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Leser-Trélat Sign: A Paraneoplastic Process?
To the Editor:
Leser-Trélat sign is a rare skin condition characterized by the sudden appearance of seborrheic keratoses that rapidly increase in number and size within weeks to months. Co-occurrence has been reported with a large number of malignancies, particularly adenocarcinoma and lymphoma. We present a case of Leser-Trélat sign that was not associated with an underlying malignancy.
A 44-year-old man was admitted to our dermatology outpatient department with a serpigo on the neck that had grown rapidly in the last month. His medical history and family history were unremarkable. Dermatologic examination revealed numerous 3- to 4-mm brown and slightly verrucous papules on the neck (Figure 1). A punch biopsy of the lesion showed acanthosis of predominantly basaloid cells, papillomatosis, and hyperkeratosis, as well as the presence of characteristic horn cysts (Figure 2). He was tested for possible underlying internal malignancy. Liver and kidney function tests, electrolyte count, protein electrophoresis, and whole blood and urine tests were within reference range. Chest radiography and abdominal ultrasonography revealed no signs of pathology. The erythrocyte sedimentation rate was 20 mm/h (reference range, 0–20 mm/h) and tests for hepatitis, human immunodeficiency virus, and syphilis were negative. Abdominal, cranial, and thorax computed tomography revealed no abnormalities. Otolaryngologic examinations also were negative. Additional endoscopic analyses, esophagogastroduodenoscopy, and colonoscopy revealed no abnormalities. At 1-year follow-up, the seborrheic keratoses remained unchanged. He has remained in good health without specific signs or symptoms suggestive of an underlying malignancy.
Paraneoplastic syndromes are associated with malignancy but progress without connection to a primary tumor or metastasis and form a group of clinical manifestations. The characteristic progress of paraneoplastic syndromes shows parallelism with the progression of the tumor. The mechanism underlying the development is not known, though the actions of bioactive substances that cause responses in the tumor, such as polypeptide hormones, hormonelike peptides, antibodies or immune complexes, and cytokines or growth factors, have been implicated.1
Although the term paraneoplastic syndrome commonly is used for Leser-Trélat sign, we do not believe it is accurate. As Fink et al2 and Schwengle et al3 indicated, the possibility of the co-occurrence being fortuitous is high. Showing a parallel progress of malignancy with paraneoplastic dermatosis requires that the paraneoplastic syndrome also diminish when the tumor is cured.4 It should then reappear with cancer recurrence or metastasis, which has not been exhibited in many case presentations in the literature.3 Disease regression was observed in only 1 of 3 seborrheic keratosis cases after primary cancer treatment.5
In patients with a malignancy, the sudden increase in seborrheic keratosis is based exclusively on the subjective evaluation of the patient, which may not be reliable. Schwengle et al3 stated that this sudden increase can be related to the awareness level of the patient who had a cancer diagnosis. Bräuer et al6 stated that no plausible definition distinguishes eruptive versus common seborrheic keratoses.
As a result, the results regarding the relationship between malignancy and Leser-Trélat sign are conflicting, and no strong evidence supports the presence of the sign. Only case reports have suggested that Leser-Trélat sign accompanies malignancy. Studies investigating its etiopathogenesis have not revealed a substance that has been released from or as a response to a tumor.
We believe that the presence of eruptive seborrheic keratosis does not necessitate screening for underlying internal malignancies.
- Cohen PR. Paraneoplastic dermatopathology: cutaneous paraneoplastic syndromes. Adv Dermatol. 1996;11:215-252.
- Fink AM, Filz D, Krajnik G, et al. Seborrhoeic keratoses in patients with internal malignancies: a case-control study with a prospective accrual of patients. J Eur Acad Dermatol Venereol. 2009;23:1316-1319.
- Schwengle LE, Rampen FH, Wobbes T. Seborrhoeic keratoses and internal malignancies. a case control study. Clin Exp Dermatol. 1988;13:177-179.
- Curth HO. Skin lesions and internal carcinoma. In: Andrade S, Gumport S, Popkin GL, et al, eds. Cancer of the Skin: Biology, Diagnosis, and Management. Vol 2. Philadelphia, PA: WB Saunders; 1976:1308-1341.
- Heaphy MR Jr, Millns JL, Schroeter AL. The sign of Leser-Trélat in a case of adenocarcinoma of the lung. J Am Acad Dermatol. 2000;43(2, pt 2):386-390.
- Bräuer J, Happle R, Gieler U. The sign of Leser-Trélat: fact or myth? J Eur Acad Dermatol Venereol. 1992;1:77-80.
To the Editor:
Leser-Trélat sign is a rare skin condition characterized by the sudden appearance of seborrheic keratoses that rapidly increase in number and size within weeks to months. Co-occurrence has been reported with a large number of malignancies, particularly adenocarcinoma and lymphoma. We present a case of Leser-Trélat sign that was not associated with an underlying malignancy.
A 44-year-old man was admitted to our dermatology outpatient department with a serpigo on the neck that had grown rapidly in the last month. His medical history and family history were unremarkable. Dermatologic examination revealed numerous 3- to 4-mm brown and slightly verrucous papules on the neck (Figure 1). A punch biopsy of the lesion showed acanthosis of predominantly basaloid cells, papillomatosis, and hyperkeratosis, as well as the presence of characteristic horn cysts (Figure 2). He was tested for possible underlying internal malignancy. Liver and kidney function tests, electrolyte count, protein electrophoresis, and whole blood and urine tests were within reference range. Chest radiography and abdominal ultrasonography revealed no signs of pathology. The erythrocyte sedimentation rate was 20 mm/h (reference range, 0–20 mm/h) and tests for hepatitis, human immunodeficiency virus, and syphilis were negative. Abdominal, cranial, and thorax computed tomography revealed no abnormalities. Otolaryngologic examinations also were negative. Additional endoscopic analyses, esophagogastroduodenoscopy, and colonoscopy revealed no abnormalities. At 1-year follow-up, the seborrheic keratoses remained unchanged. He has remained in good health without specific signs or symptoms suggestive of an underlying malignancy.
Paraneoplastic syndromes are associated with malignancy but progress without connection to a primary tumor or metastasis and form a group of clinical manifestations. The characteristic progress of paraneoplastic syndromes shows parallelism with the progression of the tumor. The mechanism underlying the development is not known, though the actions of bioactive substances that cause responses in the tumor, such as polypeptide hormones, hormonelike peptides, antibodies or immune complexes, and cytokines or growth factors, have been implicated.1
Although the term paraneoplastic syndrome commonly is used for Leser-Trélat sign, we do not believe it is accurate. As Fink et al2 and Schwengle et al3 indicated, the possibility of the co-occurrence being fortuitous is high. Showing a parallel progress of malignancy with paraneoplastic dermatosis requires that the paraneoplastic syndrome also diminish when the tumor is cured.4 It should then reappear with cancer recurrence or metastasis, which has not been exhibited in many case presentations in the literature.3 Disease regression was observed in only 1 of 3 seborrheic keratosis cases after primary cancer treatment.5
In patients with a malignancy, the sudden increase in seborrheic keratosis is based exclusively on the subjective evaluation of the patient, which may not be reliable. Schwengle et al3 stated that this sudden increase can be related to the awareness level of the patient who had a cancer diagnosis. Bräuer et al6 stated that no plausible definition distinguishes eruptive versus common seborrheic keratoses.
As a result, the results regarding the relationship between malignancy and Leser-Trélat sign are conflicting, and no strong evidence supports the presence of the sign. Only case reports have suggested that Leser-Trélat sign accompanies malignancy. Studies investigating its etiopathogenesis have not revealed a substance that has been released from or as a response to a tumor.
We believe that the presence of eruptive seborrheic keratosis does not necessitate screening for underlying internal malignancies.
To the Editor:
Leser-Trélat sign is a rare skin condition characterized by the sudden appearance of seborrheic keratoses that rapidly increase in number and size within weeks to months. Co-occurrence has been reported with a large number of malignancies, particularly adenocarcinoma and lymphoma. We present a case of Leser-Trélat sign that was not associated with an underlying malignancy.
A 44-year-old man was admitted to our dermatology outpatient department with a serpigo on the neck that had grown rapidly in the last month. His medical history and family history were unremarkable. Dermatologic examination revealed numerous 3- to 4-mm brown and slightly verrucous papules on the neck (Figure 1). A punch biopsy of the lesion showed acanthosis of predominantly basaloid cells, papillomatosis, and hyperkeratosis, as well as the presence of characteristic horn cysts (Figure 2). He was tested for possible underlying internal malignancy. Liver and kidney function tests, electrolyte count, protein electrophoresis, and whole blood and urine tests were within reference range. Chest radiography and abdominal ultrasonography revealed no signs of pathology. The erythrocyte sedimentation rate was 20 mm/h (reference range, 0–20 mm/h) and tests for hepatitis, human immunodeficiency virus, and syphilis were negative. Abdominal, cranial, and thorax computed tomography revealed no abnormalities. Otolaryngologic examinations also were negative. Additional endoscopic analyses, esophagogastroduodenoscopy, and colonoscopy revealed no abnormalities. At 1-year follow-up, the seborrheic keratoses remained unchanged. He has remained in good health without specific signs or symptoms suggestive of an underlying malignancy.
Paraneoplastic syndromes are associated with malignancy but progress without connection to a primary tumor or metastasis and form a group of clinical manifestations. The characteristic progress of paraneoplastic syndromes shows parallelism with the progression of the tumor. The mechanism underlying the development is not known, though the actions of bioactive substances that cause responses in the tumor, such as polypeptide hormones, hormonelike peptides, antibodies or immune complexes, and cytokines or growth factors, have been implicated.1
Although the term paraneoplastic syndrome commonly is used for Leser-Trélat sign, we do not believe it is accurate. As Fink et al2 and Schwengle et al3 indicated, the possibility of the co-occurrence being fortuitous is high. Showing a parallel progress of malignancy with paraneoplastic dermatosis requires that the paraneoplastic syndrome also diminish when the tumor is cured.4 It should then reappear with cancer recurrence or metastasis, which has not been exhibited in many case presentations in the literature.3 Disease regression was observed in only 1 of 3 seborrheic keratosis cases after primary cancer treatment.5
In patients with a malignancy, the sudden increase in seborrheic keratosis is based exclusively on the subjective evaluation of the patient, which may not be reliable. Schwengle et al3 stated that this sudden increase can be related to the awareness level of the patient who had a cancer diagnosis. Bräuer et al6 stated that no plausible definition distinguishes eruptive versus common seborrheic keratoses.
As a result, the results regarding the relationship between malignancy and Leser-Trélat sign are conflicting, and no strong evidence supports the presence of the sign. Only case reports have suggested that Leser-Trélat sign accompanies malignancy. Studies investigating its etiopathogenesis have not revealed a substance that has been released from or as a response to a tumor.
We believe that the presence of eruptive seborrheic keratosis does not necessitate screening for underlying internal malignancies.
- Cohen PR. Paraneoplastic dermatopathology: cutaneous paraneoplastic syndromes. Adv Dermatol. 1996;11:215-252.
- Fink AM, Filz D, Krajnik G, et al. Seborrhoeic keratoses in patients with internal malignancies: a case-control study with a prospective accrual of patients. J Eur Acad Dermatol Venereol. 2009;23:1316-1319.
- Schwengle LE, Rampen FH, Wobbes T. Seborrhoeic keratoses and internal malignancies. a case control study. Clin Exp Dermatol. 1988;13:177-179.
- Curth HO. Skin lesions and internal carcinoma. In: Andrade S, Gumport S, Popkin GL, et al, eds. Cancer of the Skin: Biology, Diagnosis, and Management. Vol 2. Philadelphia, PA: WB Saunders; 1976:1308-1341.
- Heaphy MR Jr, Millns JL, Schroeter AL. The sign of Leser-Trélat in a case of adenocarcinoma of the lung. J Am Acad Dermatol. 2000;43(2, pt 2):386-390.
- Bräuer J, Happle R, Gieler U. The sign of Leser-Trélat: fact or myth? J Eur Acad Dermatol Venereol. 1992;1:77-80.
- Cohen PR. Paraneoplastic dermatopathology: cutaneous paraneoplastic syndromes. Adv Dermatol. 1996;11:215-252.
- Fink AM, Filz D, Krajnik G, et al. Seborrhoeic keratoses in patients with internal malignancies: a case-control study with a prospective accrual of patients. J Eur Acad Dermatol Venereol. 2009;23:1316-1319.
- Schwengle LE, Rampen FH, Wobbes T. Seborrhoeic keratoses and internal malignancies. a case control study. Clin Exp Dermatol. 1988;13:177-179.
- Curth HO. Skin lesions and internal carcinoma. In: Andrade S, Gumport S, Popkin GL, et al, eds. Cancer of the Skin: Biology, Diagnosis, and Management. Vol 2. Philadelphia, PA: WB Saunders; 1976:1308-1341.
- Heaphy MR Jr, Millns JL, Schroeter AL. The sign of Leser-Trélat in a case of adenocarcinoma of the lung. J Am Acad Dermatol. 2000;43(2, pt 2):386-390.
- Bräuer J, Happle R, Gieler U. The sign of Leser-Trélat: fact or myth? J Eur Acad Dermatol Venereol. 1992;1:77-80.
Drink more coffee to prevent a second BCC
AMSTERDAM – Liberal coffee consumption was independently associated with a reduced risk of developing a second basal cell carcinoma in individuals who’ve already had a first in an analysis from the Rotterdam Study.
“This might seem surprising, but several recent studies done in both humans and mice have shown this protective effect as well. The mechanism behind it is still unclear, but we think that caffeine might help to prevent UV-induced carcinogenesis,” Dr. Joris Verkouteren said in presenting the Rotterdam Study findings at the annual congress of the European Academy of Dermatology and Venereology.
Drinking more coffee was the only protective factor identified in the study. In a multivariate regression analysis, it was associated with a 30% reduction in the relative risk of developing at least a second BCC.
In contrast, two major predictors of increased likelihood of a second BCC emerged. The strongest was having more than one primary BCC at initial presentation, which carried an associated 2.5-fold increased risk. The other risk factor was older age at diagnosis of the first BCC, associated with a 60% increase in risk, reported Dr. Verkouteren of Ermasus University, Rotterdam.
Basal cell carcinoma is the most common of all malignancies. Roughly one-third of patients who present with a first one will develop a second BCC, most often within the next couple years. This makes BCC a logical target for secondary prevention measures. The purpose of this analysis of the Rotterdam Study was to identify factors to help physicians differentiate between patients who are likely to have just one primary BCC and those who will go on to develop multiple BCCs. This would aid clinicians in selecting patients for closer monitoring and in identifying good candidates for aggressive secondary prevention interventions, such as photodynamic therapy to address the field cancerization which results from lifetime exposure to UV, he explained.
The Rotterdam Study is an ongoing prospective population-based cohort study started in 1989. This analysis included 14,976 Rotterdam residents, all at least age 45 years at entry, who have been evaluated by physican examination and detailed questionnaires every 3-4 years. Through linkage to the Dutch national histopathologic database, it was possible to identify all study participants diagnosed with BCC.
The 784 study participants who developed a first primary BCC were prospectively followed for a median of more than 4 years, during which 293 developed at least a second BCC.
Individuals who developed a second BCC at least 6 months after their first drank an average of 2 cups of joe daily, while those who did not have another BCC quaffed an average of 5 cups per day.
The median age at the time of diagnosis of a first BCC was 67.6 years in individuals who didn’t develop a second one, compared to 80.7 years in those who did.
A particularly noteworthy study finding, in Dr. Verkouteren’s view, was that many of the well-established risk factors for a first BCC were not significant predictors of a second one. A tendency to sunburn easily, light hair and eye color, male gender, smoking, a history of outdoor work -- none of these factors proved helpful in predicting which patients with a first BCC would develop another.
Dr. Tamar Nijsten, senior coinvestigator in the study, said that he is skeptical of Dr. Verkouteren’s assertion that the observed association between greater coffee consumption and reduced risk of a second BCC is probably due to a some intrinsic anti-carcinogenic effect of caffeine.
“There are people – and I am one of them – who believe that coffee consumption is associated with health status. So people who drink more coffee have, on average, a more healthy lifestyle,” said Dr. Nijsten, professor and chair of the department of dermatology at Erasmus University Medical Center, Rotterdam.
Dr. Verkouteren and Dr. Nijsten reported having no financial conflicts regarding the Rotterdam Study.
AMSTERDAM – Liberal coffee consumption was independently associated with a reduced risk of developing a second basal cell carcinoma in individuals who’ve already had a first in an analysis from the Rotterdam Study.
“This might seem surprising, but several recent studies done in both humans and mice have shown this protective effect as well. The mechanism behind it is still unclear, but we think that caffeine might help to prevent UV-induced carcinogenesis,” Dr. Joris Verkouteren said in presenting the Rotterdam Study findings at the annual congress of the European Academy of Dermatology and Venereology.
Drinking more coffee was the only protective factor identified in the study. In a multivariate regression analysis, it was associated with a 30% reduction in the relative risk of developing at least a second BCC.
In contrast, two major predictors of increased likelihood of a second BCC emerged. The strongest was having more than one primary BCC at initial presentation, which carried an associated 2.5-fold increased risk. The other risk factor was older age at diagnosis of the first BCC, associated with a 60% increase in risk, reported Dr. Verkouteren of Ermasus University, Rotterdam.
Basal cell carcinoma is the most common of all malignancies. Roughly one-third of patients who present with a first one will develop a second BCC, most often within the next couple years. This makes BCC a logical target for secondary prevention measures. The purpose of this analysis of the Rotterdam Study was to identify factors to help physicians differentiate between patients who are likely to have just one primary BCC and those who will go on to develop multiple BCCs. This would aid clinicians in selecting patients for closer monitoring and in identifying good candidates for aggressive secondary prevention interventions, such as photodynamic therapy to address the field cancerization which results from lifetime exposure to UV, he explained.
The Rotterdam Study is an ongoing prospective population-based cohort study started in 1989. This analysis included 14,976 Rotterdam residents, all at least age 45 years at entry, who have been evaluated by physican examination and detailed questionnaires every 3-4 years. Through linkage to the Dutch national histopathologic database, it was possible to identify all study participants diagnosed with BCC.
The 784 study participants who developed a first primary BCC were prospectively followed for a median of more than 4 years, during which 293 developed at least a second BCC.
Individuals who developed a second BCC at least 6 months after their first drank an average of 2 cups of joe daily, while those who did not have another BCC quaffed an average of 5 cups per day.
The median age at the time of diagnosis of a first BCC was 67.6 years in individuals who didn’t develop a second one, compared to 80.7 years in those who did.
A particularly noteworthy study finding, in Dr. Verkouteren’s view, was that many of the well-established risk factors for a first BCC were not significant predictors of a second one. A tendency to sunburn easily, light hair and eye color, male gender, smoking, a history of outdoor work -- none of these factors proved helpful in predicting which patients with a first BCC would develop another.
Dr. Tamar Nijsten, senior coinvestigator in the study, said that he is skeptical of Dr. Verkouteren’s assertion that the observed association between greater coffee consumption and reduced risk of a second BCC is probably due to a some intrinsic anti-carcinogenic effect of caffeine.
“There are people – and I am one of them – who believe that coffee consumption is associated with health status. So people who drink more coffee have, on average, a more healthy lifestyle,” said Dr. Nijsten, professor and chair of the department of dermatology at Erasmus University Medical Center, Rotterdam.
Dr. Verkouteren and Dr. Nijsten reported having no financial conflicts regarding the Rotterdam Study.
AMSTERDAM – Liberal coffee consumption was independently associated with a reduced risk of developing a second basal cell carcinoma in individuals who’ve already had a first in an analysis from the Rotterdam Study.
“This might seem surprising, but several recent studies done in both humans and mice have shown this protective effect as well. The mechanism behind it is still unclear, but we think that caffeine might help to prevent UV-induced carcinogenesis,” Dr. Joris Verkouteren said in presenting the Rotterdam Study findings at the annual congress of the European Academy of Dermatology and Venereology.
Drinking more coffee was the only protective factor identified in the study. In a multivariate regression analysis, it was associated with a 30% reduction in the relative risk of developing at least a second BCC.
In contrast, two major predictors of increased likelihood of a second BCC emerged. The strongest was having more than one primary BCC at initial presentation, which carried an associated 2.5-fold increased risk. The other risk factor was older age at diagnosis of the first BCC, associated with a 60% increase in risk, reported Dr. Verkouteren of Ermasus University, Rotterdam.
Basal cell carcinoma is the most common of all malignancies. Roughly one-third of patients who present with a first one will develop a second BCC, most often within the next couple years. This makes BCC a logical target for secondary prevention measures. The purpose of this analysis of the Rotterdam Study was to identify factors to help physicians differentiate between patients who are likely to have just one primary BCC and those who will go on to develop multiple BCCs. This would aid clinicians in selecting patients for closer monitoring and in identifying good candidates for aggressive secondary prevention interventions, such as photodynamic therapy to address the field cancerization which results from lifetime exposure to UV, he explained.
The Rotterdam Study is an ongoing prospective population-based cohort study started in 1989. This analysis included 14,976 Rotterdam residents, all at least age 45 years at entry, who have been evaluated by physican examination and detailed questionnaires every 3-4 years. Through linkage to the Dutch national histopathologic database, it was possible to identify all study participants diagnosed with BCC.
The 784 study participants who developed a first primary BCC were prospectively followed for a median of more than 4 years, during which 293 developed at least a second BCC.
Individuals who developed a second BCC at least 6 months after their first drank an average of 2 cups of joe daily, while those who did not have another BCC quaffed an average of 5 cups per day.
The median age at the time of diagnosis of a first BCC was 67.6 years in individuals who didn’t develop a second one, compared to 80.7 years in those who did.
A particularly noteworthy study finding, in Dr. Verkouteren’s view, was that many of the well-established risk factors for a first BCC were not significant predictors of a second one. A tendency to sunburn easily, light hair and eye color, male gender, smoking, a history of outdoor work -- none of these factors proved helpful in predicting which patients with a first BCC would develop another.
Dr. Tamar Nijsten, senior coinvestigator in the study, said that he is skeptical of Dr. Verkouteren’s assertion that the observed association between greater coffee consumption and reduced risk of a second BCC is probably due to a some intrinsic anti-carcinogenic effect of caffeine.
“There are people – and I am one of them – who believe that coffee consumption is associated with health status. So people who drink more coffee have, on average, a more healthy lifestyle,” said Dr. Nijsten, professor and chair of the department of dermatology at Erasmus University Medical Center, Rotterdam.
Dr. Verkouteren and Dr. Nijsten reported having no financial conflicts regarding the Rotterdam Study.
AT THE EADV CONGRESS
Key clinical point: The more coffee you drink, the less likely you will develop a second basal cell carcinoma after being diagnosed with a first one.
Major finding: Increased coffee consumption was associated with a 30% relative risk reduction for diagnosis of a second BCC.
Data source: Analysis involving more than 14,000 participants in the Rotterdam Study, an ongoing prospective population-based cohort study.
Disclosures: The presenter reported having no financial conflicts of interest.
Flurbiprofen-Induced Unilateral Eyelid Angioedema
To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.1 The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.2 These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.
A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.
Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.3 Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.4
Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.5 Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.6 In another study, Leeyaphan et al5 reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,7 localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.8 We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.
1. Roszkowski MT, Swift JQ, Hargreaves KM. Effect of NSAID administration on tissue levels of immunoreactive prostaglandin E2, leukotriene B4, and (S)-flurbiprofen following extraction of impacted third molars. Pain. 1997;73:339-345.
2. Asero R. Multiple sensitivity to NSAID. Allergy. 2000;55:893-894.
3. Nettis E, Colanardi MC, Ferrannini A, et al. Update on sensitivity to nonsteroidal anti-inflammatory drugs. Curr Drug Targets Immune Endocr Metabol Disord. 2001;1:233-240.
4. Kulthanan K, Jiamton S, Boochangkool K, et al. Angioedema: clinical and etiological aspects. Clin Dev Immunol. 2007;2007:26438.
5. Leeyaphan C, Kulthanan K, Jongiarearnprasert K, et al. Drug-induced angioedema without urticaria: prevalence and clinical features [published online ahead of print November 17, 2009]. J Eur Acad Dermatol Venereol. 2010;24:685-691.
6. Cutaneous reactions to analgesic-antipyretics and nonsteroidal anti-inflammatory drugs. analysis of reports to the spontaneous reporting system of the Gruppo Italiano Studi Epidemiologici in Dermatologia. Dermatology. 1993;186:164-169.
7. Stevenson OE, Finch TM. Allergic contact dermatitis from rectified camphor oil in Earex ear drops. Contact Dermatitis. 2003;49:51.
8. Tsuruta D, Oshimo T, Sowa J, et al. Unilateral eyelid angioedema with congestion of the right bulbar conjunctiva due to loxoprofen sodium. Cutis. 2011;87:41-43.
To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.1 The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.2 These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.
A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.
Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.3 Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.4
Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.5 Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.6 In another study, Leeyaphan et al5 reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,7 localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.8 We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.
To the Editor:
Flurbiprofen, a member of the phenylalkanoic acid derivative group of nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used to treat fever, inflammation, and pain of arthritis.1 The exact prevalence of allergic reactions to NSAIDs in the general population is not known. Rhinoconjunctivitis, bronchospasm, urticaria, angioedema, and anaphylaxis can occur as an allergic reaction to NSAIDs. Isolated angioedema following NSAID ingestion typically involves the face, particularly the periorbital skin, lips, and mouth.2 These patients may develop urticaria and/or angioedema only after NSAID ingestion, but they do not have underlying chronic urticaria. We report a rare case of isolated unilateral eyelid angioedema with flurbiprofen.
A 39-year-old man presented with the onset of unilateral angioedema of the left upper eyelid that had developed approximately 30 minutes after taking flurbiprofen (100 mg). He reported frequent use of flurbiprofen for headaches. The patient also had a history of taking aspirin, ibuprofen, diclofenac, etodolac, and naproxen sodium as needed for migraines with no prior angioedema. He had no history of chronic urticaria or allergic disease. The patient was treated with oral pheniramine hydrogen maleate and angioedema resolved after 12 hours. Three days later, the patient used flurbiprofen again for a headache. He was readmitted to our clinic with unilateral angioedema of the left upper eyelid (Figure). The symptoms started approximately 30 minutes after taking flurbiprofen. Angioedema resolved within 1 day with oral pheniramine.
Nonsteroidal anti-inflammatory drugs are the most commonly prescribed class of drugs in the world and are the most common cause of all adverse drug reactions.3 Urticaria, angioedema, and anaphylaxis are common adverse reactions to NSAIDs. The prevalence of urticaria and angioedema to NSAIDs has been reported to be 0.1% to 3% worldwide.4
Angioedema is an abrupt localized swelling of the skin and mucous membranes of the face, lips, mouth, throat, larynx, extremities, and genitalia. Angioedema generally develops over minutes to hours and resolves in 24 to 48 hours.5 Angioedema without urticaria is the clinical syndrome that can be caused by an adverse drug reaction. In an Italian review of 2137 reactions, NSAIDs were causative agents in 33.6% of patients with drug-induced angioedema.6 In another study, Leeyaphan et al5 reported that 50% of patients with drug-induced angioedema resulted from NSAIDs, commonly with ibuprofen and diclofenac. Although angioedema is due to inhibition of cyclooxygenase 1, overproduction of leukotrienes, and possibly IgE-mediated reactions to single drugs,7 localized unilateral eyelid angioedema with NSAIDs is rare. The exact mechanism of localized eyelid edema is not known.8 We believe that the unilateral eyelid angioedema in our patient was caused by flurbiprofen use because the reaction recurred when the drug was used again.
1. Roszkowski MT, Swift JQ, Hargreaves KM. Effect of NSAID administration on tissue levels of immunoreactive prostaglandin E2, leukotriene B4, and (S)-flurbiprofen following extraction of impacted third molars. Pain. 1997;73:339-345.
2. Asero R. Multiple sensitivity to NSAID. Allergy. 2000;55:893-894.
3. Nettis E, Colanardi MC, Ferrannini A, et al. Update on sensitivity to nonsteroidal anti-inflammatory drugs. Curr Drug Targets Immune Endocr Metabol Disord. 2001;1:233-240.
4. Kulthanan K, Jiamton S, Boochangkool K, et al. Angioedema: clinical and etiological aspects. Clin Dev Immunol. 2007;2007:26438.
5. Leeyaphan C, Kulthanan K, Jongiarearnprasert K, et al. Drug-induced angioedema without urticaria: prevalence and clinical features [published online ahead of print November 17, 2009]. J Eur Acad Dermatol Venereol. 2010;24:685-691.
6. Cutaneous reactions to analgesic-antipyretics and nonsteroidal anti-inflammatory drugs. analysis of reports to the spontaneous reporting system of the Gruppo Italiano Studi Epidemiologici in Dermatologia. Dermatology. 1993;186:164-169.
7. Stevenson OE, Finch TM. Allergic contact dermatitis from rectified camphor oil in Earex ear drops. Contact Dermatitis. 2003;49:51.
8. Tsuruta D, Oshimo T, Sowa J, et al. Unilateral eyelid angioedema with congestion of the right bulbar conjunctiva due to loxoprofen sodium. Cutis. 2011;87:41-43.
1. Roszkowski MT, Swift JQ, Hargreaves KM. Effect of NSAID administration on tissue levels of immunoreactive prostaglandin E2, leukotriene B4, and (S)-flurbiprofen following extraction of impacted third molars. Pain. 1997;73:339-345.
2. Asero R. Multiple sensitivity to NSAID. Allergy. 2000;55:893-894.
3. Nettis E, Colanardi MC, Ferrannini A, et al. Update on sensitivity to nonsteroidal anti-inflammatory drugs. Curr Drug Targets Immune Endocr Metabol Disord. 2001;1:233-240.
4. Kulthanan K, Jiamton S, Boochangkool K, et al. Angioedema: clinical and etiological aspects. Clin Dev Immunol. 2007;2007:26438.
5. Leeyaphan C, Kulthanan K, Jongiarearnprasert K, et al. Drug-induced angioedema without urticaria: prevalence and clinical features [published online ahead of print November 17, 2009]. J Eur Acad Dermatol Venereol. 2010;24:685-691.
6. Cutaneous reactions to analgesic-antipyretics and nonsteroidal anti-inflammatory drugs. analysis of reports to the spontaneous reporting system of the Gruppo Italiano Studi Epidemiologici in Dermatologia. Dermatology. 1993;186:164-169.
7. Stevenson OE, Finch TM. Allergic contact dermatitis from rectified camphor oil in Earex ear drops. Contact Dermatitis. 2003;49:51.
8. Tsuruta D, Oshimo T, Sowa J, et al. Unilateral eyelid angioedema with congestion of the right bulbar conjunctiva due to loxoprofen sodium. Cutis. 2011;87:41-43.
Anal high-grade squamous intraepithelial lesions cleared in 42% of gay men
MELBOURNE – High-grade squamous intraepithelial lesions are prevalent among HIV-positive gay men and a significant number of these anal lesions resolve spontaneously, according to data from a longitudinal observational cohort study.
The Study of the Prevention of Anal Cancer (SPANC) is a 3-year prospective study of the natural history of anal HPV infection, which has so far enrolled 350 homosexual men over 35 years old. Dr. Andrew Grulich from the Kirby Institute, University of New South Wales, Sydney, presented trial data at the 20th International AIDS Conference that showed a 42% clearance rate for high-grade squamous intraepithelial lesions (HSIL).
Anal lesions that result from human papillomavirus infection are difficult to treat, and there is no evidence for the effectiveness of treatment, Dr. Grulich said. Further, anal lesions are far less likely than cervical lesions to progress to cancer. However, questions remain about which men are more likely to have persistent high-grade disease and therefore are at a higher risk of progression to cancer.
Interim data from the SPANC study found a 46% prevalence of HSIL among HIV-positive gay men and a 34% prevalence among HIV-negative gay men. The higher rate among HIV-positive individuals was largely driven by a higher prevalence of more advanced anal intraepithelial neoplasia.
Men with persistent infections due to human papillomavirus (HPV) 16 – the subtype most commonly associated with anal cancer – were much less likely to clear the high-grade lesions (hazard ratio = 0.22, 95% confidence interval, 0.11-0.46), as were men with multiple subtypes of HPV.
"What we’ve been able to show is that high-grade disease is very dynamic, with one in six [gay] men getting it and of those who get it about 40% clearing it each year," Dr. Grulich told the conference.
"Not all high-grade disease requires treatment," he said. "These data suggest that treatment can be targeted at those with persistent high-grade disease because much high-grade disease diagnosed on a single occasion will simply go away."
Treatment practices for HSIL vary with some choosing a ‘watch and wait’ approach and others choosing ablative treatment. Dr. Grulich suggested treatment based on "red flags" that suggest a higher risk of progression to cancer.
"If [the patient] is HPV 16–positive, that’s a definite red flag because 90% of anal cancer is caused by that one subtype," Dr. Grulich said. Also, high-grade disease that doesn’t clear is another red flag.
"I think it’s perfectly reasonable, given the state of the science, if you’re doing high-resolution anoscopy and you diagnose (HSIL), to explain to the patient that it’s highly likely to go away but it may not, and therefore get the patient back in about a year," he said.
The study is funded by the National Health and Medical Research Council of Australia, and the Cancer Council NSW. Some authors declared financial ties to pharmaceutical companies including a manufacturer of HPV vaccines.
MELBOURNE – High-grade squamous intraepithelial lesions are prevalent among HIV-positive gay men and a significant number of these anal lesions resolve spontaneously, according to data from a longitudinal observational cohort study.
The Study of the Prevention of Anal Cancer (SPANC) is a 3-year prospective study of the natural history of anal HPV infection, which has so far enrolled 350 homosexual men over 35 years old. Dr. Andrew Grulich from the Kirby Institute, University of New South Wales, Sydney, presented trial data at the 20th International AIDS Conference that showed a 42% clearance rate for high-grade squamous intraepithelial lesions (HSIL).
Anal lesions that result from human papillomavirus infection are difficult to treat, and there is no evidence for the effectiveness of treatment, Dr. Grulich said. Further, anal lesions are far less likely than cervical lesions to progress to cancer. However, questions remain about which men are more likely to have persistent high-grade disease and therefore are at a higher risk of progression to cancer.
Interim data from the SPANC study found a 46% prevalence of HSIL among HIV-positive gay men and a 34% prevalence among HIV-negative gay men. The higher rate among HIV-positive individuals was largely driven by a higher prevalence of more advanced anal intraepithelial neoplasia.
Men with persistent infections due to human papillomavirus (HPV) 16 – the subtype most commonly associated with anal cancer – were much less likely to clear the high-grade lesions (hazard ratio = 0.22, 95% confidence interval, 0.11-0.46), as were men with multiple subtypes of HPV.
"What we’ve been able to show is that high-grade disease is very dynamic, with one in six [gay] men getting it and of those who get it about 40% clearing it each year," Dr. Grulich told the conference.
"Not all high-grade disease requires treatment," he said. "These data suggest that treatment can be targeted at those with persistent high-grade disease because much high-grade disease diagnosed on a single occasion will simply go away."
Treatment practices for HSIL vary with some choosing a ‘watch and wait’ approach and others choosing ablative treatment. Dr. Grulich suggested treatment based on "red flags" that suggest a higher risk of progression to cancer.
"If [the patient] is HPV 16–positive, that’s a definite red flag because 90% of anal cancer is caused by that one subtype," Dr. Grulich said. Also, high-grade disease that doesn’t clear is another red flag.
"I think it’s perfectly reasonable, given the state of the science, if you’re doing high-resolution anoscopy and you diagnose (HSIL), to explain to the patient that it’s highly likely to go away but it may not, and therefore get the patient back in about a year," he said.
The study is funded by the National Health and Medical Research Council of Australia, and the Cancer Council NSW. Some authors declared financial ties to pharmaceutical companies including a manufacturer of HPV vaccines.
MELBOURNE – High-grade squamous intraepithelial lesions are prevalent among HIV-positive gay men and a significant number of these anal lesions resolve spontaneously, according to data from a longitudinal observational cohort study.
The Study of the Prevention of Anal Cancer (SPANC) is a 3-year prospective study of the natural history of anal HPV infection, which has so far enrolled 350 homosexual men over 35 years old. Dr. Andrew Grulich from the Kirby Institute, University of New South Wales, Sydney, presented trial data at the 20th International AIDS Conference that showed a 42% clearance rate for high-grade squamous intraepithelial lesions (HSIL).
Anal lesions that result from human papillomavirus infection are difficult to treat, and there is no evidence for the effectiveness of treatment, Dr. Grulich said. Further, anal lesions are far less likely than cervical lesions to progress to cancer. However, questions remain about which men are more likely to have persistent high-grade disease and therefore are at a higher risk of progression to cancer.
Interim data from the SPANC study found a 46% prevalence of HSIL among HIV-positive gay men and a 34% prevalence among HIV-negative gay men. The higher rate among HIV-positive individuals was largely driven by a higher prevalence of more advanced anal intraepithelial neoplasia.
Men with persistent infections due to human papillomavirus (HPV) 16 – the subtype most commonly associated with anal cancer – were much less likely to clear the high-grade lesions (hazard ratio = 0.22, 95% confidence interval, 0.11-0.46), as were men with multiple subtypes of HPV.
"What we’ve been able to show is that high-grade disease is very dynamic, with one in six [gay] men getting it and of those who get it about 40% clearing it each year," Dr. Grulich told the conference.
"Not all high-grade disease requires treatment," he said. "These data suggest that treatment can be targeted at those with persistent high-grade disease because much high-grade disease diagnosed on a single occasion will simply go away."
Treatment practices for HSIL vary with some choosing a ‘watch and wait’ approach and others choosing ablative treatment. Dr. Grulich suggested treatment based on "red flags" that suggest a higher risk of progression to cancer.
"If [the patient] is HPV 16–positive, that’s a definite red flag because 90% of anal cancer is caused by that one subtype," Dr. Grulich said. Also, high-grade disease that doesn’t clear is another red flag.
"I think it’s perfectly reasonable, given the state of the science, if you’re doing high-resolution anoscopy and you diagnose (HSIL), to explain to the patient that it’s highly likely to go away but it may not, and therefore get the patient back in about a year," he said.
The study is funded by the National Health and Medical Research Council of Australia, and the Cancer Council NSW. Some authors declared financial ties to pharmaceutical companies including a manufacturer of HPV vaccines.
AT AIDS 2014
Key clinical point: Watchful waiting may be an option for gay men with anal high-grade squamous intraepithelial lesions if the lesion is not HPV 16 positive and has not been present for more than a year.
Major finding: Over 40% of anal high-grade squamous intraepithelial lesions clear spontaneously without treatment, with similar clearance rates for HIV-positive and HIV-negative gay men.
Data source: Interim data on 350 gay men over 35 years old enrolled in SPANC, a 3-year prospective study of the natural history of anal HPV infection.
Disclosures: The study is funded by the National Health and Medical Research Council of Australia and the Cancer Council NSW. Some authors declared financial ties to pharmaceutical companies including a manufacturer of HPV vaccines.
UV Radiation Transmittance: Regular Clothing Versus Sun-Protective Clothing
Dermatologists frequently encounter patients who inquire about the need to buy special clothing and hats that claim to block UV light rather than using their regular clothing and hats. A patient may argue that he/she has never gotten sunburned through his/her favorite T-shirt while fishing, so why does he/she need to buy special clothing? The answer to this question is not straightforward. The dermatologist could easily say yes and advise patients to buy special sun-protective clothing, which could be especially tempting if a practitioner actually sells these items in the office. However, when considering evidence-based medicine, one needs to look at the data to appropriately answer the question.
Although it is still evolving, a standard has been set for UV protection factor (UPF) in the United States as well as other countries.1 Clothing with the maximum UPF rating of 50 blocks 98% of UVA/UVB radiation. Although there are data published in the literature regarding sun-protective clothing, there are scant data in the clinical dermatologic literature.2-5 To give patients an educated answer to this question, we measured and compared UVA/UVB radiation transmittance through regular (ie, non–UPF rated) clothing versus sun-protective clothing with a UPF rating.
Materials and Methods
A digital handheld UVA/UVB meter with an absorption spectrum of 280 to 400 nm was used to measure UV energy transmitted through sample clothing articles. The meter measured UVA/UVB light with a maximum reading of 40 mW/cm2. Clothing articles were selected of varied material/color and intended use.
Regular clothing articles included a straw golf hat (Figure 1A), an off-white and blue baseball hat (70% wool)(Figure 1B), a black baseball hat (100% wool)(Figure 1C), a white athletic tank shirt (100% cotton), a white T-shirt/undershirt (100% cotton), a thin-weave blue T-shirt (100% cotton), and a conventional-weave blue T-shirt (100% cotton)(Figure 1D). The regular clothing items, with the exception of the hats, had been laundered in conventional (ie, non–UV blocking) laundry detergent and no chemicals were applied to enhance UVA/UVB blocking properties. The exact number of times the items were laundered was unknown.
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| Figure 1. Regular clothing articles included a straw golf hat (A), an off-white and blue baseball hat (B), a black baseball hat (C), and white and blue T-shirts (D). |
Sun-protective clothing articles included a polyester floral splash bucket hat and a polyester ruffled swim romper (Figure 2), both with a UPF rating of 50+. These items were purchased from a manufacturer who regularly promotes sun-protective clothing to both dermatologists and the general public. The company “guarantees” a UPF rating of 50 and advertises that these clothing articles block 98% of harmful UV rays. These items were not laundered prior to the study, and no chemicals were applied to enhance UVA/UVB blocking properties.
The UVA/UVB meter was calibrated on a clear cloudless July day in Frankfort, Illinois. An initial reading was taken without any obstruction to the sunlight. The regular and sun-protective clothing articles then were placed over the meter to measure the amount of UVA/UVB transmitted through each item. Measurements were taken for each article of clothing after the meter was covered by the respective material for 10 seconds. Care was taken to cover the meter with only 1 layer of material for each article, which was intended to mimic the degree of UVA/UVB blocking and transmittance during normal wear.
Results
The full results from the study are outlined in the Table. The unobstructed sunlight exposure exceeded the maximum measure of 40 mW/cm2, indicating there was a sufficient amount of sunlight to conduct testing.
The data show that both regular and sun-protective clothing blocked UVA/UVB rays in the 280- to 400-nm range. The Table outlines the level of UVA/UVB transmittance for each article of clothing; a lower number indicates less UVA/UVB transmittance occurred and more radiation was blocked.
Several of the regular clothing blocked more UV radiation than the sun-protective clothing; specifically, the data indicate that the baseball hats or the straw golf hat provided better protection than the sun-protective bucket hat. The black baseball hat provided the best UV protection. However, the straw golf hat provided adequate protection and better coverage, making it the best recommendation for patients.
Comment
Several of the regular items included in the study allowed less UVA/UVB transmission than the sun-protective clothing. Although our small study tested a limited number and type of articles, we assert that similar regular clothing would have similar transmittance.
There are various factors that affect UVA/UVB transmittance. Fabric construction, weight, thickness, composition, and color will affect the degree of UVA/UVB transmittance.1 In our study, the thickness, weave, and color of the fabric of the regular hats may have contributed to the superior results compared with the sun-protective hat. It could be postulated that cotton is inherently a superior fabric to the polyester sun-protective clothing fabric. With regard to the regular T-shirts, thickness, weave, and color also may have played a role in blocking UVA/UVB transmittance.
Patients may be assured of a sufficient amount of UVA/UVB blocking with sun-protective clothing. However, our study indicated that the regular clothing articles we tested provided similar, if not better, protection against UV radiation compared with the sun-protective clothing articles.
Conclusion
Based on the data, we would advise patients that they do not need to buy special sun-protective clothing that claims to block UV radiation, as regular clothing will provide equivalent protection against UVA/UVB radiation. However, these findings do not suggest that the claims for sun-protective clothing are inaccurate. Nevertheless, similar UVA/UVB blocking may be achieved with clothing already owned by patients.
1. Gies P. Photoprotection by clothing. Photodermatol Photoimmunol Photomed. 2007;23:264-274.
2. Wilson CA, Bevin NK, Laing RM, et al. Solar protection—effect of selected fabric and use characteristics on ultraviolet transmission. Textile Research Journal. 2008;78:95-104.
3. Ghazi S, Couteau C, Coiffard LJ. How to guarantee sun protection for a young sportsperson. J Dtsch Dermatol Ges. 2011;9:470-474.
4. Ghazi S, Couteau C, Coiffard LJ. What level of protection can be obtained using sun protective clothing? determining effectiveness using an in vitro method. Int J Pharm. 2010;397:144-146.
5. Morison WL. Photoprotection by clothing. Dermatol Ther. 2003;16:16-22.
Dermatologists frequently encounter patients who inquire about the need to buy special clothing and hats that claim to block UV light rather than using their regular clothing and hats. A patient may argue that he/she has never gotten sunburned through his/her favorite T-shirt while fishing, so why does he/she need to buy special clothing? The answer to this question is not straightforward. The dermatologist could easily say yes and advise patients to buy special sun-protective clothing, which could be especially tempting if a practitioner actually sells these items in the office. However, when considering evidence-based medicine, one needs to look at the data to appropriately answer the question.
Although it is still evolving, a standard has been set for UV protection factor (UPF) in the United States as well as other countries.1 Clothing with the maximum UPF rating of 50 blocks 98% of UVA/UVB radiation. Although there are data published in the literature regarding sun-protective clothing, there are scant data in the clinical dermatologic literature.2-5 To give patients an educated answer to this question, we measured and compared UVA/UVB radiation transmittance through regular (ie, non–UPF rated) clothing versus sun-protective clothing with a UPF rating.
Materials and Methods
A digital handheld UVA/UVB meter with an absorption spectrum of 280 to 400 nm was used to measure UV energy transmitted through sample clothing articles. The meter measured UVA/UVB light with a maximum reading of 40 mW/cm2. Clothing articles were selected of varied material/color and intended use.
Regular clothing articles included a straw golf hat (Figure 1A), an off-white and blue baseball hat (70% wool)(Figure 1B), a black baseball hat (100% wool)(Figure 1C), a white athletic tank shirt (100% cotton), a white T-shirt/undershirt (100% cotton), a thin-weave blue T-shirt (100% cotton), and a conventional-weave blue T-shirt (100% cotton)(Figure 1D). The regular clothing items, with the exception of the hats, had been laundered in conventional (ie, non–UV blocking) laundry detergent and no chemicals were applied to enhance UVA/UVB blocking properties. The exact number of times the items were laundered was unknown.
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| Figure 1. Regular clothing articles included a straw golf hat (A), an off-white and blue baseball hat (B), a black baseball hat (C), and white and blue T-shirts (D). |
Sun-protective clothing articles included a polyester floral splash bucket hat and a polyester ruffled swim romper (Figure 2), both with a UPF rating of 50+. These items were purchased from a manufacturer who regularly promotes sun-protective clothing to both dermatologists and the general public. The company “guarantees” a UPF rating of 50 and advertises that these clothing articles block 98% of harmful UV rays. These items were not laundered prior to the study, and no chemicals were applied to enhance UVA/UVB blocking properties.
The UVA/UVB meter was calibrated on a clear cloudless July day in Frankfort, Illinois. An initial reading was taken without any obstruction to the sunlight. The regular and sun-protective clothing articles then were placed over the meter to measure the amount of UVA/UVB transmitted through each item. Measurements were taken for each article of clothing after the meter was covered by the respective material for 10 seconds. Care was taken to cover the meter with only 1 layer of material for each article, which was intended to mimic the degree of UVA/UVB blocking and transmittance during normal wear.
Results
The full results from the study are outlined in the Table. The unobstructed sunlight exposure exceeded the maximum measure of 40 mW/cm2, indicating there was a sufficient amount of sunlight to conduct testing.
The data show that both regular and sun-protective clothing blocked UVA/UVB rays in the 280- to 400-nm range. The Table outlines the level of UVA/UVB transmittance for each article of clothing; a lower number indicates less UVA/UVB transmittance occurred and more radiation was blocked.
Several of the regular clothing blocked more UV radiation than the sun-protective clothing; specifically, the data indicate that the baseball hats or the straw golf hat provided better protection than the sun-protective bucket hat. The black baseball hat provided the best UV protection. However, the straw golf hat provided adequate protection and better coverage, making it the best recommendation for patients.
Comment
Several of the regular items included in the study allowed less UVA/UVB transmission than the sun-protective clothing. Although our small study tested a limited number and type of articles, we assert that similar regular clothing would have similar transmittance.
There are various factors that affect UVA/UVB transmittance. Fabric construction, weight, thickness, composition, and color will affect the degree of UVA/UVB transmittance.1 In our study, the thickness, weave, and color of the fabric of the regular hats may have contributed to the superior results compared with the sun-protective hat. It could be postulated that cotton is inherently a superior fabric to the polyester sun-protective clothing fabric. With regard to the regular T-shirts, thickness, weave, and color also may have played a role in blocking UVA/UVB transmittance.
Patients may be assured of a sufficient amount of UVA/UVB blocking with sun-protective clothing. However, our study indicated that the regular clothing articles we tested provided similar, if not better, protection against UV radiation compared with the sun-protective clothing articles.
Conclusion
Based on the data, we would advise patients that they do not need to buy special sun-protective clothing that claims to block UV radiation, as regular clothing will provide equivalent protection against UVA/UVB radiation. However, these findings do not suggest that the claims for sun-protective clothing are inaccurate. Nevertheless, similar UVA/UVB blocking may be achieved with clothing already owned by patients.
Dermatologists frequently encounter patients who inquire about the need to buy special clothing and hats that claim to block UV light rather than using their regular clothing and hats. A patient may argue that he/she has never gotten sunburned through his/her favorite T-shirt while fishing, so why does he/she need to buy special clothing? The answer to this question is not straightforward. The dermatologist could easily say yes and advise patients to buy special sun-protective clothing, which could be especially tempting if a practitioner actually sells these items in the office. However, when considering evidence-based medicine, one needs to look at the data to appropriately answer the question.
Although it is still evolving, a standard has been set for UV protection factor (UPF) in the United States as well as other countries.1 Clothing with the maximum UPF rating of 50 blocks 98% of UVA/UVB radiation. Although there are data published in the literature regarding sun-protective clothing, there are scant data in the clinical dermatologic literature.2-5 To give patients an educated answer to this question, we measured and compared UVA/UVB radiation transmittance through regular (ie, non–UPF rated) clothing versus sun-protective clothing with a UPF rating.
Materials and Methods
A digital handheld UVA/UVB meter with an absorption spectrum of 280 to 400 nm was used to measure UV energy transmitted through sample clothing articles. The meter measured UVA/UVB light with a maximum reading of 40 mW/cm2. Clothing articles were selected of varied material/color and intended use.
Regular clothing articles included a straw golf hat (Figure 1A), an off-white and blue baseball hat (70% wool)(Figure 1B), a black baseball hat (100% wool)(Figure 1C), a white athletic tank shirt (100% cotton), a white T-shirt/undershirt (100% cotton), a thin-weave blue T-shirt (100% cotton), and a conventional-weave blue T-shirt (100% cotton)(Figure 1D). The regular clothing items, with the exception of the hats, had been laundered in conventional (ie, non–UV blocking) laundry detergent and no chemicals were applied to enhance UVA/UVB blocking properties. The exact number of times the items were laundered was unknown.
|
|
|
|
| Figure 1. Regular clothing articles included a straw golf hat (A), an off-white and blue baseball hat (B), a black baseball hat (C), and white and blue T-shirts (D). |
Sun-protective clothing articles included a polyester floral splash bucket hat and a polyester ruffled swim romper (Figure 2), both with a UPF rating of 50+. These items were purchased from a manufacturer who regularly promotes sun-protective clothing to both dermatologists and the general public. The company “guarantees” a UPF rating of 50 and advertises that these clothing articles block 98% of harmful UV rays. These items were not laundered prior to the study, and no chemicals were applied to enhance UVA/UVB blocking properties.
The UVA/UVB meter was calibrated on a clear cloudless July day in Frankfort, Illinois. An initial reading was taken without any obstruction to the sunlight. The regular and sun-protective clothing articles then were placed over the meter to measure the amount of UVA/UVB transmitted through each item. Measurements were taken for each article of clothing after the meter was covered by the respective material for 10 seconds. Care was taken to cover the meter with only 1 layer of material for each article, which was intended to mimic the degree of UVA/UVB blocking and transmittance during normal wear.
Results
The full results from the study are outlined in the Table. The unobstructed sunlight exposure exceeded the maximum measure of 40 mW/cm2, indicating there was a sufficient amount of sunlight to conduct testing.
The data show that both regular and sun-protective clothing blocked UVA/UVB rays in the 280- to 400-nm range. The Table outlines the level of UVA/UVB transmittance for each article of clothing; a lower number indicates less UVA/UVB transmittance occurred and more radiation was blocked.
Several of the regular clothing blocked more UV radiation than the sun-protective clothing; specifically, the data indicate that the baseball hats or the straw golf hat provided better protection than the sun-protective bucket hat. The black baseball hat provided the best UV protection. However, the straw golf hat provided adequate protection and better coverage, making it the best recommendation for patients.
Comment
Several of the regular items included in the study allowed less UVA/UVB transmission than the sun-protective clothing. Although our small study tested a limited number and type of articles, we assert that similar regular clothing would have similar transmittance.
There are various factors that affect UVA/UVB transmittance. Fabric construction, weight, thickness, composition, and color will affect the degree of UVA/UVB transmittance.1 In our study, the thickness, weave, and color of the fabric of the regular hats may have contributed to the superior results compared with the sun-protective hat. It could be postulated that cotton is inherently a superior fabric to the polyester sun-protective clothing fabric. With regard to the regular T-shirts, thickness, weave, and color also may have played a role in blocking UVA/UVB transmittance.
Patients may be assured of a sufficient amount of UVA/UVB blocking with sun-protective clothing. However, our study indicated that the regular clothing articles we tested provided similar, if not better, protection against UV radiation compared with the sun-protective clothing articles.
Conclusion
Based on the data, we would advise patients that they do not need to buy special sun-protective clothing that claims to block UV radiation, as regular clothing will provide equivalent protection against UVA/UVB radiation. However, these findings do not suggest that the claims for sun-protective clothing are inaccurate. Nevertheless, similar UVA/UVB blocking may be achieved with clothing already owned by patients.
1. Gies P. Photoprotection by clothing. Photodermatol Photoimmunol Photomed. 2007;23:264-274.
2. Wilson CA, Bevin NK, Laing RM, et al. Solar protection—effect of selected fabric and use characteristics on ultraviolet transmission. Textile Research Journal. 2008;78:95-104.
3. Ghazi S, Couteau C, Coiffard LJ. How to guarantee sun protection for a young sportsperson. J Dtsch Dermatol Ges. 2011;9:470-474.
4. Ghazi S, Couteau C, Coiffard LJ. What level of protection can be obtained using sun protective clothing? determining effectiveness using an in vitro method. Int J Pharm. 2010;397:144-146.
5. Morison WL. Photoprotection by clothing. Dermatol Ther. 2003;16:16-22.
1. Gies P. Photoprotection by clothing. Photodermatol Photoimmunol Photomed. 2007;23:264-274.
2. Wilson CA, Bevin NK, Laing RM, et al. Solar protection—effect of selected fabric and use characteristics on ultraviolet transmission. Textile Research Journal. 2008;78:95-104.
3. Ghazi S, Couteau C, Coiffard LJ. How to guarantee sun protection for a young sportsperson. J Dtsch Dermatol Ges. 2011;9:470-474.
4. Ghazi S, Couteau C, Coiffard LJ. What level of protection can be obtained using sun protective clothing? determining effectiveness using an in vitro method. Int J Pharm. 2010;397:144-146.
5. Morison WL. Photoprotection by clothing. Dermatol Ther. 2003;16:16-22.
- Dermatologists routinely advise patients that clothing is a method of UVA/UVB protection.
- Regular clothing items provide similar, if not superior, UVA/UVB protection compared to sun-protective clothing.
- Physicians may confidently inform patients that regular clothing items will provide adequate UVA/UVB protection.
VIDEO: German screening initiative catches skin cancer sooner
EDINBURGH – Is population screening for skin cancer worthwhile?
Yes, Dr. Eckhard Breitbart said in a debate at the 15th World Congress on Cancers of the Skin. "Screening is not a diagnostic procedure," he noted. But the potential benefits of screening, including a significant reduction in medical costs, outweigh the potential harms related to false negative or false positive findings, added Dr. Breitbart, a dermatologist in Hamburg, Germany.
In an interview at the meeting, Dr. Breitbart reviewed the findings from his study of the impact of a population-based skin cancer screening program in Germany, and he discussed what research is needed to support such screening elsewhere.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
EDINBURGH – Is population screening for skin cancer worthwhile?
Yes, Dr. Eckhard Breitbart said in a debate at the 15th World Congress on Cancers of the Skin. "Screening is not a diagnostic procedure," he noted. But the potential benefits of screening, including a significant reduction in medical costs, outweigh the potential harms related to false negative or false positive findings, added Dr. Breitbart, a dermatologist in Hamburg, Germany.
In an interview at the meeting, Dr. Breitbart reviewed the findings from his study of the impact of a population-based skin cancer screening program in Germany, and he discussed what research is needed to support such screening elsewhere.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
EDINBURGH – Is population screening for skin cancer worthwhile?
Yes, Dr. Eckhard Breitbart said in a debate at the 15th World Congress on Cancers of the Skin. "Screening is not a diagnostic procedure," he noted. But the potential benefits of screening, including a significant reduction in medical costs, outweigh the potential harms related to false negative or false positive findings, added Dr. Breitbart, a dermatologist in Hamburg, Germany.
In an interview at the meeting, Dr. Breitbart reviewed the findings from his study of the impact of a population-based skin cancer screening program in Germany, and he discussed what research is needed to support such screening elsewhere.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
FROM THE 2014 WORLD CONGRESS ON CANCERS OF THE SKINS
Don’t overlook anus, genitalia during total body skin exam
CHICAGO – The anus and genitalia are often overlooked during total body skin examinations, leaving mucosal diseases to go unchecked, especially in women, according to Dr. Bethanee Schlosser.
She acknowledged that there is no literature to quantify the issue but said that her experience suggests mucocutaneous exams may be getting short shrift.
When Dr. Schlosser queried some 300 dermatologists assembled earlier this year, almost all said that they examine the oral cavity during total body skin exams; three-fourths responded that they routinely examine male patients’ genitalia. When asked whether they do the same for their female patients, less than 20 hands went up in the crowd.
"I think there are a couple of reasons for it," Dr. Schlosser of Northwestern University, Chicago, said at the American Academy of Dermatology summer meeting.
First, dermatologists don’t often look at the genitalia, so they may not know what the normal variations are.
Second, many patients don’t expect a dermatologist to examine genitalia. "Patients may be like, ‘You want to look where? I just have a mole on my chest.’ So it’s a matter of patient education," she said.
Third is the added time involved, and finally, some dermatologists are hesitant because they may not be comfortable managing mucosal disease should they find it.
Most dermatologists assume that gynecologists are evaluating their patients’ vulvar skin, but some gynecologists view the vulva more as "the doorway to the cervix. They may simply walk through it, not looking at what is around them, and to that effect, I don’t think it’s necessarily their fault, but their training," Dr. Schlosser said. "While vulvar disease is on the ob.gyn. board exam, the senior ob.gyn. residents rotate through our clinic with me and they routinely say they don’t get that education anywhere else."
Dr. Schlosser offered pearls for managing a number of mucosal diseases, including vulvar lichen sclerosis (VLS).
VLS affects about 1 in 600 women and can carry significant morbidity, including complete obliteration of the clitoral hood and labia minora, narrowing of the vaginal introitus, sexual dysfunction, and potential urinary obstruction, she said.
The risk of developing squamous cell carcinoma (SCC) in patients with VLS is 300-fold higher than in the general patient population. The specific risk factors for vulvar SCC are not fully elucidated in VLS, but include localized hyperkeratosis and age over 75 years.
"It’s important to realize that these older patients ... often don’t see their gynecologists because they’re told the pelvic examination is not indicated anymore," Dr. Schlosser said. "It really behooves us as dermatologists to be doing a genital exam as part of our total body skin exam."
Researchers think, but don’t have the evidence to suggest, that treating VLS changes the risk of SCC, "which is one of the hardest things to discuss with our patients," she added.
Suspicion of SCC should be raised if the patient has hyperkeratotic lesions; ulceration, even pinpoint in size, that doesn’t improve with standard therapy; erythematous, indurated plaques; or if the patient reports a change in symptom quality – previously itchy and now painful, for example – or a change in symptom distribution, such as previously all over and now localized to one spot.
"That can really herald that something bad has occurred," Dr. Schlosser cautioned.
Superpotent topical corticosteroids such as clobetasol propionate are first-line therapy for VLS, with no rationale to support the old-school treatment of topical testosterone. Maintenance therapy is common, as up to 85% of women will relapse.
Dr. Schlosser also advised physicians to educate women on how much medication to use, to send them home with a diagram of the affected area, and to use a hand mirror during the exam.
"Patients don’t want to look, but I tell them you’re not going to get better if you don’t know where to put your medication," she said.
Dr. Schlosser reported no relevant conflicts of interest.
CHICAGO – The anus and genitalia are often overlooked during total body skin examinations, leaving mucosal diseases to go unchecked, especially in women, according to Dr. Bethanee Schlosser.
She acknowledged that there is no literature to quantify the issue but said that her experience suggests mucocutaneous exams may be getting short shrift.
When Dr. Schlosser queried some 300 dermatologists assembled earlier this year, almost all said that they examine the oral cavity during total body skin exams; three-fourths responded that they routinely examine male patients’ genitalia. When asked whether they do the same for their female patients, less than 20 hands went up in the crowd.
"I think there are a couple of reasons for it," Dr. Schlosser of Northwestern University, Chicago, said at the American Academy of Dermatology summer meeting.
First, dermatologists don’t often look at the genitalia, so they may not know what the normal variations are.
Second, many patients don’t expect a dermatologist to examine genitalia. "Patients may be like, ‘You want to look where? I just have a mole on my chest.’ So it’s a matter of patient education," she said.
Third is the added time involved, and finally, some dermatologists are hesitant because they may not be comfortable managing mucosal disease should they find it.
Most dermatologists assume that gynecologists are evaluating their patients’ vulvar skin, but some gynecologists view the vulva more as "the doorway to the cervix. They may simply walk through it, not looking at what is around them, and to that effect, I don’t think it’s necessarily their fault, but their training," Dr. Schlosser said. "While vulvar disease is on the ob.gyn. board exam, the senior ob.gyn. residents rotate through our clinic with me and they routinely say they don’t get that education anywhere else."
Dr. Schlosser offered pearls for managing a number of mucosal diseases, including vulvar lichen sclerosis (VLS).
VLS affects about 1 in 600 women and can carry significant morbidity, including complete obliteration of the clitoral hood and labia minora, narrowing of the vaginal introitus, sexual dysfunction, and potential urinary obstruction, she said.
The risk of developing squamous cell carcinoma (SCC) in patients with VLS is 300-fold higher than in the general patient population. The specific risk factors for vulvar SCC are not fully elucidated in VLS, but include localized hyperkeratosis and age over 75 years.
"It’s important to realize that these older patients ... often don’t see their gynecologists because they’re told the pelvic examination is not indicated anymore," Dr. Schlosser said. "It really behooves us as dermatologists to be doing a genital exam as part of our total body skin exam."
Researchers think, but don’t have the evidence to suggest, that treating VLS changes the risk of SCC, "which is one of the hardest things to discuss with our patients," she added.
Suspicion of SCC should be raised if the patient has hyperkeratotic lesions; ulceration, even pinpoint in size, that doesn’t improve with standard therapy; erythematous, indurated plaques; or if the patient reports a change in symptom quality – previously itchy and now painful, for example – or a change in symptom distribution, such as previously all over and now localized to one spot.
"That can really herald that something bad has occurred," Dr. Schlosser cautioned.
Superpotent topical corticosteroids such as clobetasol propionate are first-line therapy for VLS, with no rationale to support the old-school treatment of topical testosterone. Maintenance therapy is common, as up to 85% of women will relapse.
Dr. Schlosser also advised physicians to educate women on how much medication to use, to send them home with a diagram of the affected area, and to use a hand mirror during the exam.
"Patients don’t want to look, but I tell them you’re not going to get better if you don’t know where to put your medication," she said.
Dr. Schlosser reported no relevant conflicts of interest.
CHICAGO – The anus and genitalia are often overlooked during total body skin examinations, leaving mucosal diseases to go unchecked, especially in women, according to Dr. Bethanee Schlosser.
She acknowledged that there is no literature to quantify the issue but said that her experience suggests mucocutaneous exams may be getting short shrift.
When Dr. Schlosser queried some 300 dermatologists assembled earlier this year, almost all said that they examine the oral cavity during total body skin exams; three-fourths responded that they routinely examine male patients’ genitalia. When asked whether they do the same for their female patients, less than 20 hands went up in the crowd.
"I think there are a couple of reasons for it," Dr. Schlosser of Northwestern University, Chicago, said at the American Academy of Dermatology summer meeting.
First, dermatologists don’t often look at the genitalia, so they may not know what the normal variations are.
Second, many patients don’t expect a dermatologist to examine genitalia. "Patients may be like, ‘You want to look where? I just have a mole on my chest.’ So it’s a matter of patient education," she said.
Third is the added time involved, and finally, some dermatologists are hesitant because they may not be comfortable managing mucosal disease should they find it.
Most dermatologists assume that gynecologists are evaluating their patients’ vulvar skin, but some gynecologists view the vulva more as "the doorway to the cervix. They may simply walk through it, not looking at what is around them, and to that effect, I don’t think it’s necessarily their fault, but their training," Dr. Schlosser said. "While vulvar disease is on the ob.gyn. board exam, the senior ob.gyn. residents rotate through our clinic with me and they routinely say they don’t get that education anywhere else."
Dr. Schlosser offered pearls for managing a number of mucosal diseases, including vulvar lichen sclerosis (VLS).
VLS affects about 1 in 600 women and can carry significant morbidity, including complete obliteration of the clitoral hood and labia minora, narrowing of the vaginal introitus, sexual dysfunction, and potential urinary obstruction, she said.
The risk of developing squamous cell carcinoma (SCC) in patients with VLS is 300-fold higher than in the general patient population. The specific risk factors for vulvar SCC are not fully elucidated in VLS, but include localized hyperkeratosis and age over 75 years.
"It’s important to realize that these older patients ... often don’t see their gynecologists because they’re told the pelvic examination is not indicated anymore," Dr. Schlosser said. "It really behooves us as dermatologists to be doing a genital exam as part of our total body skin exam."
Researchers think, but don’t have the evidence to suggest, that treating VLS changes the risk of SCC, "which is one of the hardest things to discuss with our patients," she added.
Suspicion of SCC should be raised if the patient has hyperkeratotic lesions; ulceration, even pinpoint in size, that doesn’t improve with standard therapy; erythematous, indurated plaques; or if the patient reports a change in symptom quality – previously itchy and now painful, for example – or a change in symptom distribution, such as previously all over and now localized to one spot.
"That can really herald that something bad has occurred," Dr. Schlosser cautioned.
Superpotent topical corticosteroids such as clobetasol propionate are first-line therapy for VLS, with no rationale to support the old-school treatment of topical testosterone. Maintenance therapy is common, as up to 85% of women will relapse.
Dr. Schlosser also advised physicians to educate women on how much medication to use, to send them home with a diagram of the affected area, and to use a hand mirror during the exam.
"Patients don’t want to look, but I tell them you’re not going to get better if you don’t know where to put your medication," she said.
Dr. Schlosser reported no relevant conflicts of interest.
EXPERT ANALYSIS FROM THE AAD SUMMER ACADEMY 2014
Nonsurgical Alternatives for Skin Cancer Treatment: Report From the AAD Meeting
An important topic at the 2014 Summer AAD Meeting in Chicago, Illinois, was the nonsurgical treatment of skin cancers, including adjuvant therapy, topical creams, photodynamic therapy, and radiation for melanoma and nonmelanoma skin cancers. Dr. Anthony M. Rossi discusses the benefits of some of these nonsurgical treatment options for skin cancers and describes how he uses them in his practice. He also discusses how to determine which treatment option is best for each patient and emphasizes the importance of patient compliance and close follow-up.
An important topic at the 2014 Summer AAD Meeting in Chicago, Illinois, was the nonsurgical treatment of skin cancers, including adjuvant therapy, topical creams, photodynamic therapy, and radiation for melanoma and nonmelanoma skin cancers. Dr. Anthony M. Rossi discusses the benefits of some of these nonsurgical treatment options for skin cancers and describes how he uses them in his practice. He also discusses how to determine which treatment option is best for each patient and emphasizes the importance of patient compliance and close follow-up.
An important topic at the 2014 Summer AAD Meeting in Chicago, Illinois, was the nonsurgical treatment of skin cancers, including adjuvant therapy, topical creams, photodynamic therapy, and radiation for melanoma and nonmelanoma skin cancers. Dr. Anthony M. Rossi discusses the benefits of some of these nonsurgical treatment options for skin cancers and describes how he uses them in his practice. He also discusses how to determine which treatment option is best for each patient and emphasizes the importance of patient compliance and close follow-up.
AUDIO: Unusual approaches to unusual tumors
CHICAGO – Doctors who don’t abide by accepted norms can sometimes achieve better outcomes when treating patients who have unusual and tenacious tumors. This was the theme of a session covering cases of confounding tumors at the American Academy of Dermatology summer meeting.
In an interview after the session, panel moderator and case presenter Dr. John A. Carucci, chief of Mohs and dermatologic surgery at New York (N.Y.) University, shared his thoughts on when certain kinds of imaging are more appropriate than others, even if it’s not the "usual way."
Dr. Carucci also addressed the use of postsurgical negative pressure wound therapy, radiation therapy in conjunction with Mohs surgery, and potentially controversial topics such as the use of a protein kinase inhibitor as a neoadjuvant therapy.
And what new information on staging squamous cell carcinomas has Dr. Carucci and his colleagues excited? Listen and find out. Dr. Carucci said that he had no financial conflicts to disclose.
On Twitter @whitneymcknight
CHICAGO – Doctors who don’t abide by accepted norms can sometimes achieve better outcomes when treating patients who have unusual and tenacious tumors. This was the theme of a session covering cases of confounding tumors at the American Academy of Dermatology summer meeting.
In an interview after the session, panel moderator and case presenter Dr. John A. Carucci, chief of Mohs and dermatologic surgery at New York (N.Y.) University, shared his thoughts on when certain kinds of imaging are more appropriate than others, even if it’s not the "usual way."
Dr. Carucci also addressed the use of postsurgical negative pressure wound therapy, radiation therapy in conjunction with Mohs surgery, and potentially controversial topics such as the use of a protein kinase inhibitor as a neoadjuvant therapy.
And what new information on staging squamous cell carcinomas has Dr. Carucci and his colleagues excited? Listen and find out. Dr. Carucci said that he had no financial conflicts to disclose.
On Twitter @whitneymcknight
CHICAGO – Doctors who don’t abide by accepted norms can sometimes achieve better outcomes when treating patients who have unusual and tenacious tumors. This was the theme of a session covering cases of confounding tumors at the American Academy of Dermatology summer meeting.
In an interview after the session, panel moderator and case presenter Dr. John A. Carucci, chief of Mohs and dermatologic surgery at New York (N.Y.) University, shared his thoughts on when certain kinds of imaging are more appropriate than others, even if it’s not the "usual way."
Dr. Carucci also addressed the use of postsurgical negative pressure wound therapy, radiation therapy in conjunction with Mohs surgery, and potentially controversial topics such as the use of a protein kinase inhibitor as a neoadjuvant therapy.
And what new information on staging squamous cell carcinomas has Dr. Carucci and his colleagues excited? Listen and find out. Dr. Carucci said that he had no financial conflicts to disclose.
On Twitter @whitneymcknight
EXPERT ANALYSIS FROM THE AAD SUMMER ACADEMY 2014
What Is Your Diagnosis? Granulocytic Sarcoma
A 24-year-old man presented with a 5-cm asymptomatic, indurated, well-defined nodule with a violaceous center surrounded by a greenish halo on the lower back of 3 months’ duration, along with lymphadenopathy. There was no history of trauma, weight loss, bleeding, or systemic illness. A biopsy revealed sheets of pleomorphic cells with lobulated nuclei and detectable granular cytoplasm. Immunohistochemistry showed strong myeloperoxidase activity in neoplastic cells that were CD13- and CD56-.
The Diagnosis: Granulocytic Sarcoma
Granulocytic sarcoma (GS), sometimes known as leukemia cutis, myeloid sarcoma, or an extramedullary myeloid tumor, is a rare localized collection of immature cells of granulocytic series or the cells of each maturation step in extramedullary sites. Originally described in 1811, the condition was noted after identifying an extramedullary collection of immature granulocytes involving the orbit. Then in 1853 the term chloroma was coined because of the greenish appearance of the tumor when exposed to light due to myeloperoxidase activity in the tumor cells. Finally, in 1967 the term granulocytic sarcoma was introduced because the greenish appearance was not observed in all cases, providing a more correct term.1
Granulocytic sarcoma often manifests in patients with acute myeloid leukemia, chronic myelogenous leukemia, chronic idiopathic myelofibrosis, eosinophilia, refractory anemia, or polycythemia vera, and as an isolated form in patients without apparent hematologic disorder.2
Cutaneous manifestations of leukemia can be specific (eg, GS) or nonspecific (eg, panniculitis, generalized pruritus).2,3 The tumor often appears as a solitary mass (Figure 1); however, in rare instances it can be multifocal. It usually presents as a rapidly growing nodular mass with solid consistence, and it is seen in patients of any age but most often those aged 45 to 55 years as well as in patients younger than 15 years.4
Granulocytic sarcoma is most commonly associated with acute myeloid leukemia. However, it is interesting that the chloroma appears before the onset of leukemia. Occasionally GS is associated with acute myeloid leukemia as a presenting symptom or as a manifestation of recurrence of the disease that was usually related to poor prognosis.5 In patients with GS that is associated with myeloproliferative neoplasms, the occurrence of GS frequently is associated with acute transformation of the disease and therefore a poor prognosis.6
The most common sites of involvement are bone, soft tissue, lymph nodes, and skin. The prognosis does not vary according to location.
Cutaneous B-cell lymphoma should be considered in the differential diagnosis, as it may be clinically observed as single or multiple violaceous nodules involving the head, neck, and/or trunk. Histologically, there generally is a bottom-heavy infiltrate of lymphocytes sparing the epidermis (Figure 2). Immunohistochemistry, flow cytometry, or cytochemical stains often are needed to exclude lymphoma. Pseudochloroma is a rare disease characterized by a collection of normal hematopoietic tissue in locations other than GS. It can be distinguished from GS by its constituent of mature cells.7
Granulocytic sarcoma implies a therapeutic challenge for the clinician. It should always be considered as part of a systemic disease rather than an isolated skin disorder. In patients with evidence of leukemia and GS, systemic chemotherapy is the first line of treatment. Other effective treatment regimens include radiotherapy (electron beam radiation), either alone or in combination with systemic chemotherapy (eg, hydroxyurea, methotrexate).8 If GS persists after chemotherapy, local treatment (eg, radiotherapy, surgery) should be considered with variable results.2
1. Meis JM, Butler JJ, Osborne BM, et al. Granulocytic sarcoma in nonleukemic patients. Cancer. 1986;58:2697-2709.
2. Sun NCJ, Ellis R. Granulocytic sarcoma of the skin. Arch Dermatol. 1980;116:800-802.
3. Campidelli C, Agostinelli C, Stitson R, et al. Myeloid sarcoma. Extramedullary manifestation of myeloid disorders. Am J Clin Pathol. 2009;132:426-437.
4. Pulsoni A, Falcucci P, Anghel G, et al. Isolated granulocytic sarcoma of the skin in an elderly patient: good response to treatment with local radiotherapy and low dose methotrexate. J Eur Acad Dermatol Venereol. 2000;14:216-218.
5. Neiman RS, Barcos M, Berard C, et al. Granulocytic sarcoma: a clinicopathologic study of 61 biopsied cases. Cancer. 1981;48:1426-1437.
6. Byrd JC, Edenfield WJ, Dow NS, et al. Extramedullary myeloid cell tumors in myelodysplastic syndromes: not a true indication of impending acute myeloid leukemia. Leukemia. 1996;21:153-159.
7. Beswick SJ, Jones EL, Mahendra P, et al. Chloroma (aleukaemic leukaemia cutis) initially diagnosed as a cutaneous lymphoma. Clin Exp Dermatol. 2002;27:272-274.
8. Chen WY, Wang CW, Chang CH, et al. Clinicopathologic features and responses to radiotherapy of myeloid sarcoma. Radiat Oncol. 2013;8:245.
A 24-year-old man presented with a 5-cm asymptomatic, indurated, well-defined nodule with a violaceous center surrounded by a greenish halo on the lower back of 3 months’ duration, along with lymphadenopathy. There was no history of trauma, weight loss, bleeding, or systemic illness. A biopsy revealed sheets of pleomorphic cells with lobulated nuclei and detectable granular cytoplasm. Immunohistochemistry showed strong myeloperoxidase activity in neoplastic cells that were CD13- and CD56-.
The Diagnosis: Granulocytic Sarcoma
Granulocytic sarcoma (GS), sometimes known as leukemia cutis, myeloid sarcoma, or an extramedullary myeloid tumor, is a rare localized collection of immature cells of granulocytic series or the cells of each maturation step in extramedullary sites. Originally described in 1811, the condition was noted after identifying an extramedullary collection of immature granulocytes involving the orbit. Then in 1853 the term chloroma was coined because of the greenish appearance of the tumor when exposed to light due to myeloperoxidase activity in the tumor cells. Finally, in 1967 the term granulocytic sarcoma was introduced because the greenish appearance was not observed in all cases, providing a more correct term.1
Granulocytic sarcoma often manifests in patients with acute myeloid leukemia, chronic myelogenous leukemia, chronic idiopathic myelofibrosis, eosinophilia, refractory anemia, or polycythemia vera, and as an isolated form in patients without apparent hematologic disorder.2
Cutaneous manifestations of leukemia can be specific (eg, GS) or nonspecific (eg, panniculitis, generalized pruritus).2,3 The tumor often appears as a solitary mass (Figure 1); however, in rare instances it can be multifocal. It usually presents as a rapidly growing nodular mass with solid consistence, and it is seen in patients of any age but most often those aged 45 to 55 years as well as in patients younger than 15 years.4
Granulocytic sarcoma is most commonly associated with acute myeloid leukemia. However, it is interesting that the chloroma appears before the onset of leukemia. Occasionally GS is associated with acute myeloid leukemia as a presenting symptom or as a manifestation of recurrence of the disease that was usually related to poor prognosis.5 In patients with GS that is associated with myeloproliferative neoplasms, the occurrence of GS frequently is associated with acute transformation of the disease and therefore a poor prognosis.6
The most common sites of involvement are bone, soft tissue, lymph nodes, and skin. The prognosis does not vary according to location.
Cutaneous B-cell lymphoma should be considered in the differential diagnosis, as it may be clinically observed as single or multiple violaceous nodules involving the head, neck, and/or trunk. Histologically, there generally is a bottom-heavy infiltrate of lymphocytes sparing the epidermis (Figure 2). Immunohistochemistry, flow cytometry, or cytochemical stains often are needed to exclude lymphoma. Pseudochloroma is a rare disease characterized by a collection of normal hematopoietic tissue in locations other than GS. It can be distinguished from GS by its constituent of mature cells.7
Granulocytic sarcoma implies a therapeutic challenge for the clinician. It should always be considered as part of a systemic disease rather than an isolated skin disorder. In patients with evidence of leukemia and GS, systemic chemotherapy is the first line of treatment. Other effective treatment regimens include radiotherapy (electron beam radiation), either alone or in combination with systemic chemotherapy (eg, hydroxyurea, methotrexate).8 If GS persists after chemotherapy, local treatment (eg, radiotherapy, surgery) should be considered with variable results.2
A 24-year-old man presented with a 5-cm asymptomatic, indurated, well-defined nodule with a violaceous center surrounded by a greenish halo on the lower back of 3 months’ duration, along with lymphadenopathy. There was no history of trauma, weight loss, bleeding, or systemic illness. A biopsy revealed sheets of pleomorphic cells with lobulated nuclei and detectable granular cytoplasm. Immunohistochemistry showed strong myeloperoxidase activity in neoplastic cells that were CD13- and CD56-.
The Diagnosis: Granulocytic Sarcoma
Granulocytic sarcoma (GS), sometimes known as leukemia cutis, myeloid sarcoma, or an extramedullary myeloid tumor, is a rare localized collection of immature cells of granulocytic series or the cells of each maturation step in extramedullary sites. Originally described in 1811, the condition was noted after identifying an extramedullary collection of immature granulocytes involving the orbit. Then in 1853 the term chloroma was coined because of the greenish appearance of the tumor when exposed to light due to myeloperoxidase activity in the tumor cells. Finally, in 1967 the term granulocytic sarcoma was introduced because the greenish appearance was not observed in all cases, providing a more correct term.1
Granulocytic sarcoma often manifests in patients with acute myeloid leukemia, chronic myelogenous leukemia, chronic idiopathic myelofibrosis, eosinophilia, refractory anemia, or polycythemia vera, and as an isolated form in patients without apparent hematologic disorder.2
Cutaneous manifestations of leukemia can be specific (eg, GS) or nonspecific (eg, panniculitis, generalized pruritus).2,3 The tumor often appears as a solitary mass (Figure 1); however, in rare instances it can be multifocal. It usually presents as a rapidly growing nodular mass with solid consistence, and it is seen in patients of any age but most often those aged 45 to 55 years as well as in patients younger than 15 years.4
Granulocytic sarcoma is most commonly associated with acute myeloid leukemia. However, it is interesting that the chloroma appears before the onset of leukemia. Occasionally GS is associated with acute myeloid leukemia as a presenting symptom or as a manifestation of recurrence of the disease that was usually related to poor prognosis.5 In patients with GS that is associated with myeloproliferative neoplasms, the occurrence of GS frequently is associated with acute transformation of the disease and therefore a poor prognosis.6
The most common sites of involvement are bone, soft tissue, lymph nodes, and skin. The prognosis does not vary according to location.
Cutaneous B-cell lymphoma should be considered in the differential diagnosis, as it may be clinically observed as single or multiple violaceous nodules involving the head, neck, and/or trunk. Histologically, there generally is a bottom-heavy infiltrate of lymphocytes sparing the epidermis (Figure 2). Immunohistochemistry, flow cytometry, or cytochemical stains often are needed to exclude lymphoma. Pseudochloroma is a rare disease characterized by a collection of normal hematopoietic tissue in locations other than GS. It can be distinguished from GS by its constituent of mature cells.7
Granulocytic sarcoma implies a therapeutic challenge for the clinician. It should always be considered as part of a systemic disease rather than an isolated skin disorder. In patients with evidence of leukemia and GS, systemic chemotherapy is the first line of treatment. Other effective treatment regimens include radiotherapy (electron beam radiation), either alone or in combination with systemic chemotherapy (eg, hydroxyurea, methotrexate).8 If GS persists after chemotherapy, local treatment (eg, radiotherapy, surgery) should be considered with variable results.2
1. Meis JM, Butler JJ, Osborne BM, et al. Granulocytic sarcoma in nonleukemic patients. Cancer. 1986;58:2697-2709.
2. Sun NCJ, Ellis R. Granulocytic sarcoma of the skin. Arch Dermatol. 1980;116:800-802.
3. Campidelli C, Agostinelli C, Stitson R, et al. Myeloid sarcoma. Extramedullary manifestation of myeloid disorders. Am J Clin Pathol. 2009;132:426-437.
4. Pulsoni A, Falcucci P, Anghel G, et al. Isolated granulocytic sarcoma of the skin in an elderly patient: good response to treatment with local radiotherapy and low dose methotrexate. J Eur Acad Dermatol Venereol. 2000;14:216-218.
5. Neiman RS, Barcos M, Berard C, et al. Granulocytic sarcoma: a clinicopathologic study of 61 biopsied cases. Cancer. 1981;48:1426-1437.
6. Byrd JC, Edenfield WJ, Dow NS, et al. Extramedullary myeloid cell tumors in myelodysplastic syndromes: not a true indication of impending acute myeloid leukemia. Leukemia. 1996;21:153-159.
7. Beswick SJ, Jones EL, Mahendra P, et al. Chloroma (aleukaemic leukaemia cutis) initially diagnosed as a cutaneous lymphoma. Clin Exp Dermatol. 2002;27:272-274.
8. Chen WY, Wang CW, Chang CH, et al. Clinicopathologic features and responses to radiotherapy of myeloid sarcoma. Radiat Oncol. 2013;8:245.
1. Meis JM, Butler JJ, Osborne BM, et al. Granulocytic sarcoma in nonleukemic patients. Cancer. 1986;58:2697-2709.
2. Sun NCJ, Ellis R. Granulocytic sarcoma of the skin. Arch Dermatol. 1980;116:800-802.
3. Campidelli C, Agostinelli C, Stitson R, et al. Myeloid sarcoma. Extramedullary manifestation of myeloid disorders. Am J Clin Pathol. 2009;132:426-437.
4. Pulsoni A, Falcucci P, Anghel G, et al. Isolated granulocytic sarcoma of the skin in an elderly patient: good response to treatment with local radiotherapy and low dose methotrexate. J Eur Acad Dermatol Venereol. 2000;14:216-218.
5. Neiman RS, Barcos M, Berard C, et al. Granulocytic sarcoma: a clinicopathologic study of 61 biopsied cases. Cancer. 1981;48:1426-1437.
6. Byrd JC, Edenfield WJ, Dow NS, et al. Extramedullary myeloid cell tumors in myelodysplastic syndromes: not a true indication of impending acute myeloid leukemia. Leukemia. 1996;21:153-159.
7. Beswick SJ, Jones EL, Mahendra P, et al. Chloroma (aleukaemic leukaemia cutis) initially diagnosed as a cutaneous lymphoma. Clin Exp Dermatol. 2002;27:272-274.
8. Chen WY, Wang CW, Chang CH, et al. Clinicopathologic features and responses to radiotherapy of myeloid sarcoma. Radiat Oncol. 2013;8:245.