INTRODUCTION

Actinic keratoses (AK), also known as solar keratoses, are common cutaneous lesions resulting from a localized proliferation of atypical epidermal keratinocytes, which have been damaged by ultraviolet radiation. AK occur most frequently on sun-exposed sites, such as the upper limbs, face, ears and neck. In immunocompetent patients, a small proportion of actinic keratoses are thought to undergo malignant transformation to squamous cell carcinoma (SCC). The transformation rate in organ transplant recipients is almost certainly higher, although there is no data on the exact rate. Actinic keratoses in organ transplant recipients can cause significant morbidity and also are a biomarker of prior excessive sun damage, thus acting as a clinically useful predictor for development of skin malignancy.

PATHOGENESIS

Cumulative ultraviolet (UV) radiation is the most significant etiological factor in the development of AK. Ultraviolet B radiation is absorbed by the germinal basal keratinocytes, and causes a signature mutation of the deoxyribonucleic acid (DNA), predominantly in the p53 tumor suppressor gene. These mutations lead to defective DNA repair and a reduced initiation of apoptosis in damaged cells, thus allowing propagation and accumulation of further genetic damage. The same genetic mutations are observed in both AK and squamous cell carcinoma (SCC), thus supporting similar pathogenesis.

Immunosuppressed solid organ transplant recipients are at high risk of AK and SCC. The pathogenesis is yet to be fully understood although UV-radiation-induced genetic damage remains a major etiological factor.

INTRODUCTION

As the number of living organ transplant recipients continues to rise with advances in immunosuppression, so do the long-term problems. Nonmelanoma skin cancers (NMSCs), particularly squamous cell carcinomas (SCCs) are the most common posttransplantation malignancy in countries with predominantly Caucasian populations. In subtropical Queensland, Australia, the cumulative incidence of NMSCs increased from 7% after one year of immunosuppression to 25% after 5 years, and 70% after 20 years. The mean NMSC accrual in this same population was calculated as 1.85 +/− 3.84 tumors /person/year, increasing to 3.35 +/− 4.29 tumors/person/year after 20 years of immunosuppressive therapy, representing a significant tumor load. Many of these patients can be described as having “catastrophic cutaneous carcinogenesis” with large numbers of premalignant and malignant lesions. Unfortunately, the dermatological care of transplant patients has long been reactive, rather than proactive. Patients are referred only when skin cancers develop, and often, the load of malignant and premalignant lesions can be overwhelming for any clinician. An improved model, or models, of care therefore needs to be developed for such patients.

ROLES OF THE DERMATOLOGIST IN THE CARE OF TRANSPLANT PATIENTS

The roles of the dermatologist in the skin care of transplant recipients are essentially:

• Treatment of established tumor load. This involves the diagnosis and management of skin malignancies existing at the time of initial consultation. Following diagnosis, the clinician may be able to treat the lesions, or need to liase with surgeons or other specialists to arrange treatment.

• Treatment of subsequent tumors. As new cancers develop, ongoing management will ideally remove them at the earliest possible time.

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