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Background. Trigeminal trophic syndrome is a unilateral, frequently crescent-shaped neurotrophic ulceration of the face occurring after injury to the trigeminal nerve. The appearance of the ulcers resembles other disease entities such as granulomatous disease, neoplasm, vasculitis, infection, and factitial dermatitis. Objectives. The objectives of this study are to increase awareness of this disorder and to emphasize the importance of eliciting a thorough neurologic history when evaluating facial ulcerations. Methods. Four cases are reported and, using MEDLINE, the English and non-English literature from 1982 to 2002 is reviewed. Results. Including this report, there have been 60 cases of trigeminal trophic syndrome reported from 1982 to 2002. The age at presentation ranged from 14 months to 93 years. Time of onset from injury to the trigeminal ganglion or its branches and the development of the ulcers ranged from 2 weeks to 30 years. One-third of the patients had undergone trigeminal nerve ablation for the treatment of trigeminal neuralgia and another third had a history of stroke. Other causes included craniotomy, head trauma, herpes infection. Conclusion. The majority of cases of trigeminal trophic syndrome are associated with a history of stroke or trigeminal nerve ablation. Successful surgical outcome can be achieved if the underlying neurologic pathology is addressed before the reconstructive procedure.

The growing investigation and use of epidermal growth factor receptor (EGFR) inhibitors in anticancer therapy has been motivated by their specificity for EGFR, which improves their ability to target cancer cells and enhances their safety profile compared with many other conventional chemotherapeutic agents. However, their growing use has been accompanied by an increasing incidence of cutaneous toxicities, which can cause serious discomfort and be disabling. This review illustrates the common cutaneous side effects seen in patients receiving EGFR inhibitors and discusses various options for management. With effective management of these side effects, dermatologists can play an integral role in facilitating compliance with anti-EGFR therapy and aid with effective oncologic management.

Hyaluronan (hyaluronic acid, HA) is an abundant matrix component between keratinocytes of the epidermis in vivo, but its function there remains unclear. We used a lift culture model, in which rat epidermal keratinocytes (REKs) stratify at an air-liquid interface, to ask whether HA may regulate epidermal proliferation and/or differentiation. In this model, early markers of differentiation (keratin 10), and later markers (profilaggrin, keratohyalin granules, cornified layers) are faithfully expressed, both temporally and spatially. HA, measured using two different analytical techniques, accumulated to high levels only in the presence of an intact basement membrane that seals the epidermal compartment. To test whether HA has a functional role in differentiation, Streptomyces hyaluronidase (StrepH, 1 U/ml; digests >95% of HA within 4 h) was added daily to lift cultures during stratification time-course experiments over 5 days. In StrepH-treated cultures, the expression of profilaggrin and the number and size of keratohyalin granules were significantly increased relative to controls using semiquantitative histological analyses. The StrepH-related accumulation of K10 protein and profilaggrin/filaggrin were confirmed by Western analyses. Thus, it appears that the presence of intercellular HA in the epidermis acts as a brake upon intracellular events that occur during keratinocyte differentiation.