Actinic purpura or is a common disorder of dermal connective tissue due to the damage of chronic exposure to the sun. Initially described by Bateman in 1818, it is also known as Bateman senile purpura or Bateman disease. It usually affects elderly individuals, and it is characterized by dark purple blotches on the photo-exposed areas, especially the back of the hands and the extensor surfaces of the forearm. The term solar purpura has been used by some authors as a synonym to actinic purpura, but it is preferable to reserve it to purpuric lesions which occur acutely after sun exposure.
Actinic purpura results from extravasation of the blood into the dermis after a minor trauma that is often neglected in the medical history. It is one of the signs of dermatoporosis, which indicates the skin fragility as well as skin atrophy and stellate pseudoscars.
Actinic purpura is extremely common in elderly individuals, especially those with fair skin (skin types 1 and 2) who are more sensitive to sun exposure. Its prevalence increases with age. It is estimated to be present in about 12% of individuals after the age of 50 years and up to 30% after age 75. Actinic purpura occurs equally in both genders.
Actinic purpura results from extravasation of blood into the dermis. This phenomenon is due to the skin atrophy and the fragility of the blood vessels in elderly individuals, which is exacerbated by chronic sun exposure. Actinic purpura lesions are located on sun exposed areas, like the arms, face, and neck.
Skin atrophy in dermatoporosis is due to an alteration of collagen, similar to that which is seen in osteoporosis. This pronounced skin atrophy caused by the photo-aging makes the dermal vascular network very sensitive to the slightest trauma or shearing force.
The passage of red blood cells into the dermis results in the hemosiderin deposits in the interstitial space. There is no infiltration of the vessels and usually no inflammatory reaction of the dermal tissue. The absence of phagocytosis results in delayed resorption of extravasated blood. This fact results in the formation of purple patches and macules of ecchymotic aspect.
Actinic purpura presents as patches and macules with irregular edges, with sizes ranging from 1 cm to 4 cm in diameter on average. The lesions may appear dark purple and have extensive ecchymosis. The lesions often are present on the forearm and the back of the hands. However, they can affect other areas, such as the legs, neck, and face. The surrounding skin is generally of altered quality (thin, pigmented and inelastic), and there may be evidence of other photo-aging lesions such as lentigos and actinic keratoses.
The purpuric lesions persist for about one to three weeks before resolving spontaneously. However, they do not undergo the phases of inflammation. It is possible that a residual deposit of hemosiderin in the dermis leaves a brown pigmentation. Actinic purpura, however, can continue to occur because of the already established cutaneous and vascular fragility. The ecchymotic lesions formed can cause a significant aesthetic problem and have a psychological impact; however, there is no risk of serious complications.
The diagnosis of actinic purpura is usually clinical and based on a good physical exam. In the rare cases where a biopsy is performed, the histological study will show a thinned epidermis ascending on an altered dermis with quantitatively reduced collagen fibers replaced by abnormal elastic fibers. The walls of the dermal vessels have a normal tensile structure, but there is extravasation of the red blood cells and hemosiderin deposits marked by Perls staining. In about 10% of cases, there is a neutrophilic infiltration that may lead to the misdiagnosis of actinic purpura as neutrophilic dermatosis or leukocytoclastic vasculitis.
Coagulation analysis is rarely necessary and usually, shows no abnormalities.
Actinic purpura is a benign condition that does not require specific treatment, particularly since other lesions continue to appear throughout life. The best treatment is preventive.; it is based on the intensive protection against sun exposure by wearing appropriate long-sleeved clothes. One should apply sunscreens with a high protection index (sun protection factor (SPF) greater than 50) daily to provide sufficient protection against the ultraviolet (UVB and UVA) rays. The sunscreen should be liberally applied to all sun-exposed areas regularly.
The therapeutic possibilities available for the actinic purpura lesions already formed are restricted. Tretinoin or retinoic acid (0.1%) is a derivative of vitamin A, which could theoretically reverse severe skin damage induced by ultraviolet light. Indeed, topical tretinoin is known for its role in the regeneration of dermal collagen and the reduction of the quality of abnormal elastin damaged by solar exposure. However, some authors demonstrate that the developed plaques of actinic purpura do not improve under local treatment with tretinoin.
In 2002, actinic purpura was successfully treated in one patient with tissue engineered skin; however, no similar cases have been reported.
More recently, it has been demonstrated that human epidermal growth factor may be a viable treatment of actinic purpura. It has been shown to increase the average skin thickness and reduce the number of purpuric lesions when applied twice daily for six weeks.
A citrus bioflavonoid blend has been tested for the treatment of actinic purpura. After six weeks, the treated group showed a 50% decrease in purpuric plaques with no reported side effects.
Laser therapy, which is widely used for the treatment of aging skin manifestations, is not indicated in actinic purpura. Moisturizing creams may be useful to treat frequently associated skin xerosis.
Actinic purpura is a common, benign disease of elderly individuals who have clear skin types. The disorder appears to be caused by dermal and vascular fragility induced by chronic sun exposure. It does not predispose to serious complications, and the risk of bleeding is minimal. However, it could cause significant aesthetic and cosmetic damage and induce a significant psychological impact. Treatment is limited, mainly relying on creams based on vitamin A derivatives and moisturizing creams. Photoprotection remains the best treatment, and it is based on (1) physical clothing, (2) chemical means, by the regular application of sunscreens, and especially (3) behavioral by avoiding excessive sun exposure.