eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriasis, Nails

Cindy Li, DO, Dermatologist and Cosmetic Surgeon, Department of Dermatology, Kaiser Permanente Medical Group
Richard K Scher, MD, Professor of Dermatology, University of North Carolina

Updated: Oct 29, 2009

Introduction

Background

Psoriatic nail disease has many clinical signs. Most psoriatic nail disease occurs in patients with clinically evident psoriasis; it only occurs in less than 5% of patients with no other cutaneous findings of psoriasis. An estimated 10-55% of all patients with psoriasis have psoriatic nail disease. Approximately 7 million people in the United States have psoriasis. About 150,000-260,000 new cases of psoriasis are diagnosed each year. US physicians see 1.5 million patients with psoriasis per year. Severe psoriatic nail disease can lead to functional and social impairments if left untreated.

Courtesy of Hon Pak, MD.

Pathophysiology

The pathogenesis of the psoriatic nail disorder is not completely known. Nail psoriasis may be due to a combination of genetic, environmental, and immune factors. A well-known fact is that a familial aggregation of psoriasis exists. Studies have linked psoriasis with certain human leukocyte antigen subtypes (eg, Cw6, B13, Bw57, Cw2, Cw11, B27). A T-cell–mediated inflammatory process is being investigated as part of the pathogenesis of psoriasis.

Frequency

United States

Psoriatic nail disease occurs in 10-55% of all patients with psoriasis. Approximately 7 million people in the United States have psoriasis. Psoriasis affects 2-3% of the US population. Less than 5% of psoriatic nail disease cases occur in patients without other cutaneous findings of psoriasis. About 10-20% of people with psoriasis also have psoriatic arthritis. Nail changes are seen in 53-86% of patients with psoriatic arthritis.

Psoriasis tends to run in families. In Farber's questionnaire study of 2100 patients,¹ 36% of patients reported the presence of psoriasis in at least 1 relative. Among siblings, 8% are affected if neither parent has psoriasis. This percentage increases to 16-25% if 1 parent or sibling has the disease, and it increases up to 75% if both parents are affected. If 1 twin has psoriasis, the other twin is at an increased risk of having psoriasis (25% for fraternal twins, 65% for identical twins).

International

In Scandinavia, the prevalence rate of nail psoriasis for adults with psoriasis approaches 5%. The prevalence increases with the age of the population studied.

Mortality/Morbidity

Psoriatic nail disease is not associated with mortality. In severe cases, patients may have functional and psychosocial impairments.

Sex

Both sexes are affected equally by nail psoriasis.

Age

The prevalence of nail psoriasis increases with the age of the population studied.

Clinical

History

Most psoriatic nail disease occurs in people with clinically evident psoriasis. The diagnosis of psoriatic nail disease without cutaneous psoriasis can be challenging because of the low index of suspicion and the lack of personal/family history of psoriasis.

Physical

The clinical findings associated with psoriatic nail disease correlate with the anatomical location of the nail unit that is affected by the disease. The nail unit is composed of the nail plate, the nail bed, the hyponychium, the nail matrix, the nail folds, the cuticle, the anchoring portion of the nail bed, and the distal phalangeal bones. The nail plate is the largest component of the nail unit. The nail matrix gives rise to the nail plate. Any defect to the matrix results in onychodystrophy of the growing nail plate. The proximal nail matrix forms the dorsal portion of the nail plate, whereas the distal matrix forms the ventral part of the nail plate. The clinical presentation may vary depending on the location and the severity of inflammation of the affected nail unit.

Anatomy of the nail, superior view.

Anatomy of the nail, sagittal view.

• Below is a summary of the clinical signs of nail psoriasis and the portion of the nail unit that is affected followed by a definition.
  • Oil drop or salmon patch/nail bed² : This lesion is a translucent, yellow-red discoloration in the nail bed resembling a drop of oil beneath the nail plate. This patch is the most diagnostic sign of nail psoriasis.
  • Pitting/proximal nail matrix: Pitting is a result of the loss of parakeratotic cells from the surface of the nail plate.
  • Beau lines/proximal nail matrix: These lines are transverse lines in the nails due to intermittent inflammation causing growth arrest lines.
  • Leukonychia/midmatrix disease: Leukonychia is areas of white nail plate due to foci of parakeratosis within the body of the nail plate.
  • Subungual hyperkeratosis/hyponychium: Subungual hyperkeratosis affects the nail bed and the hyponychium. Excessive proliferation of the nail bed can lead to onycholysis.
  • Onycholysis/nail bed and nail hyponychium: Onycholysis is a white area of the nail plate due to a functional separation of the nail plate from its underlying attachment to the nail bed. It usually starts distally and progresses proximally, causing a traumatic uplifting of the distal nail plate. Secondary microbial colonization may occur.
  • Nail plate crumbling/nail bed or nail matrix: Nail plate weakening due to disease of the underlying structures causes this condition.
  • Splinter hemorrhage/dilated tortuous capillaries in the dermal papillae: Splinter hemorrhages are longitudinal black lines due to minute foci of capillary hemorrhage between the nail bed and the nail plate. This is analogous to the Auspitz sign of cutaneous psoriasis, which is the pinpoint bleeding seen beneath the psoriatic plaques.
  • Spotted lunula/distal matrix: This is an erythematous patch of the lunula.
  • Psoriatic arthritis with nail changes/phalanx
• Psoriatic nail disease can also occur with onychomycosis and paronychia.
• Most people with psoriatic arthritis have nail changes that can be classified as follows:
  • Type I - Classic distal interphalangeal joint involvement (5% of patients)
  • Type II - Arthritis mutilans
  • Type III - Symmetric polyarthritis
  • Type IV - Asymmetric oligoarthritis (the most common type of psoriatic arthritis, occurring in 70% of patients)
  • Type V - Ankylosing spondylitis

Classic distal interphalangeal joint involvement in psoriatic arthritis.

This patient has extensive psoriasis, nail involvement, and joint pain.

Causes

Psoriatic nail disease may be due to a combination of genetic, environmental, and immune factors. A well-known fact is that a familial aggregation of psoriasis exists. Recent studies have linked psoriasis with certain human leukocyte antigen subtypes (eg, Cw6, B13, Bw57, Cw2, Cw11, B27). A T-cell–mediated inflammatory processing is being investigated as part of the pathogenesis of psoriasis.

Differential Diagnoses

Alopecia Areata
Lichen Planus
Onychomycosis
Pityriasis Rubra Pilaris

Other Problems to Be Considered

Idiopathic trachyonychia
Punctate keratoderma

Workup

Procedures

• Skin biopsy: A nail biopsy is needed to confirm the diagnosis of nail psoriasis in some cases and is usually taken from the nail bed.

Histologic Findings

Psoriasis can affect any part of the nail unit. Most changes occur in the nail plate. Histologic findings of nail psoriasis include mild-to-moderate hyperkeratosis, hypergranulosis, serum globules and hemorrhage in the corneum layer, papillomatous epidermal hyperplasia, and spongiosis.

Treatment

Medical Care

Many treatment options are available after the diagnosis of nail psoriasis is made. The treatments focus on improvement of the functional and psychosocial aspects of psoriatic nail disease. No curative treatment exists at the present time. Onychomycosis (if present) requires antifungal therapy for improvement. The treatment options for nail psoriasis include topical corticosteroids, intralesional corticosteroids, psoralen plus ultraviolet light A (PUVA),³ topical fluorouracil,⁴ topical calcipotriol,⁵ topical anthralin,⁶ topical tazarotene,^7,8 topical cyclosporin,⁹ avulsion therapy,¹⁰ and systemic therapy for severe cases.
 
For preventive care, keep the nails dry and protect them from trauma to avoid the Koebner effect. In areas of onycholysis, the nail plate should be trimmed to the point of separation for medications to be effective.

• Topical treatment with high-potency corticosteroid solution or ointment under occlusion with cellophane wrap at bedtime can improve nail psoriasis. Avoid long, continuous therapy with corticosteroids to avoid tachyphylaxis. Also, avoid prolonged occlusion (not to exceed 2 wk). Topical 1% 5-fluorouracil solution or 5% cream applied twice daily to the matrix area for 6 months without occlusion improves pitting and subungual hyperkeratosis. A topical preparation of a combination of high-potency corticosteroid and calcipotriol may benefit some patients.¹¹
• PUVA is very effective for cutaneous psoriasis and can improve nail psoriasis. Both oral and topical PUVA therapies have improved nail psoriasis in 3-6 months. A possible adverse effect of PUVA may be nail discoloration.
• Intralesional triamcinolone acetonide suspension of 2.5 mg/mL into the proximal nail fold is very helpful for nail matrix psoriasis (eg, pitting, ridging, leukonychia). This medication may be administered every 4-6 weeks. The proximal nail fold is sprayed first with a refrigerant spray for anesthesia, and the injection is given with a 30-gauge needle.
• Systemic therapies have been used in patients with severe cutaneous psoriasis. Few studies have shown significant improvement in nail psoriasis with long-term results. At present, 3 systemic medications are most commonly used for psoriasis and nail psoriasis: methotrexate, retinoids,¹² , and cyclosporin.¹³ All 3 agents have potential serious adverse effects and toxicities. In most cases, the psoriatic nail disease recurs after the systemic therapy is stopped. Carefully weigh the risk-to-benefit ratio in the treatment of nail psoriasis. Systemic therapies are seldom a first-line therapy for nail psoriasis. Topical treatment with calcipotriol can be used as adjunctive therapy and maintenance therapy with systemic treatment. Biological therapy for psoriasis and psoriatic arthritis may have a significant benefit for some patients with psoriatic nail disease.¹⁴
• Avulsion therapy with chemical or surgical means can be used as an alternative therapy for psoriatic nail disease. Chemical avulsion therapy includes the use of urea ointment in a special compound to the affected nail under occlusion for 7 days, and the nail is removed atraumatically. Chemical avulsion therapy is painless, involves no blood loss, and is less expensive than surgical avulsion.
• At present, no definitive and curative treatment has been agreed upon by medical experts. Discuss all treatment options for psoriatic nail disease with the patient, and choose the best individually tailored regimen.

Surgical Care

Surgical avulsion therapy can be performed for psoriatic nail disease when other treatments have failed. During surgery, the matrix can be electively ablated to prevent regrowth of the nail. This procedure is performed under local anesthesia. Inform patients of postoperative discomfort, limitations, and possible physical nail disfigurement.

Activity

Avoiding trauma to the nail, which prevents onycholysis and possible secondary microbial colonization in the nail, is important. Patients should keep psoriatic nails clean and dry.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Triamcinolone (Aristocort)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Many other topical steroids are also available.

Dosing

Adult

Topical: Apply thin film to affected area bid/tid
Intralesional: 2.5 mg/mL into proximal and/or lateral nail fold q4-6wk; proximal and/or lateral nail fold is sprayed first with a refrigerant spray for anesthesia, and injection is given with a 30-gauge needle

Pediatric

<12 years: Not established
>12 years: Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use in decreased skin circulation; prolonged use, applying over large areas, and using potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria

Betamethasone (Diprolene, Betatrex)

For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dosing

Adult

Apply thin film to affected area bid/qid until response

Pediatric

Apply as in adults

Interactions

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; decreases effect of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity; paronychia; cellulitis; impetigo; angular cheilitis; erythrasma; erysipelas; rosacea; perioral dermatitis; acne

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use in skin with decreased circulation; can cause atrophy of groin, face, and axillae; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control; do not use monotherapy to treat widespread plaque psoriasis

Clobetasol (Temovate)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Dosing

Adult

Apply to affected area bid for up to 2 wk; not to exceed 50 g/wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral or fungal skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy

Calcipotriene and betamethasone topical ointment

Calcipotriene is a synthetic vitamin D-3 analog that regulates skin cell production and development. Inhibits epidermal proliferation, promotes keratinocyte differentiation, and has immunosuppressive effects on lymphoid cells. Betamethasone is a corticosteroid that decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability. Available as a topical ointment containing calcipotriene 0.005% and betamethasone dipropionate 0.064%.

Dosing

Adult

Apply to nail area qd for up to 4 wk

Pediatric

Not established

Interactions

Coadministration with other corticosteroids may increase toxicity

Contraindications

Documented hypersensitivity; known or suspected calcium metabolism disorders; erythrodermic, exfoliative, or pustular psoriasis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause hypercalcemia; systemic absorption of topical corticosteroids has caused HPA-axis suppression, Cushing syndrome manifestations, hyperglycemia, and glucosuria; not for prolonged use (ie, >4 wk), large surface areas (ie, >30% of body surface area), or application with occlusive dressings; do not use on face, eyes, axillae, or groin; may cause contact dermatitis

Psoralens

These agents are very effective for cutaneous psoriasis and can improve nail psoriasis. They may improve nail psoriasis in 3-6 months.

Trioxsalen (Trisoralen)

Inhibits mitosis by covalently binding, in the presence of UV-A radiation, to pyrimidine bases in DNA.

Dosing

Adult

0.2-0.5 mg/kg PO 2-4 h before controlled exposure to UV-A or sunlight; not to exceed 14 d

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; history of melanoma, acute lupus erythematosus, or porphyria

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Severe burns may occur from sunlight or UV-A exposure if dose or frequency is exceeded

Methoxsalen (8-MOP, Oxsoralen)

Inhibits mitosis by covalently binding to pyrimidine bases in DNA when photoactivated by UV-A.

Dosing

Adult

0.57 mg/kg 1.5-2 h before exposure to UV light, at least 48 h apart

Pediatric

Not established

Interactions

Toxicity increases with phenothiazines, griseofulvin, nalidixic acid, tetracyclines, thiazides, and sulfanilamide

Contraindications

Documented hypersensitivity; squamous cell cancer; cataract; light sensitive diseases, such as lupus or porphyria; ingestion of photosensitizing drugs; hepatitic disease; arsenic therapy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Severe burns may occur; use only if response to other forms of therapy is inadequate

Antimetabolites

These agents inhibit cell growth and proliferation.

Fluorouracil (Efudex)

Interferes with DNA synthesis by blocking the methylation of deoxyuridylic acid and inhibits thymidylate synthetase, which subsequently reduces cell proliferation.

Dosing

Adult

5% strength recommended; apply sparingly to cover lesions bid; therapy may be required for 10-12 wk (minimum 3 wk)

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; potentially serious infections; pregnancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Incidence of inflammatory reactions may occur with occlusive dressings; porous gauze dressing may be applied for cosmetic reasons without increase in reaction

Methotrexate (Folex, Rheumatrex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).
Antimetabolite that inhibits DNA synthesis and cell reproduction in malignant cells; may suppress immune system. Satisfactory response seen in 3-6 wk following administration.

Dosing

Adult

7.5 mg test dose; check CBC count and LFT in 1 wk; 15-75 mg IM given at q1-2wk; alternatively, 10-25 mg/wk PO/IM or 2.5-7.5 mg PO q12h for 3 doses/wk

Pediatric

Not recommended

Interactions

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral MTX; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity; folic acid or its derivatives contained in some vitamins may decrease response; coadministration with NSAIDs may be fatal if high doses of MTX are used, but NSAIDS have been used safely with MTX when doses of 7.5-15 mg/wk have been used (as in treatment of rheumatoid arthritis); indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity; may increase plasma levels of thiopurines; NSAIDs increase serum levels by displacing it from albumin and inhibiting renal excretion

Contraindications

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor CBC counts monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant decrease in blood counts; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly with MTX (possibility of increased toxicity with NSAIDs, including salicylates, has not been tested)

Keratolytics

These agents cause cornified epithelium to swell, soften, macerate, and then desquamate.

Anthralin (Anthra-Derm, Drithocreme)

May upset oxidative metabolic processes, decreasing rate of epidermal cell proliferation.
Applications in excessive amounts may stain clothing.

Dosing

Adult

Apply sparingly and gently to psoriatic lesions qd

Pediatric

Not established

Interactions

Long-term corticosteroid treatment withdrawal may cause complications of rebound phenomenon (allow 1 wk interval between discontinuation of corticosteroids and initiation of anthralin therapy)

Contraindications

Documented hypersensitivity; acutely or actively swollen psoriatic lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal disease; do not apply to face or genitalia and avoid eye contact; discontinue application if redness develops

Retinoids

These agents decrease the cohesiveness of abnormal hyperproliferative keratinocytes and may reduce the potential for malignant degeneration. They modulate keratinocyte differentiation. They have been shown to reduce the risk of skin cancer formation in patients who have undergone renal transplantation.

Tazarotene (Tazorac)

Retinoid prodrug whose active metabolite modulates differentiation and proliferation of epithelial tissue; may also have anti-inflammatory and immunomodulatory properties. Mechanism of action in psoriasis is not defined. Has been shown to inhibit cornified envelope formation in human keratinocyte cultures, whose buildup is an element of the psoriatic scale. Use 0.05% or 0.1% gel.

Dosing

Adult

Begin with lowest formulation and increase as tolerated; apply thin film to cover lesion qd (2 mg/cm²); not to exceed >20% of BSA; lower frequency of application if irritation develops

Pediatric

<12 years: Not established
>12 years: Apply as in adults

Interactions

Avoid concomitant dermatologic medications and cosmetics that have a strong drying effect

Contraindications

Documented hypersensitivity; pregnancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Common adverse events reported are limited to the skin and include pruritus, burning, stinging, erythema, irritation, rash, desquamation, and irritant contact dermatitis; discontinue if excessive irritation; rinse thoroughly if contact with eyes, eyelids, or mouth; may cause severe irritation in eczematous skin; photosensitivity may occur

Acitretin (Soriatane)

Retinoic acid analog, like etretinate and isotretinoin. Etretinate is main metabolite and has demonstrated clinical effects close to those seen with etretinate. Mechanism of action is unknown.

Dosing

Adult

25 or 50 mg/d PO initially given as single dose with main meal
Maintenance dose: 25-50 mg/d PO after initial response to treatment; terminate therapy when lesions have resolved sufficiently

Pediatric

Not established

Interactions

Increases toxicity methotrexate (avoid concomitant use); interferes with effects of microdosed progestin minipill; coadministration with alcohol may enhance synthesis of etretinate, which has much longer half-life than acitretin (>120 d)

Contraindications

Documented hypersensitivity; pregnancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Do not use in severe obesity; women of childbearing age must be capable of complying with effective contraceptive measures; recommended that contraception be continued for at least 3 y after stopping treatment with acitretin; etretinate may form from acitretin, which takes about 2-3 y to clear from the body; caution if impaired renal or liver function; perform AST, ALT, and LDH tests prior to initiation of acitretin therapy at 1- to 2-wk intervals until stable and thereafter at intervals as clinically indicated

Immunosuppressives

These agents inhibit key factors of the immune system.

Cyclosporine (Sandimmune, Neoral)

Demonstrated to be helpful in a variety of skin disorders, especially psoriasis. Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft vs host disease for a variety of organs. For children and adults, base dosing on ideal body weight.

Dosing

Adult

2.5-5 mg/kg/d PO in divided doses

Pediatric

Administer as in adults

Interactions

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin

Contraindications

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UV-B radiation in psoriasis because it may increase risk of cancer

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

Vitamins

These agents are essential for normal DNA synthesis and cell function.

Calcipotriene (Dovonex)

Synthetic vitamin D-3 analog that regulates skin cell production and development. Used in the treatment of moderate plaque psoriasis.

Dosing

Adult

Apply a thin film to affected skin bid to response

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; hypercalcemia; vitamin D toxicity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue treatment if skin becomes irritated; discontinue if serum calcium level is increased outside of reference range

Follow-up

Deterrence/Prevention

• For preventive care, keep psoriatic nails dry and protect them from trauma to avoid the Koebner effect.

Complications

• Psoriatic nail disease is not associated with mortality. In severe cases, patients may have functional and psychosocial impairments.

Patient Education

• For excellent patient education resources, visit eMedicine's Psoriasis Center and Arthritis Center. Also, see eMedicine's patient education articles Nail Psoriasis, Psoriasis, Types of Psoriasis, Understanding Psoriasis Medications, and Psoriatic Arthritis.

Multimedia

Media file 1: Anatomy of the nail, superior view.

Media file 2: Anatomy of the nail, sagittal view.

Media file 3: Courtesy of Hon Pak, MD.

Media file 4: Courtesy of Hon Pak, MD.

Media file 5: Courtesy of Hon Pak, MD.

Media file 6: Classic distal interphalangeal joint involvement in psoriatic arthritis.

Media file 7: This patient has extensive psoriasis, nail involvement, and joint pain.

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Keywords

psoriasis of nails, nail psoriasis, psoriatic nails, psoriatic nail disease, psoriatic nail disorder, arthritis mutilans, symmetric polyarthritis, psoriatic arthritis, asymmetric oligoarthritis, ankylosing spondylitis

Contributor Information and Disclosures

Author

Cindy Li, DO, Dermatologist and Cosmetic Surgeon, Department of Dermatology, Kaiser Permanente Medical Group
Cindy Li, DO is a member of the following medical societies: American Academy of Cosmetic Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Richard K Scher, MD, Professor of Dermatology, University of North Carolina
Richard K Scher, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Cryosurgery, American College of Physicians, American Dermatological Association, American Geriatrics Society, American Medical Association, Association of Military Surgeons of the US, International Society for Dermatologic Surgery, New York Academy of Sciences, Noah Worcester Dermatological Society, Rhode Island Medical Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Mark G Lebwohl, MD, Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Abbott Laboratories Honoraria Consulting; Actelion Honoraria Consulting; Amgen Honoraria Consulting; Astellas Honoraria Consulting; Centocor Honoraria Consulting; DermiPsor Honoraria Consulting; Galderma  Consulting; Genentech Honoraria Consulting; Helix BioMedix Honoraria Consulting; Medicis Honoraria Investigator

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

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