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Etiology / Pathophysiology

Hematologic disorders that cause pruritus include polycythemia vera. Some conditions that cause iron deficiency, including exfoliative skin disorder, also cause pruritus. Diabetes and thyrotoxicosis are endocrine causes of pruritus.[1]

Pruritus is a frequent clinical manifestation of people with AIDS, AIDS-related Kaposi sarcoma, and AIDS-related opportunistic infections. Pruritus with or without rash has been reported in approximately 84% of people with AIDS and 35.5% of those with AIDS-related Kaposi sarcoma. The incidence of pruritus associated with AIDS-related opportunistic infections approaches 100%.[2]

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Various malignant diseases are known to produce pruritus. Hodgkin lymphoma causes pruritus in 10% to 25% of patients. In some instances, pruritus precedes diagnosis of the lymphoma [1] and may be an indicator of a less favorable prognosis when associated with significant fever or weight loss ("B" symptoms).[3] Pruritus associated with Hodgkin lymphoma is characterized by symptoms of burning and intense itching occurring on a localized skin area, frequently on the lower legs. Other lymphomas and leukemias have been associated with a less intense but more generalized pruritus. Adenocarcinomas and squamous cell carcinomas of various organs (i.e., stomach, pancreas, lung, colon, brain, breast, and prostate) sometimes produce generalized pruritus that is more pronounced on the legs, upper trunk, and extensor surfaces of the upper extremities.[1,3] Pruritus associated with malignant diseases has been observed to diminish or disappear with eradication of the tumor and reappear with recurrence of disease.[3]

Drugs associated with secondary pruritus include opium derivatives (cocaine, morphine, butorphanol), phenothiazines, tolbutamide, erythromycin estolate, anabolic hormones, estrogens, progestins, testosterone and subsequent cholestasis, aspirin, quinidine and other antimalarials, biologics such as monoclonal antibodies, and vitamin B complex. Subclinical sensitivity to any drug may be related to pruritus.[3]

Hypothesized mechanisms of pruritus have been inferred from studies of pain, since pain and itching share common molecular and neurophysiological mechanisms.[4] Both itch and pain sensations result from the activation of a network of free nerve endings at the dermal-epidermal junction. Activation may be the result of internal or external thermal, mechanical, chemical, or electrical stimulation. The cutaneous nerve stimulation is activated or mediated by several substances including histamine, vasoactive peptides, enkephalins, substance P (a tachykinin that affects smooth muscle), and prostaglandins. It is believed that nonanatomic factors (such as psychological stress, tolerance, presence and intensity of other sensations and/or distractions) determine itch sensitivity in different regions of the body.

The itch impulse is transmitted along the same neural pathway as pain impulses, i.e., traveling from peripheral nerves to the dorsal horn of the spinal cord, across the cord via the anterior commissure, and ascending along the spinothalamic tract to the laminar nuclei of the contralateral thalamus. Thalamocortical tracts of tertiary neurons are believed to relay the impulse through the integrating reticular activating system of the thalamus to several areas of the cerebral cortex. Factors that are believed to enhance the sensation of itch include dryness of the epidermis and dermis, anoxia of tissues, dilation of the capillaries, irritating stimuli, and psychological responses.[1,3,4,5]

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WebMD Public Information from the National Cancer Institute

Last Updated: October 07, 2011
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