RESUMO
OBJECTIVE: Previous studies have shown that dermatologists detect thinner melanomas than both non-dermatologists and patients in high incidence areas. The authors report depths of melanomas in a central New York practice where the incidence is low, hypothesizing that incidental melanomas detected by a dermatologist will be thinner than melanomas that are part of the chief complaint. DESIGN: A retrospective chart review examining melanoma depth to determine the importance of universal full skin exams. SETTING: Private dermatology clinic in Auburn, New York, employing one board-certified dermatologist and two physician extenders. PARTICIPANTS: Men and women who attended the clinic between 2003 and 2013 who had 235 biopsy-proven melanomas. Total patient visits in this time period was 50,699. MEASUREMENTS: Office notes were reviewed to determine the chief complaint, patient demographics, and depth of the tumor. The authors noted if the melanoma was discovered by the patient, a referring physician, dermatology physician extender, or the dermatologist. RESULTS: More than 45 percent of melanomas were an incidental finding on full skin exam. The dermatologist detected statistically thinner melanomas than melanomas that presented as the chief complaint. The dermatologist tended to detect thinner melanomas than referring physicians and patients. CONCLUSION: A significant portion of melanomas are incidentally found on full skin exam, and thinner melanomas are detected by dermatologists. Universal skin cancer screening takes little additional time, and appropriate use of physician extenders can greatly increase access to dermatological care. Full skin exams increase melanoma detection, decreases overall thickness at diagnosis, and decreases patient morbidity and mortality.
RESUMO
BACKGROUND: Pseudoporphyria is a diagnosis that is used when porphyria-like clinical lesions arise in the setting of normal porphyrin levels. This condition was first described in the 1960s and was initially related to the use of certain antibiotic drugs. In 1985, pseudoporphyria was first attributed to the use of nonsteroidal antiinflammatory drugs (NSAIDs). Subsequently, a host of NSAIDs and other drugs have been found to elicit the same clinical entity. The exact mechanism by which certain drugs create clinical lesions resembling porphyria cutanea tarda or erythropoietic protoporphyria is still unknown. A phototoxic mechanism is hypothesized. OBJECTIVE: We describe six patients diagnosed with pseudoporphyria and detail the diagnostic tests leading to the eventual diagnosis. RESULTS: The patients ranged in age from 27 to 59 years and had a female:male predominance of 2:1. The offending NSAID was DayPro (oxaprozin) for three of the patients, Relafen (nabumetone) for two of the patients, and Aleve (naproxen) for one patient. For each patient, histology and immunofluorescence was either consistent with the diagnosis of porphyria cutanea tarda or nonspecific, while serum, stool, and urine porphyrins did not support that diagnosis. Withdrawal of the offending agent provided relief from the clinical symptoms for each patient. None of our patients were rechallenged with the putative offending drug. However, prolonged avoidance has provided a sustained remission from symptoms in all six patients. CONCLUSIONS: Pseudoporphyria is a relatively rarely reported condition. Clinical suspicion with appropriate laboratory and histopathologic findings help to make this diagnosis, and exclude true porphyrias. Rechallenge with the offending drug to produce symptom relapse has been proposed to be helpful in confirming this diagnosis of exclusion. Since all 6 patients with drug-induced pseudoporphyria experienced resolution of their symptoms after discontinuing the offending agent, we propose that this clinical correlation alone is sufficient to confirm this diagnosis. Our observation of six new cases of NSAID-induced pseudoporphyria over a two-year interval suggests that this is not a rare entity.
