Clinical Dermatology

Itching frequently occurs in association with inflammatory skin diseases and in this setting, it is probably due to the action of inflammatory mediators (such as histamine, prostaglandins, and kinins) on cutaneous nerve endings. The release of proteinases during the process of inflammation may also play an important role. The same nonmyelinated nerves responsible for the transmission of light pain appear to carry these itch impulses to the brain.

Conventional wisdom suggests that all itching is qualitatively the same, but empirical observations suggest that this might not be so. For instance, patients with urticaria often complain extremely severe itching, but only rarely does this pruritus lead to excoriation. On the other hand, patients with dermatitis herpetiformis regularly scratch their lesions even when the pruritus is perceived as only moderately severe in intensity. Moreover, those individuals who are genetically atopic seem predisposed to vigorous excoriation at the slightest provocation, whereas nonatopics rarely scratch uncontrollably. From a practical standpoint, pruritus appears to depend on four major factors: (1) the type of disease-some conditions are inherently more pruritic than others; (2) the environmental condition on the skin-xerotic and sweaty skin favors itching; (3) genetic factors atopics have a lower threshold for itching than do non atopies; and ( 4) the psychologic set of the patients-itching is more severe in anxious and depressed patients. Those diseases that are, to a greater or lesser degree, inherently pruritic are listed, but the severity of pruritus experienced will be at the least partially dependent on other factors.

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