To compare the efficacy, tolerability, and cosmetic outcome of photodynamic therapy (PDT) using topical methyl aminolevulinate with cryotherapy or topical fluorouracil for treatment of squamous cell carcinoma in situ. Design: Randomized, placebo-controlled study, with follow-up at 3 and 12 months after last treatment. Setting: Forty outpatient dermatology centers in 11 European countries. Patients: Random sample of 225 patients with histologically confirmed squamous cell carcinoma in situ (lesion size, 6-40 mm) and no evidence of progression. Interventions: Treatment with PDT with methyl aminolevulinate (160 mg/g; n=96) or matching placebo cream (n=17), cryotherapy (n=82), or topical fluorouracil (5% cream; n=30). Methyl aminolevulinate or placebo cream was applied for 3 hours before illumination with broadband red light (75 J/cm 2 , 570-670 nm). Treatment was repeated 1 week later. Cryotherapy was performed with liquid nitrogen spray. Fluorouracil was applied for 4 weeks. Lesions with a partial response at 3 months were retreated. Main Outcome Measures: Clinically verified complete response of lesions; blinded and on-site assessment of cosmetic outcome (4-point rating scale). Results: At 12 months, the estimated sustained lesion complete response rate with methyl aminolevulinate PDT was superior to that with cryotherapy (80% vs 67%; odds ratio, 1.77; 95% confidence interval, 1.01-3.12; P=.047), and better than that with fluorouracil (80% vs 69%; odds ratio, 1.64; 95% confidence interval, 0.78-3.45; P=.19). Cosmetic outcome at 3 months was good or excellent in 94% of patients treated with methyl aminolevulinate PDT vs 66% with cryotherapy and 76% with fluorouracil, and was maintained at 12 months. Conclusion: Methyl aminolevulinate PDT is an effective treatment option for squamous cell carcinoma in situ, with excellent cosmesis.

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To identify potential risk factors and the yield of routine screens for early detection of malignancy associated with dermatomyositis (DM) and polymyositis (PM). Design: Retrospective study of malignancies in all patients with DM or PM followed up between the years 1981 and 2000 and a review of the relationship of DM and PM to malignancy, the usefulness of various tests or examinations for malignancy search, and the patients' course. Setting: Departments of internal medicine and dermatology in a teaching hospital. Patients: Forty consecutive adult patients with DM (33 cases) or PM (7 cases). Main Outcome Measures: (1) Rate of false-negative results of routine workup and yield (percentage of positive results) of blind malignancy search and (2) comparison of 16 characteristics in patients with malignancy vs those without. Results: Malignancy occurred in 16 patients: 13 with DM and 3 with PM. In all cases, the diagnosis of malignancy was made concurrently with or shortly after the diagnosis of DM or PM. Factors associated with malignancy were recruitment in the internal medicine department (P=.02), constitutional symptoms (PϽ.01), a rapid onset of DM or PM (P=.02), the lack of Raynaud phenomenon (PϽ .01), and a higher mean erythrocyte sedimentation rate (PϽ.01) and creatine kinase level (PϽ.01). Initial routine search failed to discover 4 malignancies, 3 of which were discovered at an advanced stage by more extensive investigations. The positive result yield of blind malignancy search was only 13% (11 of 87), but reached 28% (5 of 18) for blind abdominal-pelvic and thoracic computed tomographic scans. Conclusion: Extensive search for malignancy, particularly computed tomographic scans, may be warranted in at least a subset of patients with DM or PM and risk factors of malignancy.

To assess the rate of objective response to pegylated liposomal doxorubicin hydrochloride (Caelyx) in patients with advanced or refractory cutaneous T-cell lymphoma (CTCL).

Although cemiplimab has been approved for locally advanced (la) and metastatic (m) cutaneous squamous-cell carcinomas (CSCCs), its real-life value has not yet been demonstrated. An early-access program enrolled patients with la/mCSCCs to receive cemiplimab. Endpoints were best overall response rate (BOR), progression-free survival (PFS), overall survival (OS), duration of response (DOR) and safety. The 245 patients (mean age 77 years, 73% male, 49% prior systemic treatment, 24% immunocompromised, 27% Eastern Cooperative Oncology Group performance status (PS) ≥ 2) had laCSCCs (35%) or mCSCCs (65%). For the 240 recipients of ≥1 infusion(s), the BOR was 50.4% (complete, 21%; partial, 29%). With median follow-up at 12.6 months, median PFS was 7.9 months, and median OS and DOR were not reached. One-year OS was 73% versus 36%, respectively, for patients with PS < 2 versus ≥ 2. Multivariate analysis retained PS ≥ 2 as being associated during the first 6 months with PFS and OS. Head-and-neck location was associated with longer PFS. Immune status had no impact. Severe treatment-related adverse events occurred in 9% of the patients, including one death from toxic epidermal necrolysis. Cemiplimab real-life safety and efficacy support its use for la/mCSCCs. Patients with PS ≥ 2 benefited less from cemiplimab, but it might represent an option for immunocompromised patients.

Mutated oncogenic KIT is a therapeutic target in melanoma. We conducted a multicenter phase II trial on the KIT inhibitor nilotinib in patients with unresectable melanoma harboring KIT alteration. The primary endpoint was the response rate (complete response or partial response following Response Evaluation Criteria in Solid Tumors criteria) at 6 months. Pharmacodynamic studies using KIT sequencing, qPCR array, and immunostaining of downstream KIT effectors were performed during treatment. Twenty-five patients were included and received 400 mg oral nilotinib twice daily. At 6 months, nilotinib induced tumor response in four patients. The best overall response rate was 20% and the disease control rate was 56%, limited to patients harboring exon 11 or 13 mutations. Four patients exhibited durable response, including three persisting (3.6 and 2.8 years for two patients with stage IIIC and 2.5 years for one with IVM1b melanoma). A reduction in signal transducer and activator of transcription (STAT) 3 phosphorylation and its effectors (BCL-2, MCL-1) in tumors during follow-up was significantly associated with clinical response. In the KIT-mutated melanoma cell line M230, nilotinib reduced STAT3 signaling and STAT inhibitors were as efficient as KIT inhibitors in reducing cell proliferation. Our study evidences a significant association between STAT3 inhibition and response to nilotinib, and provides a rationale for future research assessing STAT inhibitors in KIT-mutated melanoma.

K E Y W O R D S : baboon syndrome, case report, cutaneous adverse drug reaction, nefopam, pristinamycin, secnidazole, systemic allergic dermatitis In 1984, Andersen et al 1 introduced the term "baboon syndrome" to describe a systemic contact dermatitis characterized by exanthema with involvement of the buttocks and flexure regions after the systemic absorption of a contact allergen (nickel, mercury, or ampicillin) in a sensitized patient. The rash looked like the red buttocks of a baboon. In 1983, Nakayama et al 2 published a report of 15 patients with symmetrical erythema predominantly on major flexural sites, which occurred 1 or 2 days after the breaking of a mercury thermometer. The non-contact allergic variant of baboon syndrome is also referred to as symmetrical drug-related intertriginous and flexural exanthema (SDRIFE).Since 1984, $100 cases of baboon syndrome or SDRIFE have been reported. We report 3 cases of SDRIFE, 1 each caused by pristinamycin, secnidazole, and nefopam. 3 CASE REPORTSCase 1. A 60-year-old man presented with an erythematosquamous rash of the inguinal and axillary folds and gluteal area ( Figure 1). He had been treated with candesartan for many years. He had recently been diagnosed with a bronchial infection, and was prescribed pristinamycin. The cutaneous rash appeared 2 days later. The results of laboratory tests were within normal limits, except for a mild biological inflammatory syndrome probably attributable to the infection. Histopathological analyses of a skin biopsy showed an orthokeratotic epidermis without keratinocytic necrosis, discrete spongiosis, and a lymphocytic infiltrate of the dermis with some eosinophils ( Figure S1).The clinical and histopathological signs confirmed the diagnosis of SDRIFE caused by pristinamycin, which was discontinued. The skin lesions completely regressed within 7 days. Two months later, the patient was patch tested with pristinamycin 30% pet. and 30% aq. on the back and in an inguinal fold. The results were negative on day (D) 2 and D3. The patient refused an oral provocation test. Case 2. A 44-year-old woman was treated with secnidazole for vaginitis caused by Trichomonas vaginalis. After 2 days, she developed a pruritic eczema-like eruption in the axillary, inguinal and submammary folds, with no other signs (Figure S2). She denied taking any other medication, and had a history of maculopapular exanthema caused by metronidazole and acetylsalicylic acid. Secnidazole was stopped, and topical betamethasone treatment was initiated. The lesions resolved within 4 days. SDRIFE caused by secnidazole was diagnosed, and patch tests were performed with secnidazole 30% pet. and 30% aq. These gave negative results on D2 on the back and in 1 affected area (breast), but a positive reaction on D4 on the breast (+), although the result remained negative on the back. Metronidazole and secnidazole may potentially cross-react, because both are sulfonamides.Case 3. A 68-year-old woman was referred with an erythematous Vrash of the buttocks, perineum, and axillary f...