Pruritus may be associated with dermatologic disorders, underlying systemic diseases, medication side effect, or it may be an idopathic phenomenon without any discernable etiology.  Free nerve endings located in the superficial dermis and dermo-epidermal junction of the skin and mucous membranes are responsible for the sensation of pruritus.  Many different mediators of itch (histamine, proteases, perptides, prostaglandins, leukotrienes, etc.) work at the peripheral nerve endings.  Endogenous opiates (leuenkephalins and metenkephalins) effect their role on the perception of pruritus in the central nervous system. Aquagenic pruritus is often associated with polycythemia vera.

     A thorough history and physical exam should be performed once patients present with a complaint of pruritus.  The skin should undergo close scrutiny (dermatitis, fungal infections, urticaria, etc.) and the remainder of the exam directed at detecting clues to possible underlying systemic diseases.  If there is an associated rash, examination under a Wood’s lamp (fungal infections will fluoresce) and of a 10% KOH wet mount of skin scrapings will help determine if the lesion is from a fungal infection (hyphae or budding yeast noted on microscopic examination) or represents a possible contact/allergic dermatitis (no findings on wet mount examination).  If a potential etiology is uncovered, therapy should be directed accordingly.  Fungal infections may respond to a topical or systemic antifungal; whereas, topical or oral steroids are required for allergic dermatitis.  However, if no potential etiologies are identified (lack of skin lesions) for pruritis and patients lack other signs or symptoms of underlying systemic disease, a trial of empiric therapy is warranted before proceeding with further diagnostic testing.  If the pruritus resolves with empiric therapy then a diagnosis of xerosis or atopic dermatitis may be made.  If symptoms are refractory to empiric therapy, then further evaluation is warranted.  Further testing may include CBC, chemistry panel, urinalysis, liver function panel, TSH, ESR, ANA, ferritin and iron panel, and hemoccult cards times three.  If no etiology is inferred by any of these tests, further work up may include HIV testing, chest radiography, stool examination for ova and parasites times three, SPEP, Pap smear, and skin biopsy with direct immunofluorescence.

     Empiric therapy is often with an antihistamine or an antidepressant (doxepin, amitriptyline).  Nonsedating second-generation antihistamines may be used during the morning hours with a first generation agent used before bedtime.  When there is an identifiable dermatitis, corticosteroids either orally or topically may prove effective.  Patients should be advised to limit bathing time, use a mild soap (Dove, Basis, or Tone), and to use emollients after bathing and throughout the day.  Use of a humidifier may prove helpful.  Topical antipruritic preparations (Aveeno, Caladryl, Crude coal tar 3% solution, PrameGel, Pramosone, Prax, Wuotane, Sarna, Schamberg’s lotion, Topic gel, Wibi lotion, and Zonalon) may prove effective at symptom relief; however, topical antihistamine and anesthetics should be avoided as they may exacerbate the condition.  When an identifiable etiology is present, therapy should be directed accordingly.  In some cases, treatment of the underlying disorder will result in resolution of pruritus; however, sometimes symptomatic therapy may need to be employed.  Ultraviolet light B (UV-B) is an effective therapy for the treatment of pruritus associated with chronic hemodialysis, pityriasis rosea, polymorphic light eruption, pruritic papular eruption associated with HIV, and psoriasis.  When psoralen is used in conjunction with UV-A (PUVA) it is an effective therapy for the treatment of pruritus associated with psoriasis, mycosis fungoides, and atopic dermatitis.  Pruritus associated with cholestasis may respond to treatment with cholestyramine (4 grams QD to TID), colestipol, ursodiol (600 to 900 mg/day), or phenobarbital (3 to 4 mg/kg/day).  Pruritus due to polycythemia vera may respond to cyproheptadine (4 mg TID). ).  When pruritus is refractory, naltrexone (an opiate antagonist) may be effective.  When symptoms have an acute onset and are associated with hives, treat as for anaphylaxis (epinephrine and H1 antihistamines plus or minus oral corticosteroids).  In cases which occur repeatedly and without an identifiable allergen, consider idiopathic anaphylaxisis.

     Localized perianal itching (pruritus ani) may be idiopathic or secondary to underlying pathology.  Pinworms may cause pruritus ani and are more common in the pediatric population.  Genital herpes simplex virus infection (either HSV I or II) may cause chronic or recurrent rectal itching, and should respond well to appropriate antiviral therapy (acyclovir, valacyclovir, or famcyclovir).  Anal disease which may manifest as pruritus ani includes hemorrhoids, dermatoses, fissures, polyps, and malignancy.  Empiric therapy for pruritus ani should be instituted when no underlying etiology is apparent.  Avoidance of dietary factors associated with pruritus ani should be implemented, and patients should be counseled as to proper local hygiene.  Local hygiene should include Sitz baths followed by blotting (not rubbing) and air drying (hair dryer).  A cotton ball may be placed at the anal opening to collect any moisture that may occur throughout the day.  If symptoms persist after one month of diet and hygiene recommendations, biopsies of the anus and endoscopic or radiographic examination of the rectum provide a complete evaluation.