Mild-to-Moderate Psoriasis - part 9 pptx

Table 1 Clinical Manifestations of Nail Psoriasis Based on Location of Psoriatic Change in the Nail Unit Nail unit psoriasis location Nail matrix, proximal involvement Nail bed, mid-distal matrix Nail bed only Nail bed and plate Nail bed and hyponychium Proximal nail fold Morphology due to pathologic change: Pitting—deep, irregular indentations in the nail plate Beau’s lines Onychomadesis Leukonychia Red spots in the lunula Crumbling (all matrix) Oil spots Hyperkeratosis Splinter hemorrhages Onycholysis due to distal separation of the two structures progressing proximally Subungual hyperkeratosis (when severe, this is the likely cause of onycholysis) Chronic paronychia Splinter hemorrhages Silvery classic plaques Trachyonychia Crumbling (due to total matrix involvement for a long duration) 224 Nandedkar-Thomas and Scher and splinter hemorrhages are common (15, 16). Oil spots, also known as ‘‘salmon patches,’’ refer to a yellow-orange discoloration due to psoriasis of the nail bed (Fig. 3) (17). Leukonychia is caused by mid-matrix disease. The whitish areas are likely due to adherent foci of parakeratotic cells that cannot be dislodged. Onycholysis is a distinct phenomenon that results from separation of the nail bed from the plate (Fig. 4). The separation begins distally and progresses proximally toward the matrix. The plate appears whitish rather than yellow because air becomes trapped underneath it. It is usually surrounded by a reddish hue (10) and is distinguished from true leukonychia by location. Leukonychia is usually seen on the proximal Figure 2 (See color insert) Pitting in nail psoriasis. Source: Courtesy of Maithily Nandedkar-Thomas. Figure 3 (See color insert) Oil spot in nail psoriasis. Source: Courtesy of Maithily Nandedkar-Thomas. Psoriasis of the Nails 225 portion of the plate whereas onycholysis appears whitish distally. Splinter hemorrhages are due to trauma and are analogous to the Auspitz sign asso- ciated with cutaneous psoriasis (10). Proximal nail fold plaques are marked by classic cutaneous psoriasis with silvery scales over a red base (2). This may appear as chronic paronychia (11). Nail bed psoriasis in conjunction with hyponychial involvement leads to subungual hyperkeratosis and ultimately crumbling of the nail plate (18). While there are numerous man- ifestations of nail psoriasis, very few are characteristic of psoriasis alone. The classic oil spot is the most diagnostic lesion, followed by random finger- nail pitting and subungual hyperkeratosis, respectively (12,17). Extensive onychodystrophy with painful pustules and loss of the nail plate is usually due to a more severe and distinct type of nail psoriasis known as acrodermatitis continua of Hallopeau (19). While most manifestations of nail psoriasis do not lead to scarring, pustular psoriasis remains the excep- tion. Fortunately, this debilitating disorder is rare and often isolated to a single digit (13). Unfortunatel y, despite several treatment options described in the literature, successful eradication of the disorder prior to anonychia and scarring remains poor (20). ASSOCIATION WITH PSORIATIC ARTHRITI S The most common signs of fi ngernail psoriasis are oil spots and pitting, with subungual hyperkeratosis being the most common sign associated with psoriatic Figure 4 (See color insert) Onycholysis in nail psoriasis. Source : Courtesy of Maithily Nandedkar-Thomas. 226 Nandedkar-Thomas and Scher arthritis (21). While subungual hyperkeratosis is also the most common form of toenail psoriasis, it is less often associated with arthritis. Many studies have established that patients with psoriatic distal interphalangeal (DIP) joint dis- ease are highly likely to have associated psoriatic nail changes in the same digit (22,23). One study has also suggested that extent and duration of nail disease correlates with the severi ty of DIP joint disease. Furthermore, even if arthritic changes are not clinically evident, radiographic changes may be seen in the DIP joint of the same fingertip that has visible psoriatic nail disease (24). DIP joint inflammation is not the only form of psoriatic arthritis. Moll and Wright (25) originally classified psoriatic arthritis into five types based on clinical features. Type I refers to primarily DIP bone and joint erosion, which radiographically presents as the classic ‘‘pencil in cup deformity.’’ It affects approximately 5% of all patients. The rarest is Type II, also known as arthritis mutilans, which presents as a severe mutilating arthritis that can have ocular involvement. Type III manifests as a symmetric polyarthritis that affects the small joints of the hands and feet and the large joints of the legs, such as the hips and knees. Type IV is the most common type, affecting approximately 70% of those patients who present with psoriatic arthritis. Asymmetric oli- goarthritis is the hallmark of this type of psoriatic arthritis. It affects the same joints as Type III, and may or may not present with DIP joint involvement. Type V is distinguished by axial disease that affects the spine and sacroiliac joints. It usually presents with ankylosing spondylitis. Of all the psoriatic arthritis types, this one has the least association with nail disease. The major distinguishing characteristic of psoriatic arthritis is that unlike rheumatoid arthritis, it usually presents with asymmetric joint dis- ease. Furthermore, enthesopathy is unique to psoriatic arthritis; it is not seen in rheumatoid arthritis (26). Enthesopathy specifically refers to inflam- mation occurring at the attachment site of tendons and ligaments to bone. Symptoms include joint pain, stiffness, and enthesitis with swelling at the tendon insertion points leading to ‘‘sausage d igits’’ and joint deformation (27). It is classified as a seronegative, inflammatory arthropathy, meaning rheu- matoid factor is usually negative. Much like cutaneous psoriasis, it waxes and wanes unpredictably (28). A recent study sought to determine if psoriatic nail alteration can be used as an independent predictor of psoriatic arthritis, regardless of the type (29). The study looked specifically at patients with the various types of psoriatic arthritis and found that 83% had clinically evident nail disease. As predicted, those patients with DIP involvement had more severe nail damage. Likewise, the severity of nail psoriasis directly correlated with the severity of the enthesitis and skin psoriasis. The arthr itis also tended to be progressive and unremitting in those patients. However, dactylitis and axial disease was not associated with nail disease. In fact, the lesser the nail involvement, the more likely the patient was to have the human leukocyte Psoriasis of the Nails 227 antigen (HLA)-B27 genetic haplotype, which is associated with axial rather than DIP joint disease (28). ASSOCIATED GENETIC HAPLOTYPES While the exact pathogenesis of nail psoriasis remains unclear, certain key HLA subtypes are known to be associated with certain psoriatic types (Table 2) (28,30,31). However, genetic factors alone cannot account for the occurrence of psoriasis. Environmental and immunologic factors most certainly play a role in its inception. The simultaneous onset of skin and joint disease has been correlated with an increased frequency of disease eruptions (3). Although nail changes can be evident, the severity and extent of scalp involvement has been found to be an even better marker for psoriatic arthritis (3). Apparently, worsening of scalp psoriasis is directly correlated with an increase in the number of deformed and swollen joints, sausage digits, and DIP alteration s. Therefore, while nail disease may forecast joint disease on the concomitantly affected dig- it, it is not likely to be the best predictor of psoriatic arthritis in other joints. NAIL PSORIASIS: CHILDHOOD VS. ADULT ONSET Characterizations of childhood psoriasis versus adult psoriasis are numerous and varied. A recent Asian study examining the epidemiology of childhood psoriasis in 419 patients found that boys tend to develop psoriasis at an earlier age than girls (32). Inflammatory nail changes were found in 31% of patients, with pitting being the most common finding, followed by ridging and discol- oration. Interestingly, 2.3% of patients presented with nail disease as the initial Table 2 Key Genetic Haplotypes Associated with Psoriatic Arthritis and Nail Disease Major histocompatibility class I type HLA B27 and HLA-Cw2 HLA-Cw6 HLA-Cw6 negative HLA-B13 and HLA-B57 (B17) Later onset; less nail disease; strong association with axial disease. If early onset, then linked to pediatric spondyloarthropathy, but still has a poor association with nail disease. Earlier onset; nail disease but less dystrophy than if Cw6 negative Stronger association with dystrophic nails than if Cw6 positive If more severe skin disease, then joint or nail disease 228 Nandedkar-Thomas and Scher presentation of their psoriasis. Various studies from around the world have had conflicting findings (33,34). This is likely based on varying genetic haplo- types and immunosusceptibility patterns to infectious disease that predispose to the development of psoriasis (35). A Denmark study found a female prepon- derance with childhood onset psoriasis (36). An Australian study found that the mean onset of psoriasis in children was less than five years of age, whereas most studies note onset to be between the ages of 5 and 14 (32–37). However, despite some contradictory data, certain generalities may be made regarding childhood versus adult onset nail psoriasis. When a familial history of psoriasis is found in association with juvenile-onset psoriasis, the disease course is inevitably more severe, more strongly associated with psoriatic arthritis, and more likely to display nail changes (6,38,39). Most patients, regardless of gender, develop psoriasis afte r the age of 20 (40). When childhood onset of nail psoriasis occurs, it is commonly precipitated by trauma or infectious disease (32,36,41). Also, the later the onset of cuta- neous psoriasis, the less often concomitant fingernail or toenail psoriasis occurs. This is especially true for toenail psoriasis (42). Although rare, when a child presents with nail alteration as the sole manifestation of psoriasis, an evaluation for juvenile psoriatic arthritis should be considered (43). DIAGNOSTIC CHALLENGE: ISOLATED NAIL PSORIASIS AND ITS IMPERSONATORS Onychomycosis The most common misdiagnosis for psoriatic nail disease is onychomy- cosis ( 2). It is e asy to see why this occurs, especially if subungual hyperkeratosis is the primary feature in an isolated nail. For this reason, it is prudent to perform a potassium hydroxide (KOH) wet mount, culture, or nail clipping for a periodic-acid–Schiff stain to e nsure that there is no superimposed onychomycosis. Treatment of the overlying onychomycosis often causes diminution of the hyperkeratosis, allowing the more characteristic psoriatic changes such as oil spots to be revealed. Onychomycosis does not usually cause psoriatic nail changes, but rather each condition may worsen the other (44,45). This is often difficult to eradicate. It is especially true if the super- imposed infection is due to molds rather than dermatophytes (45). Allergic Contact Dermatitis in One Nail Typically, most patients with ungual contact dermatitis also have some other skin site involved, which helps to confirm the diagnosis, although it may be confined to one digit. It is most commonly due to nail trauma or nail cosmetics (46,47). Like most diagnostic dilemmas, a thorough history and examination usually help to ascertain the correct diagnosis. Psoriasis of the Nails 229 Drug Reactions These are often seen in patients taking antibiotics such as minocycline or other phototoxic drugs (48). However, drug-induced onycholysis may occur with no associated cutaneous photosensitivity. Beau’s lines and onychomad- esis are the most common abnormalities associated with drug reactions (49). When they are also associated with onycholysis, the clinical picture can clearly mimic psoriasis (50). A careful evaluation of the history of the lesions should identify the likely culprit. Psoriatic nail changes typically have a slower onset than those due to a drug reaction, which can often be sudden and explosive. Linear Verrucous Epidermal Nevus Linear psoriasis is a rare entity whose existence has been questioned (51). It is difficult to distinguish from linear verrucous epidermal nevus, although it is likel y a true condition that has been well described in the literature (52,53). Biopsy alone may not confirm the diagnosis because histological features may overlap (54,55). Therefore, when only an isolated nail is the presenting sign, unless other presenting signs of psoriasis become manifest it may be impossible to discriminate between the two conditions (56). Lichen Striatus This is an interesting disorder that is also commonly confused with linear epidermal nevus and linear psoriasis. It is more commonly seen in children on an isolated nail. The characteristic findin g is linear trachyonychia and dystrophy of the nail plate with partial pterygium formation and then spon- taneous resolution (57). It does not present with pitting or onycholysis. Parakeratosis Pustulosa This disorde r is seen only in children. It presents with occasional isolated fingertip scaling and erythema in either the thumb or index finger. It may be a variant of psoriasis. Nail changes are always present and include onycholysis and hyperkeratosis on only one side of the nail. Typically, chil- dren have spontaneous resolution of the disorder by the time they reach puberty. However, some may later manifest widespread cutaneous psoriasis after they reach adulthood (11). Squamous Cell Carcinoma Albeit rare, there have been reports of squamous cell carcinoma (SCC) aris- ing in psoriatic nails (58–60). There is only one report of SCC arising in a psoriatic nail bed (50). Interestingly, this man had an exophytic verrucous plaque arising from a psoriatic thumbnail that became progressively larger 230 Nandedkar-Thomas and Scher over a four-month period. Finally, pain prompted the patient to report it to the physician. Because it had progressed substa ntially, the terminal phalanx required amputation. Histological exam of the amputated digit revealed well-differentiated SCC with erosion through the dermis and into the bone. The important feature of this case is that there was a delay in diagnosis because both the patient and the physician assumed that the excess hyper- keratosis was due to worsening psoriasis. DIAGNOSTIC PROCEDURE: THE NAIL BIOPSY There are numerous excellent textbooks that describe the appropriate method for punch biopsy of the nail bed versus the nail matrix (2,61–64). It is a simple straightforward procedure that is safely and routinely per- formed in the office setting. With difficult or challenging cases, the biopsy can be invaluable in ascertaining the cause of the nail abnormality. On occa- sion, both the nail bed and the matrix require biopsy simultaneously. In this case a longitudinal biopsy may be appropriate (65). MEASUREMENT OF SEVERITY: THE NAIL PSORIASIS SEVERITY INDEX It is important to have an objective scale with which to measure disease severity. The psoriasis area and severity index is used primarily for cutaneous psoriasis but does not adequately measure nail disease activity. Therefore, the nail psoriasis severity index (NAPSI) was developed to objectively quan- tify the severity of nail disease in a reproducible manner (66). It was also designed to assess efficacy of drug therapy for different manifestations of nail psoriasis (e.g., pitting vs. subungual hyperkeratosis). Using NAPSI, the nail is divided into four quadrants, each of which is then graded based on the presence or absence of nail matrix or nail bed disease. The highest score possible for each fingernail is 8 for a total of 80. If toenails are included, then the maximum total number increases to 160 (Tables 3 and 4). The sum of the scores is calculated and used to judge the severity of nail psoriasis. Not included in this grading system are proximal nail fold psoriasis, pustular psoriasis, and psoriatic arthritis. Other methods have also been proposed but we find NAPSI the least complex (67). TREATMENT OPTIONS AND COMPLICATIONS FROM THERAPY There are numerous treatments for nail psoriasis. The drugs are usuall y clas- sified as follows: steroids, biologic agents, retinoids, and other miscellaneous therapies such as chemotherapy or phototherapy. Each therapeutic class will be discussed in detail. Psoriasis of the Nails 231 Steroids and Steroid-Like Drugs The high-potency topical steroids are likely the most utilized form of ther- apy for nail psoriasis. Although they are relative ly inexpensive and readily available, tachyphyl axis occurs with prolonged use. The most effective of all steroids for nail matrix psoriasis appears to be the triamcinolone aceto- nide (2.5 mg/mL) injection administered into the proximal and/or lateral nail fold every month for six months. Some dermatologists prefer using a ring block for anesthesia prior to the injection (68). However, in our experi- ence dilution of the triamcinolone acetonide with 1% lidocaine and applica- tion of anesthetic refrigerant spray prior to rapid injection minimizes patient discomfort and increases toler ability. Both authors utilize this technique on Table 3 NAPSI Scoring System NAPSI scoring system a Nail matrix b Nail bed c Total score d 0 None None 0 1 Present in 1 quadrant Present in 1 quadrant Possible points: 1 or 2 Enter score: 2 Present in 2 quadrants Present in 2 quadrants Possible points: 2 or 4 Enter score: 3 Present in 3 quadrants Present in 3 quadrants Possible points: 3 or 6 Enter score: 4 Present in 4 quadrants Present in 4 quadrants Possible points: 4 or 8 Enter score: a For each nail, score the points as shown in the column. b This means evidence of any: (1) pitting, (2) leukonychia, (3) red spots in the lunula, or (4) crum- bling. c This means evidence of any: (1) onycholysis, (2) splinter hemorrhages, (3) subungual hyper- keratosis, or (4) oil spots/salmon patch. d There is a minimum of zero and a maximum of eight points awarded for each nail: four possible points for evidence of matrix disease and four possible points for evidence of nail bed disease. Abbreviation: NAPSI, nail psoriasis severity index. Table 4 NAPSI Scoring Table Nail scoring table—compile the score for each nail Nail 1________ Nail 2________ Nail 3________ Nail 4________ Nail 5________ Nail 6________ Nail 7________ Nail 8________ Nail 9________ Nail 10________ Final score total:_______________ Note: Minimum score is zero and maximum score is 80. Abbreviation: NAPSI, nail psoriasis severity index. 232 Nandedkar-Thomas and Scher a routine basis for psoriatic nails with good results. The major complica- tions from this therapy are hemorrhage under the nail plate and steroid- induced atrophy of the skin and subcutaneous tissues (2,69). However, in our experience, careful injection at the inflammatory pso riatic site with small amounts of steroid does not cause major atrophy. As an added positive side effect, patients report that associated painful DIP joint arthritis seems to diminish with repeated injections. Calcipotriene (Dovonex TM ) is a vitamin D 3 analog that binds to a similar steroid receptor in the skin. The cream and ointment forms have been studied in comparison to a topical steroid for use in the treatment of nail psoriasis (70). They appear to be just as effective in decreasing hyperkerato- sis. However, the ideal use of calcipotriene appears to be in combination with other oral agents such as cyclosporine or even topical steroids (71,72). Combination therapies seem to be more effective at producing clinical improvement in nail psoriasis. Biologic Agents There are several biologic agents available to combat cutaneous psoriasis. While many studies focus on plaque-type psoriasis and psoriatic arthritis with varying degrees of success (73–75), very little reproducible scientific information exists with regard to biologic agents improving nail psoriasis. Almost all of the biologic agents target either tumor necrosis factor-alpha (TNF-a) or T cells. TNF-a is required for cell-mediated inflammation (76). The key cell in the inflammatory milieu is the activated T cell (77). The induction of both cytokines is a normal host response required for the inflammatory cascade to occur. TNF-a overproduct ion and subsequent activation of T cells lead to pathologic disease states (76). Thus, the ratio- nale for use of some of these therapies is that they are designed to diminish TNF-a, which, in turn, appears to decrease the inflammatory, destructive component of psoriasis resulting in clinical improvement in disease. They can be loosely grouped as TNF-a inhibitors (etanercept, adalimumab, and infliximab) and T-cell modulators (alefacept and efalizumab). Etanercept is a TNF-a receptor antibody fusion protein, which acts like a soluble TNF-a receptor that competitively binds TNF-a (78). Thus, the bound TNF-a cannot bind to its native receptor on the target cell. This means that although the TNF-a molecule is still present, it becomes biologically inactive because it is bound to a receptor that impersonates its normal binding companion. Then the TNF-a bound etanercept is metabolized and eliminated via the liver and kidneys. Twice-weekly self-administered subcu- taneous (SQ) injections are required initially and then decrease to once weekly. The human monoclonal antibody adalimumab is also SQ injectable, which is self-administered every two weeks (76). 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