acral erythema, is a relatively common reaction to cytotoxic drugs, especially cytarabine. The classic clinical description is well demarcated tender erythematous plaques of the palms and soles beginning days to weeks after administration of the offending drug. Here we present a case of palmareplantar erythrodysethesia induced by cytarabine that initially mimicked cellulitis. Biopsy was consistent with cytotoxic changes secondary to chemotherapy. The cytotoxic reaction eventually resolved upon withdrawal of cytarabine. Commercial support: None identified.
Drug reaction with eosinophilia and systemic symptoms (DRESS): A retrospective analysis of 21 cases in a tertiary teaching hospital in Hong Kong
(Poster reference number 5215)
Johnny Chun-yin Chan, MBBS, The University of Hong Kong, Hong Kong, Hong Kong; Chi Keung Yeung, MBBS, The University of Hong Kong, Hong Kong, Hong Kong Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) is an acute, distinct and severe idiosyncratic reaction with a mortality of 8% to 10%. Owing to the rarity of the syndrome, large-scale studies are limited. Important data including the pattern of etiological agents, clinical and biochemical features and prognosis are lacking. Objective: To investigate the demographic data, clinical and biochemical characteristics, causative agents, treatment, and outcome of cases of DRESS in Hong Kong. Methods: A single center retrospective study on 21 cases of DRESS from February 2007 to February 2011. Medical records, clinical photographs, and sequential laboratory data were reviewed. An attempt was made to identify any correlation among the clinical pattern and specific causative agents. Main outcome measures: Clinical and biochemical pattern for specific drugs, treatment outcome and prognosis of DRESS. Results: Age of onset ranged from 14 to 77. No sex predilection was observed. The most common offending drug was allopurinol (28.6%), followed by phenobarbitone and trimethoprim-sulfamethoxazole. Mean latency period was 21.6 days. Exanthematous eruption was the most common cutaneous manifestation. Fever, hepatitis and eosinophilia were present in all cases. Renal impairment was observed in 7 patients (33.3%). Allopurinol-induced DRESS was associated with a higher frequency of preexisting renal insufficiency (P ¼ .02) and increased risk of renal involvement as part of the syndrome (P ¼.002). Lichenoid dermatitis was the most common histopathologic feature. Systemic corticosteroid was commenced in 15 cases (71.4%). The average initial dose was 54.6 mg/day (0.95 mg/kg/day). The mean duration of corticosteroid use was 33 weeks. Steroid-sparing agents were used in 7 cases. Two cases in the case series developed autoimmune thyroiditis and one case developed bronchiolitis obliterans organizing pneumonia on subsequent followups. The overall mortality was 4.8%. Prolonged erythroderma were observed in 2 cases induced by trimethoprim-sulfamethoxazole. Conclusion: DRESS is a form of severe cutaneous adverse reaction and associated with a variety of clinical and biochemical features. Allopurinol is a common causative agent of DRESS and its use in patients with pre-existing renal insufficiency should be cautiously monitored. Commercial support: None identified.
Diffuse truncal skin induration and ulcerations due to pentazocineinduced calcinosis cutis
(Poster reference number 5685)
Galina Y. Stetsenko, MD, University of Washington, Seattle, WA, United States; Julia Shlyankevich, University of Washington, Seattle, WA, United States; Roy M. Colven, MD, University of Washington, Seattle, WA, United States Pentazocine is a potent analgesic developed in 1967 as a ‘‘nonaddicting narcotic.’’ Subsequent abuse of this medication was recognized. We present a case of an 82year-old woman with a 7-month history of woody induration of the abdomen, back, and buttocks with nonpainful nonhealing ulcers. Her medical history included hypothyroidism and breast carcinoma status postmastectomy, in remission. Physical examination revealed confluent rock-hard induration of skin and subcutis extending from abdomen and midback to upper posterior thighs. Several 1-3 cm draining ulcers with granulation tissue and yellow-white mineral deposits present at ulcer bases were noted on thighs and back. Laboratory studies including calcium, phosphate and parathyroid hormone levels were normal. Biopsy of left lower back ulcer showed scattered dermal densely calcified nodules. No bone formation, significant inflammation, necrosis or calcium deposits associated with or around blood vessels were present. Clinical differential diagnosis for diffuse skin and soft tissue calcification includes dystrophic calcification from autoimmune connective tissue diseases, trauma, infections, genetic disorders, metastatic calcification from renal disease, cancer-related hypercalcemia, granulomatous disease or hyperparathyroidism. History of narcotics and alcohol abuse was initially denied, but was later confirmed by patient’s son. The patient injected pentazocine subcutaneously, supplied by her husband, an anesthesiologist. History of pentazocine abuse, absence of systemic diseases, and normal laboratory evaluation were supportive of the diagnosis of pentazocine-induced calcinosis cutis. Ulcers were treated with wet to dry dressings, serial debridement and skin grafts. Patient healed well; however, 7 years later she developed a similar ulcer in the vicinity of the graft site. She was planned to undergo wound care, debridement, and another skin graft, but was lost to follow-up. Pentazocine is a well-known drug of abuse among health care professionals. It can be tested for in urine by gas chromatography and mass spectrometry. Pentazocine use causes granulomatous inflammation, dystrophic calcification, and scleroderma-like changes of skin at injection sites. The mechanism of sclerodermatous changes is not known. Truncal distribution of lesions is common, as it serves to hide injection sites. Recognition of this presentation of pentazocine-induced skin ulcers is important for diagnostic considerations and avoidance of a misdiagnosis. Commercial support: None identified.
APRIL 2012
HenocheSch€ onlein purpura associated with solid-organ malignancies: A report of 3 cases from Mayo Clinic and literature review
(Poster reference number 4828)
Joshua Podjasek, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; David Wada, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; David Wetter, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States; Mark Pittelkow, MD, Mayo Clinic Department of Dermatology, Rochester, MN, United States Adult HenocheSch€ onlein purpura is rarely associated with solid-organ malignancies. We describe the cases of 3 adult patients with HenocheSch€ onlein purpura diagnosed within 3 months of the diagnosis of associated solid-organ malignancies, including pulmonary, prostate, and renal carcinomas. Two patients had complete remission with a combination of immunosuppressive therapies and treatment of the associated malignancy. The third patient had partial remission with immunosuppressive therapies but never received treatment of the associated malignancy and did not achieve complete remission before his death 10 months after diagnosis of HenocheSch€ onlein purpura. Our cases suggest that HenocheSch€ onlein purpura associated with solid-organ malignancies may be resistant to immunosuppressive therapies without treatment of the associated malignancy. Therefore, evaluation for solid-organ malignancies should be considered in adult patients without an identifiable cause of HenocheSch€ onlein purpura, especially if the disease is not self-limited or does not respond appropriately to treatment. Commercial support: None identified.
J AM ACAD DERMATOL
AB129