Dermatology and Pruritus Ani

Inflammatory diseases

Nonsexual infectious disease

Pruritus ani

Pilonidal disease

Psoriasis

Hidradenitis suppurativa

Lichen planus

Beta-hemolytic streptococcus

Lichen sclerosus et atrophicus

Fistula-in-ano

Atrophoderma

Crohn’s disease

Contact (allergic) dermatitis

Tuberculosis

Contact (irritant) dermatitis

Actinomycosis

Seborrheic dermatitis

Herpes zoster

Atopic dermatitis

Vaccinia

Radiation dermatitis

Fournier’s gangrene

Behçet’s syndrome

Tinea cruris

Lupus erythematosus

Candidiasis

Dermatomyositis

“Deep” mycoses

Scleroderma

Amebiasis cutis

Erythema multiforme

Trichomoniasis

Darier’s disease

Schistosomiasis cutis

Familial chronic pemphigus

Bilharziasis

Hailey-Hailey disease

Oxyuriasis (pinworm)

Pemphigus vulgaris

Creeping eruption (larva migrans)

Cicatricial pemphigoid

Larva currens

Bullous pemphigoid

Cimicosis (bed bugs)

Dermatitis herpetiformis

Pediculosis (lice)

Scabies

Sexually transmitted disease

Premalignant and malignant disease

Gonorrhea

Acanthosis nigricans

Syphilis

Leukoplakia

Chancroid

Mycosis fungoides

Granuloma inguinale

Leukemia cutis

Lymphogranuloma venereum

Basal cell carcinoma

Molluscum contagiosum

Squamous cell carcinoma

Herpes simplex

Melanoma

Condyloma acuminata

Bowen’s disease (AIN)

Extramammary Paget’s disease

Definitions

Accurate description of the morphology of skin lesions aids in diagnosis and follow-up of patients with pruritic complaints.
Macules are flat spots.
Papules are elevated circumscribed solid lesions.
Vesicles are separations of the epidermis from the dermis filled with serum.
Bullae are larger vesicles or blisters ≥10 mm.
Pustules contain pus.
Ulcers are surface lesions with loss of continuity of the skin and may result from rupture of vesicular lesions, infection, or trauma.
Intertrigo is inflammation seen between two opposing skin surfaces, often the result of mixed bacterial and fungal infections – associated with moisture, obesity, and poor hygiene.
Pruritus or itch is the unpleasant sensation that provokes the desire to scratch.
Primary pruritus ani is the classic syndrome of idiopathic pruritus ani.
Secondary pruritus ani has an identifiable cause or a specific diagnosis.

Physiologic Considerations

There are three different modalities of itch: (1) pruritoceptive (C mediated), (2) neuropathic (post-zoster), and (3) central or neurogenic.
Pruritoceptive fibers that mediate itch are usually unmyelinated C fibers in the epidermis and subepidermis.
These fibers may be more superficial than pain fibers and have a lower threshold for stimulation than pain fibers.
Because itch fibers are more superficial, minor mechanical stimuli (like wearing wool) may induce itch.
Although histamine (and kallikrein, bradykinin, papain, trypsin) can produce itch, topical antihistamines are not always effective to block itch.
Gastrin-releasing peptide receptors may mediate itch; thus, some H₂ blockers may have an impact on itch.
Minimal stimulation may induce itching and scratching. If there is not an adequate inhibitory feedback, a self-defeating loop may occur. Substitution of heat, cold, painful, or stinging stimulus for itch by applying alcohol or pepper extract may provide an inhibitory feedback not supplied by scratching alone.
Antidepressant medication (i.e., paroxetine) and anticonvulsant medication (i.e., gabapentin) have antipruritic effects mediated at the central nervous system level.
Itching from wound healing is associated with histamine release, release of other kinins and prostaglandins, and regeneration of nerves. Release of histamine, kinins, and prostaglandins occurs during the inflammatory phase of healing.
Antihistamines, topical anti-inflammatory agents (steroids), topical anesthetics, moisturization, petrolatum, and aloe preparations (prostaglandin inhibitors) all have beneficial effects on itching from wound healing.

Etiology of Pruritus

Table 16.2 outlines various causes of idiopathic pruritus ani.

Table 16.2

Proposed etiologies of idiopathic pruritus ani

Anatomic factors	Obesity, deep clefts, hirsutism, tight clothing
Anorectal disease	Fissure, fistula, tags, prolapsing papilla, hemorrhoids, mucosal prolapse, sphincter insufficiency, deforming scars
Antibiotics
Contact dermatitis	Chemicals in topical preparations, toilet paper, wet wipes, alcohol, witch hazel, “caine” anesthetics, fecal soiling
Dermatoses	Psoriasis, seborrheic dermatitis, atopic dermatitis, lichen planus, lichen simplex, lichen sclerosis, dermographism
Diet	Coffee (caffeinated and decaffeinated), chocolate, spicy foods, citrus fruits, tomatoes, beer, dairy products, vitamin A and D deficiencies, fat substitutes, consumption of large volumes of liquids
Diarrhea	Infectious diarrhea, irritable bowel syndrome, Crohn’s disease, ulcerative colitis
Drugs	Quinidine, colchicine, IV steroids
Gynecologic conditions	Pruritus vulvae, vaginal discharge of infection
Idiopathic
Infection	Viruses: herpes simplex, cytomegalovirus, papillomavirus; bacteria: Staphylococcus aureus, beta-hemolytic strep, mixed infections; fungi: dermatophytes, Candida species; parasites: pinworms, scabies, pediculosis; spirochetes: syphilis
Neoplasms	Bowen’s disease (AIN), extramammary Paget’s disease, squamous cell carcinoma variants, secreting villous tumors
Personal hygiene	Poor cleansing habits, over meticulous cleansing producing mechanical trauma, use of soaps
Psychogenic/neurogenic	Anxiety, neurosis, psychosis, neurodermatitis, neuropathy, “itch syndromes”
Radiation	Radiation dermatitis, sphincter compromise or leakage due to radiation proctitis
Systemic disease	Jaundice, diabetes mellitus, chronic renal failure, iron deficiency, thyroid disorders, lymphoma, polycythemia vera

There are few rigorous studies of anal pruritus.

Localized Itch Syndromes

Notalgia paresthetica is associated with itching or pain of the upper to mid-back to either side of the scapula presumed due to spinal nerve damage or entrapment. There may also be an inherited form.
Skin biopsy demonstrates increased sensory innervation.
Treatment is with topical pepper cream (capsaicin 0.025 %) which may exacerbate the symptoms during the first week of treatment, but this subsides.
Topical EMLA (2.5 % lignocaine plus 2.5 % prilocaine) may also be effective.
Dermatographism may cause anogenital pruritus.

Fecal Contamination

Regarding fecal contamination leading to pruritus, some rigorous studies have been published.
One study supports the notion that skin in different body locations reacts differently to having feces sitting upon it. Feces is probably an irritant rather than producing an allergic effect.
Anal seepage of liquid and mucous may be an important factor in pruritus symptoms.
Coffee consumption reduces the resting anal pressure in some people and may increase the chance of anal leakage.
Patients with pruritus ani have lower leak point pressures than controls. Additionally the anal inhibitory reflex seems to be more pronounced in patients with pruritus which implies that rectal distension may lead to a greater fall in anal resting pressures.

Viral Infection

Condylomata acuminata commonly cause itching.
Lesions due to herpes typically cause pain or burning versus itching.
HIV-associated lesions typically do not itch unless there is a secondary fungal infection.

Fungal Infection

Conflicting studies regarding the association of fungal infections and pruritus have been published.
If dermatophytes are cultured from the skin, there is some evidence that this may be associated with itching. Topical steroids may facilitate hyphae growth.

Bacterial Infection

Beta-hemolytic streptococci have been associated with pruritus (when cultured from the anal area).
Erythrasma (Corynebacterium minutissimum), which is probably normal skin flora, may lead to pruritus after moisture, diabetes, or obesity, allowing it to become pathogenic. This usually develops in body folds.