Recent guidelines from the American Joint Committee on Cancer (AJCC) and National Comprehensive Cancer Network (NCCN) have been proposed for the assessment of “high-risk” cutaneous squamous cell carcinomas (cSCCs). Though different in perspective, both guidelines share the common goals of trying to identify “high-risk” cSCCs and improving patient outcomes. Thus, in theory, both definitions should identify a similar proportion of “high-risk” tumors. We sought to evaluate the AJCC and NCCN definitions of “high-risk” cSCCs and to assess their concordance. Methods. A retrospective review of head and neck cSCCs seen by an academic dermatology department from July 2010 to November 2011 was performed. Results. By AJCC criteria, most tumors (n = 211,82.1%) were of Stage 1; 46 tumors (13.9%) were of Stage 2. Almost all were of Stage 2 due to size alone (≥2 cm); one tumor was “upstaged” due to “high-risk features.” Using the NCCN taxonomy, 231 (87%) of tumors were “high-risk.” Discussion. This analysis demonstrates discordance between AJCC and NCCN definitions of “high-risk” cSCC. Few cSCCs are of Stage 2 by AJCC criteria, while most are “high-risk” by the NCCN guidelines. While the current guidelines represent significant progress, further studies are needed to generate a unified definition of “high-risk” cSCC to optimize management.

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A retrospective review was performed on patients with stable melanoma brain metastases treated with HD IL-2 therapy (720,000 IU/kg per dose intravenously; 14 doses, 2 cycles per course, maximum 2 courses) from January 1999 to June 2011 at Saint Louis University. There were 5 men and 3 women; median age was 52.2 years (26.8–61.1 years). One patient started treatment with lung lesions only (after resection of melanoma brain disease) and experienced partial response. Seven patients had brain metastases at treatment initiation. Median overall survival (mOS) for entire cohort (n = 8) was 8.7 months (2.1 to 19.0 months). All patients with brain metastases at first dose (n = 7) showed progressive disease; mOS was 6.7 months (range 2.1–18.2 months) for this group. Patients received radiosurgery and whole brain radiation before and after HD IL-2 therapy. One patient had symptoms suggestive of neurotoxicity. A history of alcohol abuse was revealed during admission. The patient's symptoms improved with initiation of an alcohol withdrawal protocol. In this analysis, patients with melanoma brain metastases received HD IL-2 without treatment-related mortality. We think that HD IL-2 should be considered as a treatment option in patients with melanoma brain metastases who are otherwise eligible for therapy.

We report a 2-month-old boy with a painful ulcerated hemangioma on the lower mucosal lip extending to the vermillion border that caused feeding difficulty. It was successfully treated with topical brimonidine 0.2% and timolol 0.5%, a combination selective α2 -adrenergic agonist and nonselective β-blocker. After 6 weeks of treatment, the lesion reepithelialized and the patient's symptoms and functional complications resolved. Brimonidine 0.2% timolol 0.5% ophthalmic solution is an emerging alternative treatment for hemangiomas, offering the potential to target hemangioma growth through two synergistic mechanisms (β-inhibition and α2 -agonism) that may be especially effective for ulcerated lesions, the most common complication of infantile hemangiomas.

We report three patients with superficial haemangiomas treated topically with Combigan ophthalmic solution (brimonidine 0.2%–timolol 0.5%), a combination selective α-2-adrenergic agonist and non-selective β-blocker Food and Drug Administration-approved for use in glaucoma. Topical brimonidine 0.2%-timolol 0.5% therapy improved the appearance of haemangiomas in all the cases. Two patients did not experience any adverse effects. One patient had hypothermic episodes which were initially thought to be because of brimonidine 0.2%-timolol 0.5% therapy. However, an episode occurred a few weeks after discontinuation and brimonidine 0.2%-timolol 0.5% therapy was ruled out as a cause. Despite the benefit, off-label use of brimonidine 0.2%-timolol 0.5% therapy served as a pitfall in the evaluation of an unusual constellation of worrisome symptoms. In conclusion, brimonidine 0.2%-timolol 0.5% therapy is a promising alternative in the topical treatment of haemangiomas. It may have synergistic effects and increased efficacy by targeting haemangiomas via two mechanisms (α-agonism and β-inhibition), but the risk of unforeseen adverse effects must always be considered when prescribing off-label treatment, especially in infants.