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Summary

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Nail involvement in psoriasis is common and mostly occurs with other lesions but can also occur alone. Besides psychosocial and aesthetic impairments, patients often complain about functional impairment. Nail psoriasis is a predictor for more severe psoriasis, decreased quality of life, and a higher risk for the development of psoriatic arthritis. Onychomycosis and other differential diagnoses should be excluded prior to treatment. This article presents an overview of different clinical appearances of nail psoriasis, the essential diagnostic assessment before treatment, important differential diagnoses, and published data on treatment options for nail psoriasis.


Epidemiology

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Psoriasis is one of the most common skin diseases in Germany. The disease -prevalence is about 2.5% affecting more than 2 million people. A 2010 study published in Germany on 3,531 psoriasis patients reported that 41% had nail -involvement [1]. In a Spanish epidemiological study from 2011 (661 patients), 47.4% of psoriasis patients had nail involvement [2]. Taking various studies into account, nail involvement occurs in up to 40% of patients with mild psoriasis and 50–70% with severe disease [3, 4]. In patients with concomitant joint manifestations, i.e. psoriatic arthritis (PsA), up to 80% have nail involvement [5, 6]. Affected nails are a predilection site for the development of onychomycosis [14, 7]. Other sources report a lifetime incidence of nail psoriasis among psoriasis patients of 80–90%[8]. 5% of patients show nail psoriasis in the absence of cutaneous involvement of [9, 10]; this is a particular diagnostic challenge [11, 8].

Structure of the nail

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Knowledge of the anatomical structure of the nail is essential to understand the inflammatory processes affecting the nail in psoriasis. The nail consists of 4 epithelial structures (nail matrix, the proximal nail fold, the nail bed and the hyponychium) and the nail plate. The transparent nail plate is formed by the nail matrix and arises from below the proximal nail fold. It consists of several layers of horny, dead epithelial cells and is pushed forward by newly growing cells from the lunula. This line divides living and dead cells and is the visible part of the distal nail matrix. The nail fold surrounds the proximal and lateral boundaries around the nail plate in a horseshoe shape. The eponychium closes the space between the proximal nail fold and the nail plate and thus protects the nail matrix and the nail radix underneath the proximal nail wall against environmental influences and pathogens. At the distal end, the 0.5–1mm wide, pale yellow onychodermal band forms the margin to the adherent nail bed. The nail plate lies on the nail bed, the epithelium of which forms the bottom side of the nail plate. Anatomically, the proximal border of the nail bed is formed by the lunula; the point where the edge becomes free is the hyponychium. This, in turn, forms the transition zone between the nail bed and normal epidermis of the fingers and toes.

Clinical manifestations

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Simultaneous involvement of several nails on both hands and feet is very common. Psoriasis may affect any part of the nail, including the nail fold, nail matrix, nail bed, nail plate, and hyponychium. Yet, nail changes are often more severe if the nail matrix is affected. The severity of nail involvement is determined by the site of the inflammatory reaction. If the nail matrix is involved, there may be development of indentations (pitting), leukonychia, red patches in the lunula, and onychodystrophy. Severe nail psoriasis can result in the crumbling of the nail. If the nail bed is affected, typical “oil spots”, splinter hemorrhage, onycholysis, and subungual parakeratosis and hyperkeratosis can be observed (Table 1).

Table 1.  Clinical manifestations of nail psoriasis.
Psoriasis of the nail matrix
Nail pitting
Leukonychia
Lunula erythema and neovascularization
Crumbly nails
Psoriasis of the nail bed
Oil spots
Onycholysis
Subungual hyperkeratosis
Splinter hemorrhage

Nail pitting occurs as a result of abnormal keratinization with severe parakeratosis and an accumulation of nuclear remnants on the surface of the nail plate [12] (Figure 2). As the nail evolves from nail fold, these portions are lost, leaving behind typical indentations. These may be scattered randomly over the nail or arranged in horizontal rows. The fingernails are more often affected than the toenails. Nail pitting is not specific to psoriasis and may also occur in other skin disorders such as lichen ruber and nonspecific eczema.

image

Figure 1. Acrodermatitis continua suppurativa (Hallopeau disease).

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image

Figure 2. Onychodystrophy (a), oil spots (b), grooves (c), onycholysis (d), subungual hyperkeratosis (e), nail pitting (f).

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Psoriatic “oil spots” (areas of yellow-red discoloration) are most likely due to a PAS-positive glycoprotein. They are caused by parakeratotic changes in the nail bed, which also move distally as the nail grows [13]. Distal onycholysis usually occurs once the free edge, or hyponychium, is reached. The white color is due to air -underneath the nail plate. A “locus minoris resistentiae” may develop and significantly increase the chance of fungal infection. Onychomycosis occurs in 13–47% of patients with nail psoriasis [14]. The nails may also show a white or cloudy appearance referred to as leukonychia. Affected nails may sometimes break or crumble. The nail surface is usually soft and intact; accompanying involvement of the proximal matrix can lead to leukonychia with a rough nail surface. A thickening of the nail underneath the nail plate determines subungual hyperkeratosis. The cause is hyperproliferation of the nail bed due to a psoriatic lesion at the affected site [15]. Subungual hyperkeratosis usually displays a greasy yellow appearance. It is especially important to rule out onychomycosis if subungual hyperkeratosis is present [16].

The most severe type of nail psoriasis is total onychodystrophy, which may present with crumbling of the nail. This disorder involves the entire nail matrix which severely disrupts the formation of the nail plate. Here the nail plate is only loosely connected to the nail bed and appears to be crumbling. A form of nail involvement that is very difficult to treat occurs in acrodermatitis continua suppurativa (Hallopeau disease) (Figure 1). Sterile pustules located next to the nail plate trigger necrosis, which can lead to the loss of the entire nail plate. This highly inflammatory process may spread to the bone and represents a particular treatment challenge [17]. If the inflammatory reaction at the nail fold and nail matrix also involves the distal bone as well as adjacent tissue and skin, the disorder is referred to as pachydermoperiostosis (POPP syndrome).

The severity of nail psoriasis does not correlate closely to the extent of the skin involvement in psoriasis patients. Nor does it differ between the various types of psoriasis. Even severe nail changes are generally reversible, because they arise due to changes in the epidermal cellular kinetics and differentiation and do not lead to scarring or permanent loss of the nail. Pustular forms of psoriasis are an exception.

Etiology, genetics, and pathogenesis

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Psoriasis is a multifactorial disease in which genetic factors and environmental influences (infections, smoking, certain medications) are involved in the pathogenesis of disease. Just as in psoriasis of the skin, in nail psoriasis genetic determinants play a significant role in many patients. It is more frequent in HLA-Cw0608-negative patients. The disease course in HLA-Cw0608-positive patients in whom nail psoriasis develops at a later age appears to be more severe, while HLA-Cw-0602-positive patients with an early onset of disease more often develop psoriasis guttata and have milder nail involvement [7]. Coupling studies have identified -various susceptibility loci (PSORS) of which PSORS1 on chromosome 6p21 has been reproducible in all studies. Located in this region, the HLA-CW*0602 allele has the strongest association to the disease, especially in patients with type I psoriasis. The risk to develop psoriasis vulgaris is 9 times higher in heterozygous carriers of this “risky” allele and 23 times higher in homozygous carriers[18]. Other studies have shown an association with genetic variations which affect important cytokine pathways in psoriasis, including TNF-α[19] and IL-23 [20, 21].

The close anatomic relationship between the nails, tendinous attachment to the bone, and the periosteum explains the significantly higher prevalence of nail psoriasis in patients with psoriatic arthritis [22]. Histological studies of the functional unit have improved our understanding of the basis of this connection between the nail and the joint. These results have shown that the extensor tendon of the distal phalanges of the fingers not only inserts on the dorsal aspect of the distal phalanx, but also has connections further distally via the fibrous connective tissue as far as the nail radix [23]. These data suggest that the micro-anatomical origin of nail psoriasis lies in the relationship between enthesitis and joint disease [24]. In addition, the entheses and the skin share anatomical similarities. Both have poorly vascularized tissue (epidermis, fibrocartilage) and well vascularized tissue (dermis, bone) joined by a bounding surface. Observations such as those mentioned above support the concept that there is a group of diseases, such as psoriatic arthritis and nail psoriasis, in which an autoimmune inflammatory reaction affects a certain site primarily due to tissue-specific factors (microtrauma, altered permeability, increased tissue stress). The nail is just as much a part of the anatomical functional unit of the enthesis as of the skin [25]. The fascia of the enthesis transitions into and is continuous with the nail radix. A research group led by McGonagle [26] and Tan [27] used MRI of the finger to study the anatomical correlations. Histologically, and with high-resolution MRI, one could see that the extensor tendon which crosses the distal interphalangeal (DIP) joint is connected with the nail radix and matrix via tendinous fibers surrounding the radix. In PsA there is nearly always enthesitis of the DIP joint in the early phase of disease. The inflammatory reaction may be severe, even affecting the nail matrix. This close relationship between the nail, tendinous attachment to the bone, and periosteum may explain why patients with psoriatic arthritis, who typically have inflammatory changes affecting the DIP joint, often develop inflammation of the nail, too.

Diagnosis

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The diagnosis of psoriatic nail changes can usually be made based on clinical appearances, especially if the patient also has typical skin lesions. Given that nail psoriasis rarely manifests (1–5%) without psoriasis, the patient history or clinical findings usually reveal plaque psoriasis or psoriatic arthritis. In patients with nail changes affecting individual fingers or toes, onychomycosis should be ruled out with a plain specimen and fungal culture. If the nail changes are of uncertain origin, without accompanying skin changes, a biopsy may be useful in order to confirm the diagnosis. Because nail growth is slow, photo documentation is essential to assess therapeutic outcomes in nail psoriasis.

Differential diagnostic considerations

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The most important epidemiological and clinical differential diagnosis is onychomycosis, which usually affects the toenails. The clinical diagnosis is only presumptive. The detection of spores and mycelia in microscopy or fungal cultures is required to confirm the diagnosis. Although the nails may exhibit all features of nail psoriasis, onycholysis, slower nail growth, and a chronic progressive course are more common in onychomycosis (Table 2). Histological examination shows marked hyperkeratosis and an accumulation of neutrophils as well as patchy hypergranulosis with papillomatous hyperplasia of the nail bed. Hyphae and spores in the subungual, hyperkeratotic tissue and on the bottom side of the nail plate are diagnostic proof of onychomycosis.

Table 2.  Distinguishing nail psoriasis from onychomycosis (modified after Haneke 2010. In: ìDifferentialdiagnosen der Nagelpsoriasis, Ligatur; Verlag für Klinik und Praxis 2010).
 Nail psoriasisOnychomycosis
FrequencyMost frequent skin disease with nail involvementMost frequent nail disorder
Age-dependencyTwo age peaks (Children/adolescents and patients aged 40–60 years)Frequency increases with age
Clinical changes
PittingVery common, numerousRare
OnycholysisCommonCommon
DiscolorationYellow or brown/redNone, yellow (also brown, etc.)
LeukonychiaRareQuite rare
Splinter hemorrhageRareVery rare
Nail growthSomewhat fasterGenerally slower
OtherOften psoriasis of the skin, only up to 5% have isolated nail involvementOften additional clinical signs of tinea pedum, manuum, or corporis
HistologySevere hyperkeratosis with collection of neutrophils and serum inclusions, often columnar parakeratosis containing pyknotic neutrophilsSevere hyperkeratosis with accumulation of neutrophils and serum inclusions
 Focal hyperkeratosisFocal hypergranulosis
 Hyperplasia of the nail bedPapillomatous hyperplasia of the nail bed
 Spongiosis and mononuclear exocytosisSpongiosis and mononuclear exocytosis
 Psoriasis pitting: indentations in the nail plateHyphae and spores in the subungual hyperkeratosis and underside of the nail plate

Common differential diagnostic considerations also include nail changes associated with eczema, and less often with lichen planus (Table 3). Other less common skin diseases such as pityriasis rubra pilaris, Darier disease, collagen disorders, bullous autoimmune diseases, and various genodermatoses may also be associated with nail abnormalities. If solitary nails are affected, the presence of a tumor, such as subungual melanoma or epithelial tumor of the nail, should be considered. The differential diagnosis of nail changes should also include metabolic and systemic diseases.

Table 3.  Differential diagnoses for nail psoriasis.
Onychomycosis
Eczema with nail involvement
Lichen planus
Acute palmoplantar pustulosis
Reiter disease
Pityriasis rubra pilaris (type I)
Darier disease
Lupus erythematosus
Mycosis fungoides
Bowen disease
Alopecia areata
Erythema exudativum multiforme
Acrokeratosis paraneoplastica (Bazex syndrome)
Antiphospholipid syndrome
Dermatomyositis
Scleroderma
Pemphigus vulgaris and pemphigoid variants
Systemic diseases (e.g., hepatopathy, amyloidosis, anemia, gout)
Vitamin deficiencies
Toxic substances causing nail damage

Evaluating the severity of nail psoriasis

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The most common methods to determine disease severity, such as PASI and DLQI, do not include specific features of nail psoriasis and accordingly do not differentiate between influences due to psoriasis or nail involvement. A number of scores have been specifically developed in order to assess the level of severity and to evaluate the course of disease [28]. The NAPSI has been the most widely used in clinical studies; the NPQ10 score specifically documents the quality of life; the NAPPA, the newest tool, measures the three aspects – objective status, quality of life, and treatment benefit to the patient.

NAPSI score

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The nail psoriasis severity index (NAPSI) was one of the first scores created for the measurement of nail involvement. The affected nail is divided into 4 quadrants; in each of these the alteration in both nail matrix and nail bed are evaluated (Figure 3). The individual values (0–4) are added for each nail, so that the maximum score for each hand or foot is 40. The total score for all nails ranges between 0 and 160. The higher the NAPSI score, the worse is the nail involvement. The score is reproducible and objective [29, 30]. A further, validated development is the Modified Nail Psoriasis Severity Index [31].

image

Figure 3. Determining the NAPSI score.

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NPQ10 score

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

In France, Ortonne and colleagues have developed a scoring system that evaluates the effects of nail psoriasis on quality of life. This instrument consists of 10 questions (pain and limitations of the daily life), and the final score is calculated by adding the individual scores to a total between 0 and 100. Higher scores indicate a lower quality of life. The validation study reported clinically relevant impairment in the quality of life of patients with nail psoriasis in terms of physical, psychological, and social effects [32].

NAPPA score

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The newest and the internationally best validated method of measuring the severity of nail psoriasis is the NAPPA score (Nail Assessment in Psoriasis and Psoriatic Arthritis). This instrument evaluates the quality of life of patients as well as the benefit of the treatment over the course of the disease. It is the only survey that covers the various dimensions of the burden of the nail involvement. The validity, ease of use, and patient acceptance have been shown to be very good [33]. Determining clinical severity is very straightforward. NAPPA has been used in clinical studies as well as in routine care.

Impact on quality of life

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Severe nail psoriasis is correlated with severe skin lesions (as measured by the affected body surface area [BSA] and PASI score) [34] and a longer disease course [5]. One German study with 3,531 patients reported that the duration of disease in patients with nail psoriasis was significantly longer (21.9 vs. 18.1 years), the average severity of disease as measured by PASI (12.7 vs. 9.3) was greater, and the percentage of patients with PsA higher (26.0 vs. 12.7%) [1] (Table 4). 72.8% of respondents had nail psoriasis, and among these patients the quality of life parameters compared with psoriasis patients without nail involvement was significantly poorer (DLQI 7.2 vs. 5.3; EQ5-D 60.1 vs. 67.3). Absenteeism is also higher among patients with nail involvement (9.8 vs. 3.3 days annually). Patients with nail involvement are hospitalized more often due to psoriasis. In addition, patients with nail involvement more often have a positive family history of disease. The results have been confirmed by a study on a large cohort of patients in the German Psoriasis Association [35]. Nail psoriasis was shown to cause psychological stress as well as pain and physical restrictions.

Table 4.  Comparison of psoriasis patients with and without nail involvement (modified after Augustin, Radtke et al. 2010) [1]; n = 3.531.
 With nail involvementWithout nail involvement
IndicatorsWomenMenWomenMen
  1. 1PASI: Psoriasis Area Severity Index; 2DLQI: Dermatology Life Quality Index (0 = no impairment; 30 = maximum impairment), 3in last 5 years.

PASI1 > 2015.6%21.4%8.7%12.2%
DLQI2 > 1038.3%32.2%28.5%25.5%
Positive family history45.6%43.0%41.6%32.0%
Inpatient treatment329.2%34.8%14.3%14.9%
Psoriatic arthritis28.7%24.4%13.7%11.9%

De Berker and colleagues have reported that 93% of patients perceive their nail psoriasis as an important social problem which influences their professional life in particular; 52% of patients report frequent pain [36]. Restrictions on daily working life were very common [37].

Psoriatic onychodystrophy is often considered by dermatologists to be a -negligible “secondary problem.” Yet the clinical problems due to stigmatization, limitations on everyday activities, secondary infections, and pain can indeed reach serious clinical dimensions. In regard to isolated nail psoriasis, the risk-to-benefit ratio of systemic treatment should be considered. In many patients, nail psoriasis leads to functional limitations of manual skills. A survey of 1,728 patients with nail changes showed that more than half (51.8%) had pain and more than 90% reported cosmetic impairment. 77% wanted to have their nails treated. Armesto and colleagues [2] suggested in their epidemiological study of 611 patients that patients with nail psoriasis are significantly more often affected by comorbidities, more severe psoriasis, more often have psoriatic arthritis, and on the whole have more prolonged disease.

Therapy

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Nail psoriasis is often overlooked in outpatient and clinical care, and, despite its dramatic effects on the quality of life, many patients fail to receive specific treatment, even when it is the very reason the patient visited his doctor in the first place [37]. One problem is the limited effectiveness of the available preparations and the short remission times. Given the anatomical structure of the nail, it is difficult to achieve sufficiently high concentrations of topical antipsoriatic drugs in the nail plate, nail bed, or nail matrix. Good penetration of the agent is essential. The choice of treatment depends on clinical presentation and patient-related factors. Systemic treatment is indicated in patients with severe nail psoriasis or moderate-to-severe psoriatic skin lesions. Systemic therapy should also be favored if there is concomitant joint involvement (psoriatic arthritis). The choice of the treatment depends on various factors which may include the patient's history and the examination: these include age, sex, appearance of the nail psoriasis, disease course, accompanying diseases and therapies, individual patient preferences, as well as advantages and risks of treatment. The correct diagnosis made by a dermatologist is the starting point for proper treatment planning (Table 5).

Table 5.  Treatment options for nail psoriasis.
Topical treatment
Urea
Corticosteroids, intralesional
Corticosteroids + calcipotriol combination preparation
Vitamin D3 derivatives (calcipotriol, tacalcitol)
5-fluorouracil
Anthralin
Tazarotene
Laser therapy
Pulsed dye laser
Phototherapy
UVA / PUVA
Systemic therapy
Fumaric acid esters
Cyclosporine A
Methotrexate
Retinoids
Biologicals
Adalimumab
Etanercept
Golimumab (if concomitant PsA)
Infliximab
Ustekinumab

Topical therapy

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

The fundamental challenge for topical therapy arises from the fact that the antipsoriatic agents can only very slowly penetrate into the nail plate – or not at all. This results in a low concentration of the active agent at the target site of the immunological process. External agents are available in different vehicles (tinctures, ointments, creams, and nail polish). Topical corticosteroids may be injected intralesionally (e.g., using Dermo-Jet injections), achieving higher concentrations at the site of the inflammation. Tinctures and creams may be massaged into the proximal and lateral nail folds and the effects of the substances may be increased with occlusion.

Urea: Specially designed preparations for nail psoriasis are available in 15% urea in a stable nail polish. Hyperkeratosis may be treated with a user-friendly polish that may be precisely applied. After the solvent has evaporated, the polish dries and the urea concentration increases to 50%, which results in a keratolytic effect. With daily use, denaturation of the damaged nail keratin occurs as a result of the breaking of the hydrogen bonds and induces re-growth of the nail keratin. After 6 months of treatment with a urea-based polish, nail thickness is reduced and the nail appears smoother and healthier.

Corticosteroids: Intralesional steroid injections are a traditional form of treatment which offer safe and effective treatment of nail psoriasis, especially if the nail matrix is involved. Injection dosages, concentrations, and the frequency of injections have not yet been standardized. In various, mostly open, uncontrolled studies, triamcinolone acetonide in concentrations of 10 and 40mg/ml has been injected weekly or monthly [38, 39, 40, 41, 42]. Although there are only a few randomized, double-blind studies in the literature, the available evidence suggests that the intralesional injection of corticosteroids is especially effective in alleviating nail matrix changes and also counteracts pitting. Specific dosages are injected directly into the nail structure or nearby using a needle or Dermo-Jet syringe. The injection frequency varies: some studies report one-off injections [43] while others report weekly or monthly administration [40, 42]. Other sources, including the authors, recommend administration every 3–4 weeks (4–6 injections) or monthly injections for the first 6 months, then 4 injections spread over another 6 months, and then every 2 months for the following 6–12 months. Disadvantages of intralesional corticosteroid use are pain related to the injection as well as the risk of atrophy of the proximal nail fold or even tendon rupture [4]. Most patients prefer the Dermo-Jet syringe over needle injections as it is significantly less painful. Topical steroids may also be applied in a cream or solution to the nail fold and periungual regions, if necessary under occlusion [44, 45, 46]. The response rates vary depending on the strength of the steroid and duration of treatment [47].

Calcipotriol: Rigopoulos and colleagues [48] treated 62 patients in an open study with topical calcipotriol once daily overnight on 5 days a week as well as -clobetasol propionate cream twice a week for a total of 6 months; after this clobetasol propionate cream was given twice a week for a total of 6 months. The authors reported a reduction of fingernail hyperkeratosis of around 35.2% after 2 months and around 32.6% for the toenails. After 6 months of treatment, this increased to 72.3% for the fingernails and 69.9% for the toenails. A case series on the safety and efficacy of topical calcipotriol on 24 patients with nail psoriasis showed that the special qualities of this treatment may lie in the reduction of onycholysis, hyperkeratosis, and nail discoloration [49]. After stopping therapy, the patients’ nail condition generally worsened again. Topical treatment with calcipotriol, especially in combination with steroids, is thus a possible treatment option [50, 51, 52].

5-fluorouracil: Only limited and badly outdated data are available on topical 5-fluouracil therapy (5-FU). A randomized, double-blind study found that after 12 weeks of application of 1% fluorouracil, none of the preparations were superior to the vehicle [53]. A prospective study by Fredriksson [54] examined the effectiveness of 1% 5-FU solution on 20 patients with severe nail hyperkeratosis, pitting, and onycholysis. The solution was applied twice daily for 6 months around the nail and massaged into the nail fold. After treatment the majority of patients (17/20) had significant improvement of 25% over baseline with regard to hyperkeratosis and pitting. In patients in whom onycholysis predominated, the treatment was not effective and is therefore not recommended.

Anthralin: In a study by Yamamoto and colleagues [55], in 20 patients topical therapy with 0.4–2% anthralin in vaseline was administered once daily for 30 minutes. Then the agent was rinsed off with water and 10% triethanolamine cream was applied to prevent pigmentation due to use of the drug. Within 5 months of treatment, 12 of the 20 patients (60%) had significant or moderate improvement, with improvement of the onycholysis and paronychia and reduced nail pitting. In 20% the treatment was ineffective. The main side effect was pigmentation of the nail plate. There is still insufficient evidence for making recommendations on the use topical anthralin.

Tazarotene: A double-blind, randomized, controlled study examined the administration of tazarotene 0.1% gel in 31 patients for 24 weeks [56]. The results showed a reduction in onycholysis and nail pitting, yet there was no significant effect on subungual hyperkeratosis, leukonychia, and splinter hemorrhage. Another double-blind, randomized study compared the efficacy of a 12-week regimen of tazarotene cream to clobetasol propionate. No statistically significant differences were found in terms of efficacy. Nail pitting, hyperkeratosis, and onycholysis improved significantly in both treatment arms.

Phototherapy: Phototherapy is an important part of psoriasis therapy and has also effectively been used against nail psoriasis. Either UVA or UVB light may be used. UVA light is able to penetrate the nail bed and the hyponychium. Published case series have shown that continuous irradiation can achieve moderate improvement in onycholysis as well as nail discoloration and subungual hyperkeratosis. In one study on systemic PUVA therapy, symptoms improved by around 50% in 70% of treated patients, [57]. Another study on topical PUVA therapy showed that 4 out of 5 treated patients had significant improvement in onycholysis and nail pitting decreased [58].

Systemic therapy

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

Fumaric acid esters are compounds of fumaric acid, a metabolic product of the human body. They were approved for psoriasis treatment in Germany in 1995. The dosage is gradually increased based on an established dosage scheme. The maximum recommended dosage is 1.2 g/day (6 tablets daily), although this is not always necessary for effective treatment. Limitations include commonly occurring gastrointestinal side effects and intermittent flush as well as occasional lymphocytopenia, which may necessitate a dosage reduction or premature discontinuation of treatment. The goal is to find an individual dosage with which the psoriasis may be treated effectively without major side effects. There are no available results from controlled studies on the treatment of nail psoriasis, but only from isolated case studies [59]. Treatment may be attempted if there are no contraindications.

Cyclosporine A has been used since 1983 in transplantation medicine; it was approved in 1993 for interval therapy (short-term/induction therapy) and continuous long-term treatment of psoriasis. It reduces skin symptoms via immunosuppression resulting from the inhibition of T-cell activation and diminished release of inflammatory mediators. Depending on the dosage, 50–70% of patients (2.5 to 5mg/kg of body weight) have partial remission of around 75% (or Psoriasis Area and Severity Index [PASI] 75) after an average of 12 weeks, and 30 to 50% experience complete remission (PASI 90). The data on nail psoriasis are sparse. In an uncontrolled study by Syuto and colleagues [60] on 16 patients, cyclosporine was given at a dosage of 3mg/kg of body weight. 14 out of 16 patients had marked improvement, 10 out of 16 had significant improvement, and 2 healed completely. In a comparative study on 54 patients by Feliciani and colleagues [61], some of the patients were given combination therapy consisting of cyclosporine and topical calcipotriol; 33 patients received cyclosporine monotherapy. After 3 months, 79% of patients who were given combination therapy had a “good” or “excellent” result compared with 48% who were given monotherapy. The combination with topical preparations for treating psoriasis vulgaris may thus be a useful option, especially considering that the dosage may be reduced if local therapy with vitamin D3 analogues or corticosteroids is simultaneously administered, without compromising effectiveness.

Various drug interactions must be considered when using cyclosporine. On the one hand, these may alter the bioavailability of cyclosporine or other drugs, while on the other hand there is an increased risk of adverse effects. Cyclosporine is contraindicated in patients with relevant kidney dysfunction, inadequately controlled hypertension, severe infection, or a history of or current malignancy [62]. After one to two years at most, given the potential side effects of the drug – especially nephrotoxicity, hypertension, and an increased risk of malignancy – a critical assessment must be made as to whether to continue treatment.

Methotrexate (MTX) is one of the primary immunosuppressants used to treat severe inflammation. The preparation was initially developed for the treatment of neoplasms because it inhibits the proliferation of rapidly dividing cells such as cancer cells. The effectiveness of folic acid antagonists was first reported in 1951. In 1991 in Germany MTX was approved for the treatment of severe psoriasis. Contraindications arise mainly due to toxic effects on the liver and kidneys in association with certain prior illnesses. There is also a risk of bone marrow suppression. MTX is generally initiated at 5 to 15mg/weekly and then the dosage is adapted individually. The recommended maintenance dose is 5 to 22.5mg/weekly. Parenteral administration is preferred over oral use because it is more effective and better tolerated. It is no longer customary to give an established test dosage before the actual maintenance dose. In patients who respond to treatment, the drug becomes clinically effective after four to six weeks.

A number of studies on the clinical efficacy of MTX in patients with nail psoriasis exist: Gümüsel and colleagues reported that for a starting dosage of 15mg/weekly there was an average reduction in NAPSI of around 43.3% after 24 weeks of treatment. Compared to systemic therapy with cyclosporine, with an average reduction in NAPSI of around 37.2%, MTX was significantly superior, especially in regard to the response of psoriasis in the nail matrix region [63]. In a randomized clinical study, Reich and colleagues reported a 36.8% improvement in the NAPSI score after 24 weeks of MTX treatment. After 52 weeks of therapy, the average NAPSI reduction was 39.3%. Careful monitoring of laboratory parameters is essential. Indications for stopping treatment and further tests include elevated transaminase levels over three times normal, anemia, decreased leukocyte or thrombocyte counts in peripheral blood, increased creatinine levels, acute dyspnea and cough, as well as severe infections. Usually a decrease in leukocytes and thrombocytes is seen seven to ten days after the last dosage is given. MTX should be discontinued in patients who develop severe leukocytopenia, diarrhea (dehydration), ulcerative stomatitis, nephrotoxicity, or pulmonary toxicity. An increase in mean corpuscular hemoglobin (MCH) is a common occurrence and indicates the development of megaloblastic anemia. Folic acid substitution (5mg) the day after taking MTX can help avoid mild side effects of MTX [62]. The administration of methotrexate may slow down nail growth.

Acitretin is a vitamin A derivative (retinoid). It is less effective in plaque psoriasis than other systemic drugs, but it is especially useful in patients with pustular forms of disease. At the beginning of oral administration, the drug is usually -administered in higher dosages, and over the course of disease the dosage is reduced to a minimum level. A marked response is usually not evident until after four to eight weeks. Tosti and colleagues gave 36 patients with isolated nail psoriasis acitretin (0.2–0.3mg/kg of body weight) for 6 months, achieving an average NAPSI reduction of around 41%[64]. Complete or nearly complete healing was achieved in almost 25% of patients. Retinoids often cause dry skin and mucous membranes with a feeling of tension or itching. Acitretin is often given in combination therapy, for instance with phototherapy. As monotherapy, systemic retinoids may only be recommended in certain situations. They should not be given to women of child-bearing age. One should recall when treating nail psoriasis with systemic retinoids that they promote the development of paronychia.

Adalimumab is a human monoclonal antibody that targets TNF-α. Adalimumab binds with high affinity and specificity to soluble and membrane-bound TNF-α. This prevents binding to the TNF-α receptor (p55 and p75) and blocks the biological effect of TNF-α. The drug is given by subcutaneous injection every 14 days. Van den Bosch and colleagues [65] reported that treatment led to an average NAPSI reduction of about 45% after 12 weeks of therapy and about 65% after 20 weeks. A study by Thaci and colleagues [66] reported that after 16 weeks there was an average NAPSI reduction of 39.5%. In placebo-controlled studies, the most commonly reported side effect were reactions at the injection site (adalimumab: 20%; placebo: 14%). In the event of a severe side effect or infection, adalimumab should be discontinued and the symptoms treated. Treatment is feasible for the doctor and patient. Similar to reduced antibody formation seen in simultaneous use of MTX and infliximab, the combination of MTX and adalimumab could also counteract the antibody formation and presumably prolong the treatment response.

Etanercept is a fusion protein that is composed of 2 p75 components of the TNF-α receptor which are coupled with the Fc portion of a human IgG1 immunoglobulin. As a soluble receptor etanercept binds free TNF-α, but not membrane-bound TNF-α, and blocks the inflammatory cascade triggered by it. It thus has anti-inflammatory and immunosuppressant properties. The initial therapy consists of twice weekly subcutaneous injection of 50mg for 12 weeks. A dosage of 50mg/weekly has been approved for maintenance therapy. Given the pharmacokinetics of etanercept, it is not necessary to adjust the dosage in patients with restricted kidney and liver function. After absorption, etanercept enters the various tissues and bodily fluids, including the synovial fluid. In a post hoc analysis by Luger and colleagues, the administration of etanercept 25mg twice weekly led to an average reduction in the NAPSI scores of around 51% after 54 weeks (711 patients with psoriasis, of whom 80% had nail involvement) [67]. The average NAPSI reduction after 12 weeks of therapy was 28.9%.

Golimumab is a human monoclonal antibody. In the framework of binding to the human TNF-α, golimumab forms high affinity stable complexes with soluble as well as membrane-bound bioactive forms of TNF-α and thus prevents TNF-α from binding to the corresponding receptors. The preparation is approved for use as monotherapy as well as in combination with methotrexate for the treatment of psoriatic arthritis, if the response to prior treatment with a disease-modifying anti-rheumatic drug (DMARD) was inadequate. Treatment with 50mg golimumab every 4 weeks has been shown to achieve an average improvement in NAPSI after 14 weeks of 25% and after 24 weeks of 33%[68]. Based on current studies, its efficacy against cutaneous psoriasis appears to not be quite as high as for the other TNF-α antagonists which have been approved for systemic treatment of psoriasis.

Infliximab is a chimeric monoclonal antibody that blocks free and receptor-bound TNF-α. The dosage is adjusted according to the patient's weight and administered intravenously.

Infliximab is an IgG1 immunoglobulin with human sequences in the constant regions and murine sequences in the complementarity determining regions of the light and heavy chains. The most comprehensive investigation of the -efficacy in nail psoriasis is from a phase III, multicenter, double-blind, placebo-controlled study for the evaluation of long-term efficacy and safety of infliximab in patients with moderate to severe plaque psoriasis. The primary endpoint of the study was the percentage of patients with at least a 75% improvement in Psoriasis Area and Severity Index (PASI) score compared to baseline. The -percentage of improvement in NAPSI in weeks 10, 24, and 50 was examined -separately. Infliximab led to complete eradication of nail psoriasis in 6.9% of patients within 10 weeks, 26.4% after 24 weeks, and 44.7% after 50 weeks [69, 70]. The average reduction in NAPSI was 28.9% after 12 weeks of treatment and 51% after 54 weeks of treatment. Complete healing was reported after 54 weeks in 30% of patients. Based on the label for psoriasis vulgaris for nail psoriasis as well, in the induction phase the infusions are adjusted by weight (5mg/kg of body weight), given on day 0, week 2, week 6 and then every 8 weeks. Acute infusion reactions are common and are usually mild, consisting of chills, headache, flush, nausea, dyspnea, or infiltration at the infusion site. The probability of an infusion reaction is higher in patients with infliximab–specific antibodies. Yet anaphylactoid reactions – irrespective of having infliximab-specific antibodies – are also possible. These require surveillance of the patient during the infusion and for one hour after the infusion. Renewed administration of treatment after a longer interval may cause arthralgia, myalgia, angioedema, or other acute reactions [62].

Contraindications for the use of TNF-α antagonists include acute or chronic infections, especially latent tuberculosis, advanced cardiac insufficiency (NYHA class III–IV), as well as pregnancy and nursing. Tuberculosis should be ruled out before starting therapy. Extra caution is warranted in patients with hematological changes (leukocytopenia, thrombocytopenia), demyelination processes, and prior neoplasms.

Ustekinumab is a recombinant, completely human, monoclonal antibody which binds with high affinity and specificity to the common p40 protein subunit of the cytokines IL-12 and IL-23, and thus selectively blocks differentiation and expansion of helper T cells (Th)1 and Th17. In a phase III study, using a standard dosage of ustekinumab 45 mg, after 12 weeks of treatment there was a reduction of the median NAPSI of around 25%; and after 24 weeks of around 50%[71]. An initial dose of 45mg is recommended at week 0, followed by a 45mg dose in week four and then every 12 weeks. For patients weighing >100kg the dosage per injection is 90mg. Ustekinumab is approved for the treatment of moderate-to-severe psoriasis vulgaris in adults in whom other systemic therapies including cyclosporine A, methotrexate, and PUVA failed, are contraindicated, or are not tolerated.

Adjuvant measures

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis

In addition to using medication to treat nail psoriasis, patients should be informed about adjuvant therapies which can positively influence the course of disease and healing. Routine visits to a podiatrist may be indicated in patients with -severe disease. This can help avoid mistakes in proper nail and foot care. The patient should be informed by his physician about meticulous nail care. Measures to protect the nails can be an important part of treatment success. These include protecting the fingers by wearing gloves when handling chemically or physically aggressive materials at home or at work. Patients should preferably keep their fingernails and toenails cut short. Injuries to the nails, especially the cuticles, should be avoided. When washing the hands, it is important to dry off the tips of the fingers carefully with a paper tissue to absorb moisture that can get under the fingernails. Acetone-based nail polish removers should be avoided. Patients who have nail psoriasis of the toes should wear light shoes that breathe and do not create pressure on the feet.

Conclusions for clinical practice

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis
  • • 
    Involvement of the nails in psoriatic inflammatory reactions is a major problem for most patients.
  • • 
    Nail involvement is a predictor for a severe disease course in patients with psoriasis. By definition, it may result in a higher severity of disease and may make other treatment goals necessary.
  • • 
    Management includes careful diagnosis; in particular, onychomycosis must be ruled out. Another special diagnostic consideration is the possibility of psoriatic arthritis.
  • • 
    Local therapy with corticosteroids and vitamin D analogues, as well as with UV therapy, should be attempted initially, but the effects are more limited than in skin lesions.
  • • 
    In patients with severe disease, severe impairment of QoL, or topical treatment fails, systemic therapy with conventional or biological agents is warranted.
  • • 
    For patients on systemic therapy, routine evaluation of the level of severity and photo documentation are advised.
  • • 
    In order to enhance the success of topical and systemic treatment, routine nail care and protective measures are helpful.

References

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis
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Fragen zum CME-Artikel Nagelpsoriasis

  1. Top of page
  2. Summary
  3. Epidemiology
  4. Structure of the nail
  5. Clinical manifestations
  6. Etiology, genetics, and pathogenesis
  7. Diagnosis
  8. Differential diagnostic considerations
  9. Evaluating the severity of nail psoriasis
  10. NAPSI score
  11. NPQ10 score
  12. NAPPA score
  13. Impact on quality of life
  14. Therapy
  15. Topical therapy
  16. Systemic therapy
  17. Adjuvant measures
  18. Conclusions for clinical practice
  19. References
  20. Fragen zum CME-Artikel Nagelpsoriasis
  • 1
    Welche belegten Assoziationen weist die Nagelbeteiligung bei Psoriasis vulgaris auf?
    • a) 
      Geringere Wahrscheinlichkeit einer Psoriasis-Arthritis
    • b) 
      Geringeres Aufkommen an Alkohol-Abusus
    • c) 
      Höherer klinischer Schweregrad der kutanen Herde (PASI)
    • d) 
      Geringere Rate an Arbeitsunfähigkeit
    • e) 
      Niedrigere Häufigkeit einer positiven Familienanamnese
  • 2
    Welche genetischen Merkmale gelten auch für die Nagelpsoriasis?
    • a) 
      Nagelpsoriasis weist nur eine geringe Vererbbarkeit auf
    • b) 
      Nagelpsoriasis ist häufiger bei HLA-Cw0608-negativen Patienten zu finden.
    • c) 
      HLA-Cw-0602-positive Patienten entwickeln keine Guttata-Formen der Psoriasis
    • d) 
      Die Risikoallele für Nagelpsoriasis liegen ausschließlich auf Chromosom 3
    • e) 
      Kopplungsstudien haben bislang keine Suszeptibilitätsloci für Psoriasis identifiziert
  • 3
    Welches der nachfolgenden Merkmale findet sich bei Nagelpsoriasis und beruht in erster Linie auf Entzündungen der Nagelmatrix?
    • a) 
      Onychodystrophie
    • b) 
      Onychodystonie
    • c) 
      Subunguale Hyperkeratose
    • d) 
      Splitterblutungen
    • e) 
      Psoriatischer Ölfleck
  • 4
    Welches der nachfolgenden Merkmale findet sich bei Nagelpsoriasis und beruht in erster Linie auf Entzündungen des Nagelbettes?
    • a) 
      Onychodystrophie
    • b) 
      Grübchen (Tüpfelnägel)
    • c) 
      Subunguale Hyperkeratose
    • d) 
      Onychodystonie
    • e) 
      Paronychie
  • 5
    Welches der nachfolgenden Evaluationsinstrumente wurde spezifisch für die Nagelpsoriasis entwickelt?
    • a) 
      DLQI
    • b) 
      NASA
    • c) 
      NFR-30
    • d) 
      NAPPA
    • e) 
      NVK-1
  • 6
    Welches der nachfolgenden Therapeutika ist in seiner klinischen Wirksamkeit bei Nagelpsoriasis bisher nicht durch publizierte kontrollierte Studien geprüft (Stand Dezember 2012)?
    • a) 
      Ustekinumab
    • b) 
      Dapson
    • c) 
      Infliximab
    • d) 
      Adalimumab
    • e) 
      MTX
  • 7
    Welche Aussage zu therapieunterstützenden Maßnahmen bei Nagelpsoriasis ist zutreffend?
    • a) 
      Eine podologische Versorgung ist bei gleichzeitiger Systemtherapie kontraindiziert
    • b) 
      Das Schuhwerk ist bei Nagelpsoriasis der Zehen von nachrangiger Bedeutung
    • c) 
      Nagelpflege sollte nicht durch den Patienten erfolgen
    • d) 
      Acetonhaltige Nagellackentferner unterstützen die Ablösung betroffener Nägel
    • e) 
      Hautschutzmaßnahmen an den Fingern sind bei Umgang mit Irritantien in Beruf und Haushalt anzuraten
  • 8
    Welche Aussage zur topischen Therapie der Nagelpsoriasis trifft zu?
    • a) 
      Für die Wirksamkeit topischer Vit.-D-Analoga gibt es keine Evidenz
    • b) 
      Wegen ihres atrophogenen Potentials dürfen topische Glukokortikosteroide nur über wenige Tage eingesetzt werden
    • c) 
      In der Therapie mit topischen Glukokortikosteroiden sind intraläsionale Injektionen und Dermojet-Behandlungen weniger wirksam als Salbenanwendungen
    • d) 
      Die Fototherapie ist eine weitere mögliche Therapieoption
    • e) 
      Für Anthralin und Tazaroten liegen keine Erkenntnisse aus klinischen Studien vor
  • 9
    Welche weitere Hautkrankheit kann bei Nagelpsoriasis in der Differentialdiagnostik ausgeschlossen werden?
    • a) 
      Onychomykose
    • b) 
      Lichen ruber planus
    • c) 
      Subunguale Tumoren
    • d) 
      Ekzemnägel
    • e) 
      Keine der genannten
  • 10
    Nagelpsoriasis an den Fingern geht bei betroffenen Patienten mit z.T. erheblichen psychosozialen Belastungen einher. Welcher der genannten gehört nicht dazu?
    • a) 
      Eingeschränkte Funktionsfähigkeit bei manuellen Tätigkeiten
    • b) 
      Scham und sozialer Rückzug
    • c) 
      Verminderte Lebensqualität
    • d) 
      Höheres Psychoserisiko
    • e) 
      Erhöhter Aufwand mit der Nagelpflege

Liebe Leserinnen und Leser,

der Einsendeschluss an die DDA für diese Ausgabe ist der 19. April 2013. Die richtige Lösung zum Thema –Systemische Sklerodermie – Fokus auf dermatologischen Aspekten. Teil 2: Diagnostik, Therapieì in Heft 11 (November 2012) ist: 1a, 2c, 3e, 4e, 5d, 6d, 7d, 8c, 9b, 10d.

Bitte verwenden Sie für Ihre Einsendung das aktuelle Formblatt auf der folgenden Seite oder aber geben Sie Ihre Lösung online unter http://jddg.akademie-dda.de ein.