eMedicine Specialties > Dermatology > Nails

Pachyonychia Congenita

Aleksej Kansky, MD, PhD, Professor, Department of Dermatology, Ljubljana University Faculty of Medicine, Slovenia

Updated: Mar 23, 2007

Introduction

Background

Pachyonychia congenita (PC) is a rare form of hereditary palmoplantar keratoderma (PPK). Müller made the first documented observation in 1904 (Müller, 1904). The next reports were published in 1905 by Wilson (Wilson, 1905) and in 1906 by Jadassohn and Lewandowsky (Jadassohn, 1906). In the dermatologic literature, PC is better known as Jadassohn-Lewandowsky syndrome.

The condition is rare. According to the Pachyonychia Congenita Project Mission Statement less than 300 were reported. Certain reports include larger series of cases: Moldenhauer and Ernst reviewed 93 cases and described 6 new cases (Moldenhauer, 1968). Puente reported 26 cases (Puente, 1955), Kumer and Loos reported 23 cases (Kumer, 1935), and Su reported 12 cases (Su, 1990). Fourteen cases from Slovenia (Franzot, 1981) and 25 cases from Croatia (Videnic, 1991) are reported. Additional reports on larger series of patients describe 19 patients from China (Xiao, 2004) and 13 patients of Italian descent (Terrinoni, 2001).

Various classifications for PC have been proposed. Currently 2 distinct syndromes of PC are recognized: (1) PC-1, or the Jadassohn-Lewandowsky type, which is designated as Mendelian Inheritance in Man (MIM) entry 167200 (McKusick, 1994), and (2) PC-2, or the Jackson-Lawler type, which is designated as MIM entry 167210.

For a definitive classification of PC, more data about genotypic-phenotypic correlation in the same patients is needed.

Pathophysiology

PC results from mutations in the genes encoding epidermal keratinocyte keratins. Specifically the 1A and 1B helical encasing regions of keratins K6a, K6b, K16, and K17 are the most frequent sites of mutations, for example, removal of 1 of 2 adjacent asparagine residues (N170/171) in the 1A encoding region of K6a. The mutation is likely to have a deleterious effect on protein structure as it interferes with the assembly of polypeptides forming the keratin skeleton of epidermal cells (Bowden, 1995). Further mutations are 325A to G in the 1A domain of K17 (Xiao, 2004) or 275A to G in the same domain (Feng, 2003).

Interestingly, a case was reported in which, in addition to the missense mutation 124L to R, a 23 bp deletion (1244-1266del) and a separate 1 bp deletion (1270delG) in exon 6 in the helix termination motif (HTM) in the K16 gene were described (Smith, 2000). The author believes that the loss of the HTM sequence may render the mutant less capable to influence the filament assembly and thus provoke a milder phenotype.

In most cases, an autosomal dominant mode of inheritance is described; however, autosomal recessive inheritance is also mentioned in the literature.

Sporadic PC cases in which no family linkage can be established may be the result of new mutations. However, an unknown affected father seems to be a further possibility.

The concept that in addition to the known mutation of the keratin gene, a second mechanism (probably an additional mutation) is needed for the expression of PC was first mentioned by Cockayne in 1933. He studied the then-available pedigrees of PC patients and noted that the pedigrees did not exactly match the principle of autosomal dominant inheritance (Cockayne, 1933). Lately, a similar view was expressed by MacLean, who introduced the term of a second modifying mutation within a keratin gene (Maclean, 2005). He also stated that approximately 10% of PC patients referred to his laboratory lacked detectable mutations in any of the 4 appropriate keratins

Findings from the present authors' clinical studies of a relatively large series of patients with PC support Cockayne's theory.

Frequency

United States

The disorder is rare. In the United States, only a few reports exist.

International

According to the Pachyonychia Congenita Project Mission Statement, less than 300 cases have been reported worldwide. No data are available about the incidence in various countries. However, in Slovenia, a rate 0.7 case per 100,000 inhabitants is reported. In Croatia, a comparable rate of 0.53 case per 100,000 persons is reported.

Mortality/Morbidity

The lesions in PC do not endanger the patient's life.

Race

Most likely, all races can be affected.

Sex

PC affects both sexes equally.

Age

• The affected nails are usually present at birth, but they may appear later, as they do in PC tarda.
• Paller et al described 5 patients in whom the disfigured nails appeared when they were aged 10-30 years. However, molecular biologic analysis was not available to verify the diagnosis. In PC tarda, thickened nails appear during adult life, which is probably not so rare. However, in the last 10 years, at least 2 cases of PC tarda were reported (Lucker, 1995; Hannaford, 2000). According to Connors, the PC tarda was, in one case, linked to the missense mutation K354N in the central 2B domain of K16. In the other case PC-2 2 was found to be caused by a missense mutation in the second half of the 1A domain of K17, N109D (Smith, 2004; Xiao, 2004).

Clinical

History

• Parents notice the lesions soon after their child's birth.
• Paller et al described 5 patients in whom the disfigured nails appeared when they were aged 10-30 years, as they do in PC tarda.

Physical

• Jadassohn-Lewandowsky type, or PC-1, is the more common variant. Mutations of the genes encoding keratins K6a and K16, which disrupt the keratin filament assembly, characterize the disorder. In PC-2 mutations in the keratin genes K6b and K17 are found
  • The nail changes are the most prominent feature. The nail plate is substantially thickened and brownish-gray with a rough surface. Usually, all fingers are affected; the toenails may also be affected, but this finding is less characteristic. The thickened fingernails may expand into periungual tissue, causing a pressure-provoked paronychia.
  • Circumscribed or diffuse hyperkeratoses are expressed on the palms and soles. Periodically, blisters may appear in hyperkeratotic areas, especially in children. Hyperhidrosis often accompanies the hyperkeratoses.
  • Follicular hyperkeratosis is observed on the face (eg, temples, front, eyebrows) and on the extensor aspect of the proximal parts of the extremities.
  • Leukokeratosis of the oral mucosa is a prominent sign especially of PC-1. Patchy whitish areas may be seen on the back of the tongue, on the buccal mucosa, and, sometimes, on the gingiva. In some patients, early tooth decay is observed.
  • Oral leukokeratosis is not a precancerous lesion. It is differentiated from leukoplakia or cancer either by performing an oral biopsy or by recognizing its presence in patients with other symptoms of PC.
  • Steatocystoma multiplex is generally considered a hallmark for PC-2, but according to the author's observations and some data from the literature (Ward, 2003), it may also appear later in life in patients with PC-1.
• Jackson-Lawler type, or PC-2, is less frequent compared with PC-1.
  • Patients have a thickened nail plate, and, eventually, other symptoms appear. The symptoms are similar to those in PC-1; however, PC-2 is characterized by natal teeth and the consistent presence of steatocystoma multiplex. A subset of mutations in the keratin K17 gene cause steatocystoma multiplex (MacLean, 2005).
  • Hair anomalies (eg, unruly hair) are also described. A new PC subtype was described in 2 patients (van Steensel, 2001), which included severe and generalized hypotrichia with thickened nails, as in PC. No mutations in keratin genes encoding K6a, K6b, K16, or K17 were detected. The author has also observed a similar case.
  • PC-2 is linked to mutations in the genes for keratin 6b and K17.
  • Sebaceous cysts may appear later in life.
• Corneal opacities and cataracts are rare. Reports of such findings were made prior to the classification of PC into PC-1 and PC-2 types.
• Cicatricial alopecia is an uncommon symptom.
• A thickened nail plate may occasionally be observed in the dominant form of dystrophic epidermolysis bullosa. in Clouston syndrome, in fungal infections in immunologically suppressed patients

Causes

An autosomal dominant mode of inheritance is observed in most cases of PC, but sporadic cases do occur. An autosomal recessive mode of inheritance has also been mentioned.

• Cockayne was the first to express the opinion that the presence of an additional factor, probably a second genetic mutation, is necessary for the expression of the disease (Cockayne, 1933). A similar view was expressed by MacLean in 2005.
• Munro was the first to propose that the genetic defect in PC is linked to the keratin gene cluster on chromosome 17 (Munro, 1994).
  • In a detailed molecular biologic analysis, McLean et al found that PC is caused by mutations on chromosomes 16 and 17.
  • More detailed molecular analysis revealed that PC was caused by mutations in the genes encoding the epidermal keratinocyte keratins K6a, K6b, K16, or K17 (McLean, 1995); these mutations are responsible for the clinical manifestations.
  • Bowden reported in 1995 that one of the adjacent asparagine residues in the 1A helical encoding region of K6a (N170/N171) was deleted in 5 patients from Slovenia. The mutation is provoking a deleterious effect on assembly of peptides. A mutation of F174S phenylalanine to serine was found in 1 patient. Further described mutations are 325 A to G in the 1A domain of K17 (Xiao, 2004) and 275A to G in the same domain (Feng, 2003).
• Rare genetic variants are described in each syndrome. Some of these appear to be due to mutations that occur elsewhere in the keratin genes.
  • Most well-studied mutations occur at the ends of the helical-rod domains disrupting the keratin filament assembly.
  • More data on mutations and symptoms in a larger number of patients are needed, for an exact genotype/phenotype correlation.

Differential Diagnoses

Candidiasis, Cutaneous

Workup

Laboratory Studies

• Molecular DNA analysis reveals missense mutations, deletion mutations, substitution mutations, and other mutations of keratin genes K6a, K6b, K16, and K17.
• Oral leukokeratosis is to be differentiated from leukoplakia or cancer either by performing oral biopsy or by recognizing its presence in patients with other symptoms of PC.
• In babies, PC can be misdiagnosed as candidiasis; PC can be misdiagnosed as onychomycosis later in life.
  • The occasional detection of a few Candida spores but no hyphae excludes onychomycosis.
  • To confirm candidal infection, mycologic investigation should reveal multiple spores and hyphae.
  • A detailed investigation of the fingernails in 8 patients with PC-1 in whom the diagnosis was verified by molecular biologic analysis did not reveal a candidal infection. Only a few spores and no hyphae were seen in 4 patients, while in the other 4, neither spores nor hyphae were found (Kansky, 1998).

Histologic Findings

The hyperkeratotic lesions of the skin and oral mucosa show acanthosis, hyperkeratosis, and parakeratosis. Premalignant changes are not observed.

Electron microscopy can be performed by using plantar or palmar skin samples. Electron microscopy shows thickened and clumped intermediate filaments, as well as enlarged keratohyaline granules. In the broadened granular layer, thick masses of tonofilaments and large, irregular keratohyaline granules are present. In the spinous layer, thick masses of tonofilaments are found at the periphery of the cells.

Treatment

Medical Care

Currently, no ideal treatment for the thickened nail plate is available, although a few therapeutic options have been suggested.

• The thickened nail plate can be softened by using 20% salicylic acid ointment or 20-40% urea and 10% salicylic acid in an emulsifying ointment with occlusive dressings.
• After the nail plate is softened, it can be mechanically abraded, which is sometimes performed by patients even without softening. This abrasion may be followed by additional softening of the nail plate.
• A 5% 5-fluorouracil cream can be applied twice daily. 5-Fluorouracil cream can be applied after thinning or abrasion of the nail plate to suppress the hyperproliferative activity of the nail matrix.
• Systemic treatment with retinoids (acitretin, retinoic acid) in a daily dose of 1 mg/kg is partially effective; the nail plate becomes thinner and its surface becomes smoother.
  • The adverse effects include potential liver damage, which can be demonstrated by increased liver enzyme levels; an increase in serum lipid levels; hyperostosis; and, the most dangerous, teratogenicity in pregnant women. The benefit-to-risk ratio must be carefully evaluated if treating females of childbearing age.
  • Minor adverse effects are dry and itchy skin, cracking of palmar and plantar skin, nose bleeding, dry mucosa, cheilitis, hair loss, and paronychia.Exostoses and calcination of ligaments and tendons are other minor adverse effect that particularly affect children.
  • Serious adverse effects are headache and brain edema.

Surgical Care

The affected nails can be removed under local or general anesthesia; however, unless the nail matrix is partially removed, nails regrow. After a complete removal of the nail matrix, a disfiguring anonychia may result.

In general, surgical ablation is not recommended, but it can be performed upon a patient's insistence.

Consultations

• A psychiatrist may be consulted if the patient has psychiatric problems related to the abnormal nails.
• A geneticist may be consulted for genetic counseling.

Diet

• Dietary changes seem to have no effect. During eventual systemic treatment with retinoids, the intake of saturated lipids must be limited.

Activity

Certain leisure activities (eg, bowling, soccer) or occupations that require the use of fine movements with hands or fingers should be discouraged.

Medication

Medications are used to reduce the symptoms associated with this syndrome. Cure is not yet possible.

Retinoids

Retinoids are a family of drugs related to vitamin A.They regulate the differentiation and proliferation of epithelial cells. Some also possess antitumoral activity.

Acitretin (Neotigason, Soriatane)

Retinoic acid analogues such as acitretin and isotretinoin are relatively widely used in dermatology. Etretinate is the main metabolite. The detailed mechanisms of action are still being studied.

Dosing

Adult

0.5-1 mg/kg/d PO; after 2-3 mo, reduce dose by half or one third initial dose; during systemic treatment with retinoids, monitor liver enzyme levels, serum lipid profile, and glucose values during therapy

Pediatric

Generally not recommended because of possible severe adverse effects

Interactions

Increases toxicity of 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 (>120 d)

Contraindications

Documented hypersensitivity to retinoids; hyperlipemia; liver diseases; diabetes mellitus

Precautions

Pregnancy

X - Contraindicated in pregnancy

Precautions

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

Antineoplastics

These agents inhibit cell growth and proliferation.

Fluorouracil (Carac, Efudex, Fluoroplex)

Interferes with DNA synthesis by blocking methylation of deoxyuridylic acid, inhibiting thymidylate synthetase and subsequently cell proliferation.

Dosing

Adult

Apply 5% formulation topically bid

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; potentially serious infections

Precautions

Pregnancy

X - Contraindicated in pregnancy

Precautions

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

Keratolytics

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

Salicylic acid (20%) ointment

By dissolving the intercellular cement substance salicylic acid produces desquamation of the horny layer of skin, while not affecting structure of viable epidermis.
Hydrate skin and enhance effects of medication by soaking affected area in warm water for 5 min prior to use. Remove any loose tissue with brush, washcloth, or emery board and dry thoroughly. Improvement should generally occur in 1-2 wk.

Dosing

Adult

Apply to affected area and cover with occlusive dressing

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; prolonged use in infants, diabetics, and patients with impaired circulation not recommended; use on moles, birthmarks, or warts with hair growing from them, genital or facial warts, or warts on mucous membranes, irritated skin, or any area infected or reddened also contraindicated

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Avoid contact with mucous membranes, normal skin surrounding warts, and eyes; immediately flush with water for 15 min if contact with eyes or mucous membranes occurs; avoid inhaling vapors

Urea (Ureacin-40)

Promotes hydration and removal of excess keratin in conditions of hyperkeratosis.

Dosing

Adult

Apply to affected area and cover with occlusive dressing

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; viral skin disease

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Do not use near eyes; caution if applied to broken or swollen skin

Salicylic acid (20%), urea (40%), and hydrophilic ointment compound

Compounded in the pharmacy. Promotes hydration and removal of excess keratin in conditions of hyperkeratosis.

Dosing

Adult

Apply to affected area and cover with occlusive dressing

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; prolonged use in infants, diabetics, and patients with impaired circulation not recommended; use on moles, birthmarks, or warts with hair growing from them, genital or facial warts, or warts on mucous membranes, irritated skin or any area infected or reddened also contraindicated; viral skin disease

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Do not use near eyes; caution if applied to broken or swollen skin; avoid contact with mucous membranes, normal skin surrounding warts, and eyes; immediately flush with water for 15 min if contact with eyes or mucous membranes occurs

Follow-up

Further Outpatient Care

• Patients receiving systemic retinoids require appropriate laboratory monitoring, including serum pregnancy testing.

Complications

• Paronychia may occur due to the ingrowing of the thickened nail plate.
• Adverse effects observed during treatment with retinoids include dryness of the skin and mucous membranes, nose bleeding, dry eyes, cheilitis, and transient hair loss.

Prognosis

• Nail findings persist, while other manifestations may become less severe later in life.

Patient Education

• Patients and their relatives should be informed that PC does not endanger an individual's life, but it may impair his or her quality of life.
• The patient may be informed that, at present, no effective treatment is available; however, gene therapy treatment may become available in the future.
• A genetic counselor should inform the carrier that this gene has an autosomal dominant inheritance pattern and that PC can affect one half of his or her progeny.

Miscellaneous

Medicolegal Pitfalls

• Failure to correctly diagnose PC may result in the inability to provide genetic counseling, correct treatment, or adequate treatment.
• PC can be misdiagnosed as candidiasis or onychomycosis, and unnecessarily treated with antimycotics.

Multimedia

Media file 1: The most prominent feature is a substantially thickened, brownish gray nail plate with a rough surface.

Media file 2: Leukokeratosis of the oral mucosa is a prominent sign. Patchy whitish areas may be seen on the back of the tongue; the buccal mucosa; and sometimes, the gingiva.

Media file 3: Hyperkeratotic lesions of the skin may involve acanthosis, hyperkeratosis, and parakeratosis.

References

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Keywords

PC, Jadassohn-Lewandowsky syndrome, polykeratosis congenita (Touraine), palmoplantar keratoderma, PPK, keratosis disseminata circumscripta, leukokeratosis linguae, PC-1, Jadassohn-Lewandowsky type, PC-2, Jackson-Lawler type, pachyonychia congenita tarda, MIM 167200, MIM 167210

Contributor Information and Disclosures

Author

Aleksej Kansky, MD, PhD, Professor, Department of Dermatology, Ljubljana University Faculty of Medicine, Slovenia
Aleksej Kansky, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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
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

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
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

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

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