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Approaching the Pruritic Patient

»What is the most common symptom of dermatologic disease?
»What is an “itch”?
»Is an itch a separate modality of pain or a submodality of pain?
»What causes an itch?
»Describe the difference between localized and generalized pruritus.
»What is the best approach to evaluation of a patient with localized pruritus?
»What are the common causes of localized pruritus?
»What is notalgia paresthetica?
»What is the physician’s best approach when seeing a patient with generalized pruritus?
»After obtaining a complete history and physical examination, what clinically oriented classification scheme should be followed?
»What are common causes of generalized pruritus?
»How prevalent is an underlying systemic disease in a patient who seeks medical attention for pruritus?
»What is “winter itch”? In which patient population is it common?
»The patient complains that “wool makes me itch” or “I am allergic to wool.” What disease does this patient probably have?
»What treatment should the physician consider if a patient presents with pruritus and “hives”?
»What disease should the physician consider if the patient volunteers that his spouse also suffers from itching?
»Is pruritus in HIV-infected patients common? What are the common causes of pruritus in these patients?
»Which psychiatric disorder often presents with intractable pruritus?
»Which patients with renal failure experience “renal itch”?
»Which patients with liver disease are most likely to experience pruritus? What is the best screening laboratory test?
»What are the common causes of cholestic pruritus?
»Which hematologic disorders are known to present with pruritus?
»Is generalized pruritus a common symptom of endocrine disorders?
»Can itching cause skin disease?
»What is the best symptomatic treatment for a patient with pruritus?

 
 
 

What causes an itch?

Itch is mediated by a number of local and central substances. Histamine, produced by skin mast cells, is the classical pruritus mediator. Pricking the skin with histamine produces pruritus in most individuals; however, histamine does not account for all pruritus. Other pruritus mediators include prostaglandin, serotonin, tachykinins, cytokines, and opioid receptors. Prostaglandin E1 lowers the threshold of the skin to itching provoked by histamine. Serotonin, 5-hydroxytryptamine (5-HT), may regulate itch by acting on 5-HT3 receptors. Tachykinins, such as the neuropeptide substance P, cause pruritus for reasons attributable to histamine release from mast cells. Cytokine interleukin-2 may be an important peripheral mediator of itching. Opioid receptors in the central nervous system regulate the intensity and quality of perceived itch.


Understanding pruritus mediators can help classify itch accordingly to origin. The classification of itch includes:
  1. pruritoceptive—cutaneous nerves are activated by pruritogens at sensory endings,
  2. neuropathic—diseased or lesion pruritic neurons generate itch,
  3. neurogenic—itch caused by mediators acting centrally, and
  4. psychogenic. Although classifications are important, there are limitations as itch can have more than one origin.
Bernard JD, editor: Itch: mechanisms and management of pruritus, New York, 1994, McGraw-Hill.

Buddenkotte J, Steinhoff M: Pathophysiology and therapy of pruritus in allergic and atopic diseases. Allergy 65:805-821, 2010.