O'Brien J P
Br J Dermatol. 1978 Jan;98(1):1-13. doi: 10.1111/j.1365-2133.1978.tb07327.x.
Actinic damage (actinic elastosis) affecting the internal elastic lamina appears to be the prime cause of 'age change' and arteritis of the temporal artery. Resorption and removal of altered elastin (elastolysis) is an integral part of the pathology of actinic damage. Actinic irradiation is probably responsible for the destruction and disappearance of a vast number of arterioles in elastotic skin. The intimate connection between temporal arteritis and polymyalgia rheumatica prompts the belief that the vascular and other internal malign components of the temporal arteritis/polymyalgia rheumatica syndrome might likewise be due, albeit indirectly, to the same actinic cause. Actinic elastotic damage at the body surface could have this effect by provoking a state of systemic elastolysis. Although ultraviolet (uv) light is often regarded as the sole cause of actinic elastosis, penetrating infrared (heat) irradiation may deserve a large or even a dominant share of the blame.
影响内弹性膜的光化性损伤(光化性弹力组织变性)似乎是颞动脉“老化改变”和动脉炎的主要原因。变性弹性蛋白的吸收和清除(弹性蛋白溶解)是光化性损伤病理的一个组成部分。光化性照射可能是导致弹力组织变性皮肤中大量小动脉破坏和消失的原因。颞动脉炎和风湿性多肌痛之间的密切联系使人相信,颞动脉炎/风湿性多肌痛综合征的血管及其他体内有害成分可能同样间接归因于同一光化性病因。体表的光化性弹力组织变性损伤可能通过引发全身性弹性蛋白溶解状态而产生这种影响。尽管紫外线常被视为光化性弹力组织变性的唯一原因,但穿透性红外(热)照射可能应承担很大甚至主要责任。