Investigation into Psoriasis INTRODUCTION: Psoriasis is a inflammatory non-infectious dermatological condition. It is primarily characterised by defined erythematous plaques that commonly present with large silver coloured scales. (Hunter, 1995) Psoriasis is present due to increased epidermal proliferation from excessive cell division in the basal layers. The period of cell turnover falls from 28 to 5 days due to the proliferation. It is now believed that Psoriasis is primarily a genetic disorder that is triggered by some form of stress (Psoriasis Association, 1999; Hunter, 1995) Many forms and variations of Psoriasis exist with most effect the lower extremity and foot. The literature reviewed suggests that 1-3% of most world population suffer from Psoriasis and it is most often seen between the ages of 15-40 years. Regardless of the form or variety of Psoriasis present, the condition is unsightly and almost always uncomfortable for the sufferer. The condition is lifelong and characterised by chronic, recurrent exacerbations and remissions that are emotional and physically stressful. Many therapies have been trialed in the past but only several have proven to be successful in the treatment of various Psoriatic presentations. (Psoriasis Association, 1999; Habif, 1996)) OVERVIEW: Psoriasis is considered to be one of the most common skin diseases that is experienced, and it is usually found in populations and individuals of good general health. Psoriasis is classified as a papulosquamous disease and was originally considered to be a form of leprosy. (Roenigk, 1991;Solomons, 1988) Hunter (1995) Solomons (1988) and Dockery and Crawford (1999) all stated that approximately 2% of the general population present with the various forms of Psoriasis. The Australian Psoriasis Association (1999) wrote that the prevalence of Psoriasis is now in the order of 4-5% and steadily rising. Psoriasis is generally a chronic condition and is usually characterised by well-defined papules, or plaques of varying size. These lesions are reddish and covered with dull silvery scales. Various types of Psoriasis are found and these commonly are seen on extensor surfaces, but also may appear on the elbows, knees, back, scalp, dorsum of the feet and can involve fingernails and toenails. Several variants of Psoriasis may even cover almost all of the body. The distinct clinical presentation of Psoriatic plaques is usually sufficient for diagnosis of the condition. The key presentation of Psoriasis is called Auspitz sign, and this is the characteristic red scaling papules that form round or oval plaques overlayed with adherent silvery scale. (Solomons, 1988) The variations of Psoriasis that can be seen are: (Solomons, 1988; Hunter, 1995; Habif, 1996) Stable Plaque Psoriasis Arthropathic Psoriasis Guttate Psoriasis Pustular Psoriasis Erythrodermic or exfoliative Psoriasis HIV induced Psoriasis Keratoderma Blenorrhagicum (Reiter's Syndrome) Light Sensitive Psoriasis
PATHOLOGY 
Figure 1: Histology of Psoriasis (Adapted from Hunter, 1995) The histological presentation of Psoriasis affected dermal layers presents a unique appearance. Hyperkeratosis is present on the very outer layer with characteristic thinning of the papillae area of the Malpighian layer. Lengthening of the dermal-epidermal folds is seen and capillary loops are somewhat dilated and tortuous within. This results in the blood vessels of the dermis lying much closer to the adjacent hyperkeratotic surface and this can result in regular bleeding. (Solomons, 1988, Hunter, 1995; Habif, 1996) Munro cited in Hunter, Savin and Dahl (1989) described Polymorphonuclear leucocyte microabscesses that commonly appear under the hyperkeratosis within the horny layer of the skin. This unique histological appearance accounts for the clinically scaly appearance of Psoriasis and explains why pinpoint bleeding results when the scales are forcibly removed. (Solomons, 1988; Hunter, 1995) The Australian Psoriasis Association (1999) stated that the altered histopathology seen in Psoriasis is not so much a reflection of the disease, but of the normal skin reproduction cycle at fault. The skin repair process has been activated and the observed appearance is on skin under repair. ETIOLOGY Previously, the cause of Psoriasis was postulated by several authors to be linked to Leprosy. Many other authors believed the etiology was unknown, but thought that many factors contributed to its appearance. It is now believed that Psoriasis is essentially a genetic disorder that is triggered by some form of stress. (Psoriasis Association, 1999) The evidence presented within the literature does not conclusively state the etiology of Psoriasis but the factors that appear to contribute to its appearance are listed below: Solomons (1988) stated that the familial incidence of all cases is about 30 %. Hunter, (1995) described a 15% chance that an off spring would develop Psoriasis if one parent was affected. This rose to 50% if both parents were sufferers. The Psoriasis Association of Australia (1999) suggested that the appearance of Psoriasis is solely a Genetic disposition that is expressed due to a form of stress. Hunter (1995) stated that the increased epidermal proliferation was due to increased levels of prostaglandins, leukotrienes and hydroxyeicosatetraenoic acids in the epidermis. Hunter, Savin and Dahl (1989) stated that altered Arachidonic acid metabolism resulted in decreased Cyclic Nucleotides, raised Polyamines and raised Proteases when Psoriasis is seen. Hunter (1995, p. 949) stated that "The inflammatory reaction may be part of an immunological response to as yet unknown antigens". Hunter (1995) wrote that the increased epidermal cell proliferation of Psoriasis.was related to increased replication and metabolism of dermal fibroblasts. Predisposing Factors: With no definite cause of Psoriasis, many factors have been found that contribute to the occurance of the disorder: Trauma. Laceration or previous surgical site can cause a Psoriatic appearance commonly called Kőbner or Koebner phenomenon. (Hunter, 1995; Habif, 1996) Inflection. Beta-haemolytic streptococcal throat inflections or tonsillitis can trigger Guttate Psoriasis. (Hunter, 1995; Solomons, 1988) Climate. Psoriasis is most commonly seen in northern hemisphere areas and is linked to winter months when duration of sunlight is shortened (Solomons, 1988) Age. The most common age is between 15-30 years. (Solomons, 1988) Drugs. Lithium, Beta antagonists and Anti-malarials or potent local and systemic corticosteroids may worsen Psoriatic appearance.(Hunter, 1995) Sunlight. Rarely ultraviolet radiation from the sun of artificial source can worsen the condition. This occurs in approximately 10% of cases (Hunter, 1995; Hunter, Savin and Dahl, 1989) Psychological upsets / Emotional disturbances. (Solomons, 1988; Hunter, 1995; Habif, 1996; Psoriasis Association, 1999)
SPECIFICS: COMMON PRESENTATIONS ON THE LOWER EXTREMITY: Psoriasis Vulgaris / Stable Plaque Psoriasis: Dockery and Crawford (1999) and Hunter (1995) stated that Psoriasis Vulgaris was the most common type of Psoriasis seen. Psoriasis Vulgaris is the most stable form of Psoriasis and most easily managed. It's appearance is characteristic with a well defined, non-inflammatory, red based lesion covered with a uniform silver scale. Most commonly this type of Psoriasis persists unchanged for months and even possibly years, but disappearances and reoccurrences are inevitable Once a remission has occurred a temporary white, brown or red macule may remain. (Habif, 1996). The most common areas effected are he elbows, knees and lower back, but the scalp, nails, flexure surfaces, palms and the napkin area are other common locations (Hunter, 1995) Figure 2 clearly presents the characteristic appearance. 
Figure 2: The typical plaque of Psoriasis Vulgaris (Dockery and Crawford, 1999) 
Figure 3 : Psoriasis is sometimes confused with severe eczematous dermatitis. (Dockery and Crawford, 1999) Guttate Psoriasis: Guttate Psoriasis is seen prominently in children and adolescents as 30% of all presentations are under 20 years of age. Commonly Guttate Psoriasis appears after a streptococcal pharyngitis (tonsillitis) has occured. A rash like appearance of numerous small round red macules appear. This occures rapidly and the individual lesion range in size from pinpoint to 1 cm. The lesions are usually droplet shaped, red in colour, and scaly with appearance mainly on the trunk and extremities but not the palms or soles. This rash often clears but it may continue and form a plaque like Psoriatic appearance. (Dockery and Crawford, 1999; Hunter, 1995; Hunter, Savin and Dahl, 1989) Erythrodermic Psoriasis: Eythrodermic Psoriasis is a particularly unpleasant variation of Psoriasis. With this variant, the skin also becomes red and scaly but almost all of the body can be effected. Due to the inflammatory nature, the individual shivers uncontrollably in an effort to compensate for the considerable heat loss experienced. The effects of Dithranol, tar or the withdrawal of systemic or topical corticosteroids can initially stimulate this variation. (Hunter, 1995) 
Figure 4: Erthyrodermic Psoriasis (National Psoriasis Foundation, 1999) Pustular Psoriasis: Pustular Psoriasis is a rare but serious variant that is the most confusing diagnostically (Dockery and Crawford, 1999). The onset of Pustular Psoriasis is commonly sudden and many small sterile pustules erupt. These eruptions occur usually on the arch of the feet and middle section of the palms and have an erythematous base. Zumbusch Psoriasis, is a variation of Pustular Psoriasis that effects the entire body. This serious condition requires hospital admission as the patient is very ill. (Fitzpatrick, et al, 1997; Habif, 1996) The lesions of Pustular Psoriasis begin as usually deep-seated pustules that evolve into dusky-red macules. A brown crust may cover the area, although eruption of the sites is most common appearance. Eventually the lesions change, forming deep yellow coloured pustules that do not rupture, but dry up and turn brown and scaly. At several stages in the pustules cycle it may present similar to Vesicular Tinea Pedis, however it is not as pruritic and remains very local as it only usually effects both soles and palms. (Fitzpatrick, et al, 1997) Typically Pustular Psoriasis presents as a chronic, persistent symmetrical condition and is also referred to within the literature as Acropustulosis, pustular acrodermatitis, acodermatitis continua, and dermatitis reopens. (Solomons, 1988; Hunter, 1995; Dockery and Crawford, 1990; Habif, 1996) 
Figure 5 : PUSTULAR PSORIASIS (Dockery and Crawford, 1999) 
Figure 6: PUSTULAR PSORIASIS. (Dockery and Crawford, 1999) Psoriatic Arthritis: Psoriatic Arthritis is a distinct form of arthritis that is seen in 20% of all Psoriasis sufferers. It is more likely to appear when severe skin based Psoriasis is present. Commonly five presentation of arthritis are seen with associated Psoriasis: Asymmetrical arthritis Symmetrical arthritis Distal Interphalangeal joint disease Arthritis Mutilans Ankylosing Spondylitis
Most commonly Psoriatic Arthritis involves the distal interphalangeal joints of the toes and fingers. Due the high incidence of distal digit involvement, manifestations involving the nail are seen in 80% of cases. The most common characteristic is asymmetrically swelling of the distal interphalangeal joint of the finger or toe. This presentation is referred to as a Sausage digit. Hunter, Savin and Dahl (1989) and Habif (1996) stated that Psoriatic arthritis can be differentiated from other forms of Arthritis as no rheumatoid factor or nodules are found. Despite active treatments of Psoriatic arthritis the codition may well prove to be very progressive and deforming to the joint and nail. 
Figure 7: PSORIATIC ARTHRITIS. Sausage digit. (Dockery and Crawford, 1999)  
Figure 8: PSORIATIC ARTHRITIS. (National Psoriasis Foundation, 2000) Nail involvement of Psoriasis: The involvement of the finger or toe nail is very common in patients with any form of Psoriasis. In some instances, the abnormalities of the nail plate may exist before other signs of Psoriasis are seen. Therefore, it is important to differentiate the Psoriatic nail involvement from Onychomycosis and other complaints. Common changes to the nail plate that are seen with Psoriasis are: Pitting Onycholysis Subungual debris Severe deformity with the matrix involvement.
The occurrence of nail involvement with Psoriasis sufferers is 30%, but if Psoriatic Arthritis is present 80% are effected. (Dockery and Crawford, 1999) 
Figure 10: TOTAL NAIL INVOLVEMENT. (Dockery and Crawford, 1999) 
Figure 11: PUSTULAR PSORIASIS. (Dockery and Crawford, 1999) 
Figure 12: Hand involvement ( Psoriasis Association, 1999) Differential Diagnosis: Discoid Eczema Pityriasis Rosea Secondary Syphilis Seborrhoeic Eczema Cutaneous T cell lymphoma Tinea Ungum Lichen Planus Pityriasis Rosea Mycosis Fungiodes
(Hunter, Savin and Dahl, 1989; Roenigk, 1991; Habif, 1996) DIAGNOSIS: Most variations of Psoriasis can be diagnosed by the characteristics of the lesion and it's presentation pattern (Roenigk, 1991; Habif, 1996). Solomons (1988) stated that biopsy is necessary to assist in identification while Hunter (1995) wrote that biopsy is seldom necessary as the clinical picture is usually characteristic. Throat swabbing for beta haemolytic streptococci is recommended to be performed when Guttate psoriasis is suspected (Hunter 1995) while Habif (1996) recommends ESR and Rheumatoid factor tests to be completed for suspected Psoriatic Arthritis cases. Hunter, Savin and Dahl (1989) stated that skin and nail scrapings might be required to exclude Tinea Pedis presentations. TREATMENT: General Measures: Along with Eczema, Psoriasis patients require a confident and optimistic approach on the part of the practitioner in the management of the disease and itâs manifestations. Explanation, reassurance and instructions are vital, otherwise the resolution will be slow and reoccurences are common as a large component of the etiology is suspected to be stress related. (Solomons, 1988; Psoriasis Association, 1999) Hunter, Savin and Dahl (1989) stated that physical and mental rest could be beneficial when other specific managements are occurring. It is cleared described by the authors that the disease must be kept in perspective and the treatment should never become more troublesome than the condition itself. Topical Measures: Texts such as the definitive 'Psoriasis' by Roenigk and Mailbach (1991) contains no less than 450 pages describing various treatment regimes. Below is a list of the more commonly used methods: Coal Tar Preparations ALPHOSYL® (Stafford-Miller), IONIL-T® (Galderma), LINOTAR GEL® (Linotar), POLYTAR® (Stiefel), PSOR-ASIST® (Sunspot), SEBITAR® (Ego), The mode of action is to inhibit the DNA synthesis of the skins constituent cells. This limits the proliferation and slows the abnormal cycle. (Solomons, 1988; Hunter, 1995; MIMS, 1998)Dithranol DITHRASAL® (DermaTech), DITHROCREAM® (Hamilton), EGODERM® (Ego) Dithranol inhibits the DNA synthesis. This product is used in a short contact application for only 30 minutes. It is more irritant and tricky than coal tar preparations but its use has become more widespread. (Hunter, 1995; MIMS, 1998)Calcipotriol DAIVONEX® (Hamilton) This Vitamin D analogue that reduces the epidermal proliferation and restores a more normal skin construction.. This preparation is an odourless, colourless and it can causes a transient irritation. (Hunter, 1995; MIMS, 1998)Topical Corticosteroids Hunter (1995) stated that patients and doctors like these preparations, as they are clean and initially effective. Unfortunately their long-term use is contraindicated as once withdrawal happens, rapid relapse occurs that is more difficult to treat than the original presentation.Ultraviolet Radiation Psoriatic patients under normal circumstance improve with normal sunlight. This can be difficult to achieve during the winter months and the use of medium wave ultraviolet radiation can be provided via the use of sun beds. Combination therapies of ultraviolet, coal tar preparations and Dithranol can be used to achieve quick resolution of symptoms. (Hunter, Savin and Dahl, 1989)Systemic Treatment When Psoriasis fails to respond to local measures, systemic drugs can be used. Various regimes for treatment are detailed within the literature. The most common are listed below: PUVA Photochemotherapy with Psoralen + UVA. Hawk and Legrice (1994) found that use of PUVA in both oral and topical forms completely cleared chronic hand and foot Psoriasis 50-60% of the time Retinoids Methotrexate (folic acid antagonist) METHOBLASTIN® (Pharmacia & Upjohn), METHOTREXATE® (David Bull) Cyclosporin. NEORAL® (Novartis), SANDIMMUN® (Novartis) . No treatment
Guttate Psoriasis is a self-limiting condition and requires no treatment, however rapid clearing can be achieved with UV phototherapy. Hunter, Savin and Dahl (1989) summarised the recommended treatments for various forms of Psoriasis. The table, in an adapted form is included as Table 1. Type of Psoriasis | Treatment Choice | Alternative Treatments | Stable Plaque | Short contact Dithranol | Tar | Extensive Stable Plaque (> 20% surface area) | PUVA Retinoids | Short contact Dithranol, UVB, Tar | Widespread small Plaques | UVB | Tar | Guttate | Emollients while erupting UVB | Weak Tar preparations , Mild local steroids | Facial | Mild local steroids UVB | | Flexural | Mild to moderate potent local steroids + antifungal UVB | | Pustular Psoriasis of hands and feet | Moderately potent or potent local steroid UVB | Retinoids | Acute erythrodermic, unstable or generalised pustular | In-patient treatment with Ichthammol paste Local steroids may be used initially and then UVB | Retinoids, Methotrexate |
Table 1 : Psoriasis Treatments (Adapted from Hunter, Savin and Dahl, 1989) Figure 13 graphically shows the quick effects of local steroid application in the effort to treat pustular psoriasis on the foot. 
Figure 13: PUSTULAR PSORIASIS. Left = BEFORE. Right = AFTER (Dockery and Crawford, 1999) NEW DEVELOPMENTS: A research team from the Royal Children's Hospital Research foundation in Melbourne has developed a new strategy for treatment of Psoriasis. This treatment revolves around production of an anti-gene called antisense oligonucleotides that is designed to reduce the production of the proteins that that allow the increased proliferation of the dermis to occur. The only problem currently faced by the researchers is how to get the therapeutic molecules to penetrate the layers of hyperkeratosis or scale on the outer surface. (Psoriasis Association, 1999) The Australian Psoriasis Association (1999) warns that almost every conceivable outlet is selling ineffective scam treatments that are alleged to effectively treat Psoriasis. Many of these products do nothing for the Psoriasis] PROGNOSIS: A permanent cure for Psoriasis of any form is impossible. Where there is a marked familial tendency and /or a regular Psoriatic response to emotional upsets, relapses are more likely. In general the greater the faith of the patient in the Practitioners handling of the disease, and the patients insight into it, and treatment, the longer are the periods of remission seen. (Solomons, 1988) SUMMARY Psoriasis is a papulosquamous disease that effects between 4-5% of the population. Originally the disease was thought to be linked to Leprosy but this was dismissed. No conclusive explanation of the etiology of Psoriasis exists, but some authorities believe it is most probably genetic orientated and triggered by a miscellaneous stress. Psoriasis has an underlying alteration to the histopathology of the skin and can present in many forms. The most common form of Psoriasis is the stable Plaque presentation that has a well-defined red plaque formation with borders of silvery grey scaling. Various other forms are particularly evident on sufferers and can cause much aggravation and frustration. Pustular, Arthropathic, guttate and Erthyrodermic are common presentations. Traditionally several topical preparations have been utilised for the treatment of the Psoriatic plaques, but the effect of these somewhat varies between patients. Applications of Coal Tar, Dithranol, Steroids, Retinoids, Methotrexates and Ultraviolet light therapy with Psoralins are commonly listed. New etiological specific treatments are currently being developed here in Australia. The most important aspect of management for Psoriasis sufferers is ensuring the patient does not take the disease state out of perspective. It is the responsibility of both the practitioner and patient to ensure the appropriate mind set and treatment regime is upheld to ensure effective management is afforded. REFERENCES Dockery, G. L. and Crawford, M. E. 1999. Colour atlas of Foot and Ankle Dermatology. Lippincott-Raven, Philadelphia. Fitzpatrick, T. B., Johnson, R. A., Wolff, K., Polano, M. K. Suurmond, D. 1997. Colour Altas and Synopsis of Clinical Dermatology (3rd Ed). McGraw Hill, New York. Habif, T. P. 1996. Clinical Dermatology - A colour Guide to Diagnosis and Therapy (3rd ed.) Mosby, St Louis. Hunter, J. A. A., Savin, J. A. and Dahl, M. V. 1989. Clinical Dermatology. Blackwell Scientific Publishing, London. Hunter, J. A. A. 1995. Diseases of the Skin. In. Edwards, C. R. W., Bouchier, I. A. D., Haslett, C. and Chilvers, E. R. (eds) Davidson's Principles and Practice of Medicine (17th ed). Churchill Livingstone, Edinburgh. pp. 948-953. MIMS, Januaray 1998. 34 (6) MediMedia Australia, St Leonards. Psoriasis Association Inc. 1999. What is Psoriasis? [Online] Available: http://www.psoriasis.org.au Roenigk, H. H. 1991. Skin Manifestations of Psoriasis. In. Roenigk, H. H. and Maibach, H. I. (eds.) Psoriasis: Second Edition, Revised and Expanded. Marcel Dekker Inc, New York pp. 3-8 Solomons, B. 1988. Lecture Notes on Dermatology. P. G. Publishing Pte Ltd., Singapore
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