Spontaneous remission of solar keratoses: the case for conservative management

Abstract

One thousand and forty people aged 40 years and over, 616 (59.2%) of whom had solar keratoses, were followed for 12 months. Two hundred and twenty-four people (36.4%) had a spontaneous remission of at least one of their solar keratoses. A total of 485 lesions (25.9%) underwent spontaneous remission out of the 1873 lesions that were present at the first examination of these 224 people. There was no significant difference between the number of lesions present at the initial examination in those who had a spontaneous remission compared with those who did not. There was a 21.8% increase in the total number of solar keratoses in the 1040 people studied in the 12-month period, due to new lesions forming at the same time as remissions were occurring. The incidence rate of squamous cell carcinoma occurring in the people with solar keratoses was 0.24% for each solar keratosis present at the original examination. With a substantial proportion of solar keratoses remitting spontaneously, plus the low rate of malignant transformation and the low potential for metastasis to occur from squamous cell carcinoma arising in a solar keratosis, the rationale of treating all solar keratoses appears questionable.

Id3 induces a caspase-3- and -9-dependent apoptosis and mediates UVB sensitization of HPV16 E6/7 immortalized human keratinocytes

“…Different studies have estimated the AK regression rates at 21% (Harvey et al, 1996), 25.9% (Marks et al, 1986), and 29% per year (Frost et al, 2000) for new lesions, and 74% per year for prevalent lesions (Frost et al, 2000). In contrast, the rates of AK progression to SCC are much lower, with rate estimates of 0.2% (Marks et al, 1986), 0.1% (Marks et al, 1988), and 0-1.1% per year (Frost et al, 2000). While the exact details are yet to be elucidated, an insight into the molecular mechanisms of AK regression can be gleaned from studies in which expression of immortalizing and survival proteins were examined in normal skin, porokeratosis, AK, SCC in situ, and invasive SCC (Park et al, 2004).…”

Loss of heterozygosity analysis of keratoacanthoma reveals multiple differences from cutaneous squamous cell carcinoma

“…Although there may be histological differences between sporadic KA and MSSE, many consider the MSSE a form of familial KA (Straka and Grant-Kels, 1991;Schwartz, 1994); reports of multiple KAs occurring sporadically also suggest overlap (Witten and Zak, 1952). A final reason for interest in the genetics of KAs is the finding that another cutaneous lesion, actinic keratoses (AK) (small scaly red lesions occurring on UVR-exposed skin showing varying degrees of dysplasia), which also show a high rate of spontaneous regression (Marks et al, 1986), show a frequency of allelic loss similar to, if not higher than, SCC (Rehman et al, 1994). One of a number of interpretations of the allelotype data of AK is that accumulation of genetic change in skin tumours may be associated with both progression and regression (Rees, 1994;Rehman et al, 1994 (Straka and Grant-Kels, 1991;Schwartz, 1994).…”

Keratoacanthomas have an immunosuppressive cytokine environment of increased IL-10 and decreased GM-CSF compared to squamous cell carcinomas

“…Suggestions include distinct entities, KAs may be a benign tumour in a spectrum with the more aggressive SCC at the malignant end, or KAs may represent a 'self-healing' or regressing form of SCC (Le Boit, 1995), much like actinic keratoses which also frequently regress spontaneously (Marks et al, 1986). The mechanism of KA resolution has also not been determined.…”