Entitlement eligibility guidelines

Psoriasis is a chronic inflammatory skin disease involving accelerated proliferation ofthe epidermis layer of the skin. It generally consists of erythematous, well-demarcatedpapules and rounded plaques, covered by silver-colored scales.
Diagnosis from a qualified medical practitioner is required. The diagnosis can be madeclinically; no specialized tests are required.
The characteristic anatomy of psoriasis is hyperproliferation of the epidermal layer ofskin. Epidermal cell turnover at sites affected by psoriasis is approximately 10 timesthe cell turnover of normal epidermal cells. All types of psoriasis have similarhistiological features. Psoriasis develops into characteristic plaques at some timeduring the disease.
There are several common variants of psoriasis: guttate psoriasis - where numerous small papular lesions with silveryscaling evolve suddenly over the body, often 1 to 3 weeks afterstreptococcal pharyngitis; inverse psoriasis - where plaques evolve in intertriginous areas; theseplaques lack the typical silver scale because of maceration and moisture; pustular psoriasis - where superficial pustules may stud typical plaques,be confined to the palms and soles, or be associated with a raregeneralized erythematous skin condition accompanied by fever andleukocytosis; erythrodermic psoriasis - where there is generalized erythema and scalecovering the entire body; psoriasiform - where there are lesions resembling psoriasis.
Entitlement Eligibility Guidelines - PSORIASIS
Psoriasis is a common skin disease which affects approximately 1% of the generalpopulation. It may begin at any age, although the peak age of onset is between ages 15and 25. Persons with onset at an early age tend to have more severe disease. Thosewith onset before the age of 40 are likely to be HLA-Cw6 positive; however, not allpeople with HLA-Cw6 develop psoriasis, and psoriasis occurs in other HLA types. Genetic factors play an important role. About 44% of persons with psoriasis have anaffected parent. Racial factors play a more important role than geographical location inthe prevalence of psoriasis. The lesions of psoriasis are distinctive. Psoriatic lesions begin as red, scaling papulesthat coalesce to form round-to-oval plaques, which can easily be demarcated from thesurrounding normal skin. The scale is adherent, silvery white, and reveals bleedingpoints when removed (Auspitz’s sign). Trauma to skin may induce new skin lesions(Koebner’s phenomenon). Scaling may become extremely dense, especially on thescalp. Scaling forms, but is macerated and dispersed in intertriginous areas; therefore,the psoriatic plaques of skin folds appear only as smooth, red plaques with a maceratedsurface. The most common site for an intertriginous plaque is the intergluteal fold.
Nails often show small pitting depressions on the surface of the nail bed, and acharacteristic red-brown discoloration of the surface that resembles an oil stain underthe nail. Subungual collections of keratotic material are common, with distal separationof the nail from the nail bed. Mucous membranes are rarely involved. The extensorsurfaces of the arms and legs, and the scalp are the most commonly affected sites. Skin trauma increases the risk for involvement, but any epidermal surface can becomeinvolved.
The disease may remain localized to a few areas, or may cause continuous generalizeddisease, occasionally resulting in total body erythema and scale, i.e. erythrodermicpsoriasis.
Clinical course is characterized by chronicity and seasonal fluctuations, with aworsening in winter as dry skin leads to epidermal injury, and improvement in thesummer secondary to sun exposure.
There is no curative agent for psoriasis, and treatment suppresses the condition only aslong as it is administered. Sunlight has been reported as beneficial and is arecommended treatment in many cases.
Entitlement Eligibility Guidelines - PSORIASIS

The precise causes of the abnormal cellular proliferation and inflammationare unknown.
There is an increased prevalence in individuals with human leukocyteantigens HLA-B17, B13, and BW37 and Cw6. However, not all theseindividuals will develop psoriasis; thus, HLA type alone does not fullyexplain the etiology involved in psoriasis. It appears to be a multifactorialdisease in persons who are genetically predisposed.
Skin trauma or other interruption to skin Skin trauma or other interruption to skin may cause the initialmanifestation of psoriasis, contribute to psoriasis, and/or aggravateexisting psoriasis. Skin trauma or other interruption to skin must interrupt the integrity of boththe epidermal and dermal layers of the skin.
“Skin trauma” may result from a wound, cut, laceration, gunshot wound, orabrasion of the skin.
“Other interruption to skin” may result from disorders which producecutaneous vesicles, including drug reactions and dermatitis, and fromexternal forces which damage the skin, including chemical, thermal (e.g.
frostbite), and electrical burns.
Entitlement Eligibility Guidelines - PSORIASIS
Skin trauma or other interruption to skin must be significant enough toresult in the Koebner phenomenon, i.e. the development of isomorphicpsoriatic lesions. The lesions must occur at the site of the trauma or otherinterruption to skin. The lesions should develop within weeks of thetrauma or other interruption to skin.
Certain medications may cause or aggravate psoriasis.
Treatment should be ongoing at time of clinical onset or aggravation,although drug-induced aggravation may occur up to several months afterthe medication is first taken.
As drug-induced psoriasis may continue, improve or disappear ondiscontinuation of the drug, evidence of a chronic condition is required.
Drugs may also produce temporary flare-ups or exacerbations. Thesetemporary flare-ups or exacerbations must lead to permanent aggravationof psoriasis to be considered pensionable. Drug-induced aggravation can be unpredictable and severe.
LithiumLithium is a known cause of psoriasis in susceptible individuals, and can aggravate existing psoriasis. Pre-existing psoriasis is not,however, a general contraindication to lithium treatment, and thedisease does not permanently worsen in many lithium-treatedpersons.
Beta-blocker: oral or parental (by injection)Beta-blockers have been recognized to cause psoriasiform, i.e. apsoriasis-like eruption, and to aggravate true psoriasis. Thesedrugs may be used to treat hypertension, certain heart conditions,thyrotoxicosis, and as a preventative for migraines.
Anti-malarial, e.g. hydroxychloroquine and chloroquineAnti-malarials may aggravate psoriasis, although pre-existingpsoriasis is not contra-indicated in persons who have psoriasis andneed prophylactic treatment for malaria. Chloroquine is also usedto treat other conditions, including Rheumatoid Arthritis and certaindermatological disorders.
Systemic and topical steroidsThese drugs may aggravate psoriasis. However, it is important tonote that they may also cause flare-ups which may or may notrepresent permanent worsening. It is recognized that withdrawal VETERANS AFFAIRS CANADA
Entitlement Eligibility Guidelines - PSORIASIS
after prolonged use of steroids can frequently result in a severeflare-up of psoriasis, notably pustular psoriasis. Anxiety and depressive disorders for aggravation only Anxiety and depressive disorders may aggravate psoriasis. While the roleof stress is felt to be acute in most cases and is not considered to lead topermanent worsening, clinical studies support the fact that anxiety ordepressive disorders, when chronic or severe, may aggravate psoriasis insome individuals. For an anxiety or depressive disorder to aggravate psoriasis, the followingshould be evident:The anxiety or depressive disorder must attract a diagnosis under DSM-IV; andMedical intervention must have been sought for the anxiety or depressivedisorder; andIncreased signs/symptoms of psoriasis should be ongoing or recurrent forat least 6 months.
It is recommended that each case be examined on its individual merits,taking into account the chronicity and severity of the anxiety or depressivedisorder. Respiratory streptococcal infections in Guttate Psoriasis only The medical literature supports an association between acute respiratorystreptococcal infections and the development and aggravation of guttatepsoriasis.
Streptococcal lesions in other parts of the body are excluded. No specific strain of the streptococcal bacteria has been identified.
The guttate variant of psoriasis usually develops or is aggravated one tothree weeks after the respiratory streptococcal infection. Because guttate psoriasis may resolve spontaneously within weeks ormonths, it is necessary to ensure that it is chronic, i.e. in existence formore than 6 months, before a relationship can be recognized for pensionpurposes.
Entitlement Eligibility Guidelines - PSORIASIS
Psoriasis may become particularly severe in individuals who are HIV infected. It may become guttate in appearance and more refractory totreatment. Inability to obtain appropriate clinical management Exclusions:
Despite research efforts to date, there is a lack of sufficient evidence at this timeto establish, for pension purposes, causation and /or aggravation between thefollowing and psoriasis:• *While there is some medical research linking cigarette smoking to “palmoplantarpustulosis”, this is regarded by many to be an entity separate from psoriasis. MEDICAL CONDITIONS WHICH ARE TO BE INCLUDED IN


Photochemotherapy with oral methoxsalen (psoralen) and ultraviolet A radiation(PUVA) can increase the risk in the following conditions, therefore, medicalconsutation(s) should be requested:• basal cell carcinoma • malignant melanoma • squamous cell carcinoma (skin)• cutaneous genital tumours in men• cataracts VETERANS AFFAIRS CANADA
Entitlement Eligibility Guidelines - PSORIASIS
1. Australia. Department of Veterans Affairs: medical research in relation to the Statement of Principles concerning Psoriasis, which cites the following asreferences:1) Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, and Kasper DL (Eds) (1994) Harrison's Principles of Internal Medicine. McGraw-Hill, New York,13th Ed. p276.
2) Christophers E and Kruiger GG (1987) Epidermis: disorders of cell kinetics and differentiation in Dermatology in General Medicine. Fitzpatrick TB, Eisen AZ, WolffK, Freedberg IM and Austen KF (Eds.) New York: McGraw-Hill Book Company. p.
3) Baker H (1986) Psoriasis in Textbook of Dermatology. Vol. 2. Rook A, Wilkinson DS, Ebling FJG, Champion RH and Burton JL (Eds.) Fourth Edition. Oxford:Blackwell Scientific Publications. p. 1472.
4) Higgins EM and du Vivier AWP (1994) Cutaneous Disease and Alcohol Misuse. Br Med Bulletin. Vol. 50(1) pp. 85-98.
5) Krueger GG and Duvic M (1994) Epidemiology of Psoriasis : Clinical Issues. J Invest Dermat. Vol. 102. pp.14S-18S.
6) Farber EM and Nall L (1994) Psoriasis in the Tropics. Dermatological Clinics. Vol.
7) Elder JT, Henseler T, Christophers E, Voorhees JJ and Nair RP (1994) Of genes and antigens: the inheritance of psoriasis. J Invest Dermat. Vol. 103. pp.150S-153S.
8) Theeuwes M and Morhenn V (1995) Allelic Instability in the Mitosis Model and the Inheritance of Psoriasis. J Am Academy Derm. Vol. 32. pp. 44-52.
9) Krueger, G.G. and Duvic, M. (1994) op cit. pp. 14S-18S.
10) Brandrup F, Holm N, Grunnet N, Henningsen K and Hansen HE (1982)Psoriasis in monozygotic twins: variations in expression in individuals withidentical genetic constitution. Acta Dermatovener (Stockholm). Vol. 62. pp. 229-236.
Elder JT, Nair RP and Voorhees JJ (1994) Epidemiology and the genetics ofpsoriasis. J Invest Dermat. Vol. 102. pp. 24S-27S.
Naldi L, Parazzini F, Brevi A, Peserico A, Veller Fornasa C, Grosso G, Rossi E,Marinaro P, Polenghi MM, Finzi A, Galbiati G, Recchia G, Cristofolini M,Schena D and Cainelli T (1992) Family history, smoking habits, alcoholconsumption and risk of psoriasis. Br J Derm. Vol. 127. pp. 212-217.
Arnett FC, Reveille JD and Duvic M (1991) Psoriasis and psoriatic arthritisassociated with HIV infection. Rheumatic Clinics of North America. Vol. 17(1).
pp. 59-78.
Entitlement Eligibility Guidelines - PSORIASIS
White SH, Newcomer VD, Mickey MR and Terasaki PI (1972) Disturbance ofHLA Antigen Frequency in Psoriasis. NEJM. Vol. 287(15) pp. 740-743.
Barker JNWN, Mitra RS, Griffiths CEM, Dixit VM and Nickoloff BJ (1991)Keratinocytes as Initiators of Inflammation. The Lancet. Vol. 337, Jan. 26. pp.
Ros AM (1992) Photosensitive Psoriasis. Seminars in Derm. Vol. 11(4). pp.
O'Doherty CJ and MacIntyre C. (1985) Palmoplantar pustulosis and smoking. BMJ. Vol.291. pp. 861-864.
Mills CM, Srivastava ED, Harvey IM, Swift GL, Newcombe RG, Holt PJA andRhodes J (1992) Smoking habits in psoriasis: a case control study. Br JDermatology. Vol. 127. pp. 18-21. Poikolainen K et al. (1994) Smoking, alcohol and life events related topsoriasis. Br J Derm. Vol. 130. pp. 473-477.
Poikolainen K, Reunala T, Karvonen J, Lauharanta J and Kärkkäinen P (1990)Alcohol intake: a risk factor for psoriasis in young and middle aged men? BMJ.
Vol. 300. pp. 780-783.
Farber EM and Nall L (1993) Erythrodermic Psoriasis. Cutis. Vol. 51. pp. 79-82.
O'Doherty CJ and MacIntyre C (1985) op cit. p. 863.
Chaput JC, Poynard T, Naveau S, Penso D, Durrmeyer O and Suplisson D(1985) Psoriasis, alcohol and liver disease. BMJ. Vol. 291. p. 25.
MacGregor RR (1986) Alcohol and Immune Defense. JAMA. Vol. 256(11). pp.
1474-1479. Fitzpatrick TB et al. (Ed.) (1987) Dermatology in General Medicine. New York:McGraw-Hill Book Company. p. 478.
Menter A. and Barker JNWN. (1991) Psoriasis in Practice. The Lancet. Vol.
338. July 27. pp. 231-234.
Duvic M, Rios A and Brewton GW (1987) Remission of aids-associatedpsoriasis with zidovudine. The Lancet. Sept. 12, p. 627.
Belsito DV, Sanchez MR, Baer RL, Valentine F and Thorbecke GJ (1984)Reduced Langerhans` cell IA antigen and ATPase activity in patients withAIDS. NEJM. Vol. 310(20). pp. 1279-1282.
Forster SM, Seifert MH, Keat AC, Rowe IF, Thomas BJ, Taylor-Robinson D,Pinching AJ and Harris JRW (1988) Inflammatory joint disease and HIVinfection. BMJ. Vol. 296. pp. 1625-1627.
Ellis, C.N. Gorsulowsky DC, Hamilton TA, Bilings JK Brown MD, HeadingtonJT, Cooper KD, Baadsgaard O, Duell EA, Annesley TM Turcotte JG andVoorhees JJ (1986) Cyclosporin Improves Psoriasis in a Double-blind Study. JAMA. Vol. 256(22). pp. 3110-3116.
Ramsay B and O`Reagan M (1988) A Survey of the Social and PsychologicalEffects of Psoriasis. Br J Derm. Vol. 118. pp. 195-201.
Entitlement Eligibility Guidelines - PSORIASIS
Menter A. and Barker JNWN. (1991) Psoriasis in Practice. The Lancet. Vol.
338. July 27. pp. 231-234 Peserico A, Zanetti G, Padovan S, Bertoli P, Veller Fornasa C, Cipriani R,Ambrosio GB, Zamboni S and Pagnan A (1988) Relationship Between BodyWeight and Blood Pressure and Some Metabolic Parameters in PsoriaticPatients. Br J Derm. Vol. 118. pp. 191-194.
2. Bork, Konrad, and Brauninger, W. Diagnosis and Treatment of Common Skin Diseases. Toronto: W. B. Saunders, 1988. 3. Cotran, Ranzi. S., Vinay Kumar, et al. Robbins Pathologic Basis of Disease. 4. Fauci, Anthony S. and Eugene Braunwald, et al, eds. Harrison’s Principles of Internal Medicine. 14th ed. Montreal: McGraw-Hill, 1998. 5. Fitzpatrick, Thomas B., Arthur Z. Eisen, et al, eds. Dermatology in General Medicine. 4th ed. Montreal: McGraw-Hill, 1993. 6. Goldman, Lee and J. Claude Bennett. Cecil Textbook of Medicine. 21st ed. 7. Goroll, Allan H. and Albert G. Mulley,Jr. Primary Care Medicine. Office Evaluation and Management of the Adult Patient. 4th ed. Philadelphia: Lippincott Williams &Wilkins, 2000. 8. Habif, Thomas P. Clinical Dermatology. 3rd ed. Toronto: Mosby-Year Book, 1996.
MAY 1, 2002

Source: https://www.veterans.gc.ca/pdf/dispen/eeg/psoriasis.pdf


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