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    Current Diagnosis

    • A careful history and physical examination will reveal a clear exposure, a sick contact, a recent travel, or clues to a systemic disease.

    • Antihistamines are effective in treating histamine-mediated pruritus, but they are less effective in mechanisms involving serotonin, leukotrienes, etc.

    • Initial testing in the absence of improvement with nonpharmacologic methods or antihistamine should include complete blood counts, thyroid-stimulating hormone, renal and liver panel, human immunodeficiency virus (HIV) test, and chest radiograph.

    • Chronic pruritus may precede a systemic illness, especially in older adults. Hodgkin lymphoma is the malignant disease most strongly associated with pruritus and occurs in up to 30% of patients diagnosed with pruritus.

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    Current Therapy

    • Acute and localized pruritus may resolve with nonpharmacologic methods, such as skin hydration with hypoallergenic, alcohol-free, and fragrance-free moisturizing creams; decreasing the length of showers and baths as well as the temperature of the water; identifying material that may irritate the skin either in jewelry or clothing items; and avoiding scratching.

    •   Wound care of scratch lesions includes any cellulitic portions.

    • First-line pharmacologic treatments may include the use of antihistamine and antipruritic creams. Antipruritic agents may be used as second-line treatments.

    • In the absence of improvement, the management of chronic pruritus should be directed at the underlying cause.

    Pruritus is defined as an unpleasant sensory percetion that causes the desire to scratch. While it shares similarities with pain, the neurophysiology of pruritus is distinct: pain causes withdrawal, whereas pruritus induces the reflex of reaching out and scratching.

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    Pruritus can be distinguished as acute or chronic, with the latter defined by the International Forum for the Study of Itch (IFSI) as lasting for 6 or more weeks.

    Despite many classifications over the years, there is no uniform, clinically based classification of pruritic diseases to assist in the diagnosis and management of patients with pruritus. The classification chosen for this chapter focuses on clinical signs and distinguishes between the disease with and without primary or secondary skin lesions.

    1.   Group 1: Pruritus of primary diseased, inflamed skin

    2.   Group 2: Pruritus of primary nondiseased, noninflamed skin

    3.   Group 3: Pruritus with chronic secondary scratch lesions

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    The sensation of pruritus stems from a number of different causes. It is generally transmitted through slow-conducting unmyelinated C fibers and free nerve endings located superficially in the skin, which appear to be more sensitive to pruritogenic substances than pain receptors. Histamine, neuropeptide substance P, serotonin (a key component in several diseases), bradykinin, mast cell tryptase, and other unknown mediators (e.g., in uremic pruritus, cholestatic pruritus), may be involved in the genesis of pruritus. Impulses are transmitted from the dorsal root ganglion to the spinothalamic tract. Pruritus then generates a spinal reflex response, the scratch, which is as innate as a deep tendon reflex. Other pathogenic mechanisms include neuropathic (e.g., herpes zoster) and immune-mediated (atopic dermatitis). Lastly, opioids are known to modulate the sensation of pruritus, both peripherally and centrally.

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    Clinical Manifestations

    Pruritus is among the most common symptoms in dermatology. Other associated symptoms depend on the etiology and may include urticarial skin lesions, dry skin, jaundice, and thyroid-related symptoms. Left untreated, itch and its associated scratching increase the risk of chronic skin changes and secondary infection.

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    Differential Diagnosis

    The patient’s work-up further places him or her in one of the following categories:

    1.   Primary diseased, inflamed skin

    •   Inflammatory: Atopic and contact dermatitis, psoriasis, dry skin, drug reactions

    •   Infectious: Mycotic, bacterial and viral infections, folliculitis, scabies, pediculosis, arthropod reactions, and insect bites

    •   Autoimmune: Bullous dermatoses, especially dermatitis herpetiformis, bullous pemphigoid, and dermatomyositis

    •   Dermatoses of pregnancy

    •   Neoplasms: Cutaneous T-cell-lymphoma (especially erythrodermic variants), cutaneous B-cell lymphoma, leukemic infiltrates of the skin

    2.   Primary nondiseased, noninflamed skin

    •   Endocrine and metabolic diseases: Chronic renal failure, liver diseases/cholestasis, hyperthyroidism, malabsorption, perimenopausal pruritus

    •   Infectious diseases: HIV infection, helminthosis, parasitosis

    •   Hematologic and lymphoproliferative diseases, iron deficiency, polycythaemia vera, Hodgkin and Non-Hodgkin lymphoma

    •   Visceral neoplasms of the cervix, prostate, or colon, carcinoid syndrome

    •   Pregnancy: Pruritus gravidarum with and without cholestasis

    •   Drug-induced pruritus: Opioids, ACE-inhibitors, amiodarone, hydrochlorothiazide, estrogens, simvastatin, hydroxyethyl starch, allopurinol

    3.   Pruritus with chronic secondary scratch lesions (The underlying origin may be a systemic disease or a skin disease.)

    •   Neurogenic origin (without neuronal damage), such as hepatic itch

    •   Neuropathic diseases (neuronal damage causes itch)

    •   Multiple sclerosis, neoplasms, abscesses, cerebral or spinal infarcts, brachioradial pruritus, postherpetic neuralgia, vulvodynia, small fiber neuropathy

    •   Somatoform pruritus (e.g., obsessive-compulsive disorders)

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    •   Basic measures to lessen drying of skin: Limit bathing to short, cool showers with soap applied only to oily skin areas. A mild moisturizing cream is preferably applied immediately after bathing to lock in moisture. The patient’s home should be humidified, especially during dry, cold winter months. Avoid contact irritants, such as wool, fiberglass, and detergents.

    •   Nonspecific therapy: A wheal and flare response is a marker of histamine-induced pruritus in patients with urticaria or an allergic dermatitis. These patients benefit from long-acting antihistamines. Concurrent H1 and H2 blockers increase therapeutic effectiveness.

    •   Treatment specific: Itching gradually recedes as the primary systemic condition improves.

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    Pruritus is accompanied by intense scratching. Skin may thicken, displaying lichen simplex chronicus: a localized skin thickening often appearing over the posterior neck, extremities, scrotum, vulva, anus, and buttocks. In prurigo nodularis, a variant of lichen simplex chronicus, some nodules develop over areas within easy scratching reach, such as the extensor arms and legs. Impetigo may result from superinfected excoriations in patients with atopic dermatitis.

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    Ikoma A., Rukwied R., Ständer S., et al. Neurophysiology of pruritus: Interaction of itch and pain. Arch Dermatol.


    Ständer S., Weisshaar E., Mettang T., et al. Clinical classification of itch: A position paper of the International Forum for the Study of Itch. Acta Derm Venereol. 2007;87:291–294.

    Zirwas M.J., Seraly M.P. Pruritus of unknown origin: A retrospective study. J Am Acad Dermatol. 2001;45:892–896.

    Cho Y.L., Liu H.N., Huang T.P., Tarng D.C. Uremic pruritus: Roles of parathyroid hormone and substance P. J Am Acad Dermatol. 1997;36:538–543.

    Ganesh E., Maxwell L.G. Pathophysiology and management of opioid-induced pruritus. Drugs. 2007;67:2323–2333.

    Krajnik M., Zylicz Z. Understanding pruritus in systemic disease. J Pain Symptom Manage. 2001;21:151–168.

    Reamy B. A diagnostic approach to pruritus. Am Fam Physician.


    Moses S. Pruritus. Am Fam Physician. 2003;68:1135–1142.

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