diagnosis of psoriasis

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Diagnosis : Physicians usually diagnose psoriasis by examining the affected skin. Less often, a small piece of skin affected by the psoriasis is cut out and examined under a microscope. A microscopic examination of tissue taken from the affected skin patch is required to make a definitive diagnosis of psoriasis and to distinguish it from other skin disorders. Usually in psoriasis, the examination will show proliferation of dry skin cells but without many signs of inflammation or infection. Changes in the nails typical of psoriasis are often strong indicators of psoriasis

Psoriasis is characterized by dysfunction of keratopoesis .the major pathological features are parakeratosis . munnro abscesses and an increased number of mitoses. Acantosis and spongiosis are often seen . the dermal-epidermal border is well marked. The upper derma shows papillomatosis and dilation of capillaries with excess of perivascular neutrophilic infilteration . the nerve fibers are Dystrophic, with enalarged neurolema and central cylinder. It’ s also reported that the stratum granulosum is thinned or absent .

It can be difficult for the doctor to diagnose psoriasis in the early stages, when the disease may be limited to rough patches on the elbows. Certain symptoms, such as a dandruff-like scalp condition or what looks like a fungal infection, may be hard to recognize as psoriasis. Nail pits may be a sign of early psoriasis, but they may also be a sign of other conditions. The diagnosis is straightforward if the doctor examines the skin and sees thick, red, flaky patches-the plaques characteristic of psoriasis.

In people with psoriatic arthritis, the arthritis usually follows the appearance of psoriasis. Typically, psoriatic arthritis first appears in the finger and toe joints closest to the nail. Other forms of psoriatic arthritis may be more difficult to diagnose. The joints may be affected in no recognizable pattern. Unlike , psoriatic arthritis cannot be diagnosed by a blood test and also x-ray may taken for diagnosis
Also see Ref :

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1-" THE HISTOPATHOLOGY OF PSORIASIS ", G. DE ROSA, C. MIGNOGNA, Department of Biomorphological and Functional Sciences, Pathology Section, “Federico II” University of Naples, Italy

2-" Rook’sTextbook of Dermatology ", Tony Burns, Stephen Breathnach, Neil Cox, Christopher Griffi ths, This edition fi rst published 2010, © 1968, 1972, 1979, 1986, 1992, 1998, 2004, 2010 by Blackwell Publishing Ltd, ISBN: 978-1-4051-6169-5

3-" ROBBINS AND COTRAN PATHOLOGIC BASIS OF DISEASE, 8/E",ISBN: 978-1-4160-3121-5, Copyright © 2010 by Saunders, an imprint of Elsevier Inc.

Differential diagnosis with psoriasis

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The characteristics already defined are usually sufficient to enable the diagnosis to be made, but doubt may arise in atypical cases, in particular sites, and when psoriasis is complicated by or alternates with other diseases. In seborrhoeic dermatitis, the lesions are lighter in colour, less well-defined and covered with a dull or branny scale. Eczema at times develops a psoriasiform appearance, especially on the legs. Hyperkeratotic eczema of the palms is a common cause of misdiagnosis. Colour, scratch-evoked scaling and well-defined margins are suggestive of psoriasis, and nail changes may be diagnostic. Lichen planus should give rise to difficulty only when the two diseases alternate or coexist, especially when present as hypertrophic lesions on the legs, as penile lesions and on the palms. The violaceous colour, glistening surface and presence of oral changes are usually decisive. Lichen simplex can resemble psoriasis closely, particularly on the scalp and near the elbow. The intensified skin markings, rather ill-defined edge and the marked itching are characteristic, and the point of the elbow tends to be avoided. Pityriasis lichenoides chronica can closely resemble guttate psoriasis, but the lesions are usually less evenly scattered, have a brownish red or orange brown colour and are capped by an opaque soft "mica-like" scale. Candidiasis shows a glistening deep red colour suggestive of psoriasis, particularly in the flexures, but scaling tends to be confined to the edge, and small satellite pustules and papules are usually evident outside the main area. Tinea cruris has a well-defined, often polycyclic edge, but Trichophyton rubrum infections, especially of the palm, cause difficulty. If corticosteroids have been applied, scaling may be absent and the diagnosis must be made by microscopy and culture. Less common causes of confusion are pityriasis rubra pilaris and secondary syphilis. The resemblance to pityriasis rubra pilaris . An association of psoriasis and cardiovascular disease (CVD) has long been recognized. CVD risk is highest in those with more severe disease, with standarized mortality rates reaching , particularly in younger patients. Much of this risk is due to coexistence of known CVD risk factors, including type II diabetes mellitus, dyslipidaemia, hypertension and obesity, increasingly referred together as the " metabolic syndrome". However, emerging evidence suggests that the risk may in part remain even after controlling for known risk factors. Taken together, these studies indicate that treating patients with moderate or severe psoriasis requires attention to these important general medical issues.

Dermatitis, Atopic , Pityriasis Rosea , DermatitisContact , Reactive Arthritis , Gout and Pseudogout , Syphilis , Pityriasis Alba , Tinea
See also for more informations about misdiagnose of psoriasis

 Also see Ref :

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1-" THE HISTOPATHOLOGY OF PSORIASIS ", G. DE ROSA, C. MIGNOGNA, Department of Biomorphological and Functional Sciences, Pathology Section, “Federico II” University of Naples, Italy

Stages of development of psoriatic plaque

The early stage consists in elongation and dilatation of blood vessels of the papillary derma, with associated aedema and lymphocytic infiltrate (perivascular cuffing). Vessels are dilated and tortuous, with some neutrophils in their lumen. Lymphocytes and neutrophils emerge from the vessel reaching the epidermis (“squirting” papilla). Rare erythrocytes extravasated may be found. Epidermis during this phase, is quite normal.Shortly after, there is a thickening of epidermis with loss of granular cell layer and formations of mounds of parakeratosis, which is thought to result from a markedly shortened cellular turnover time. Keratinocytes proliferate and mature rapidly, so that terminal differentiation is incomplete. Thus, squamous keratinocytes aberrantly retain intact nuclei and release few extracellular lipids that normally cement adhesion of corneocytes.

The resulting poorly adherent stratum corneum leads to the characteristic scales or flakes of psoriasis lesions. Scattered neutrophils are seen at the edge of mounds of parakeratosis: they represents the earliest manifestation of Munro microabscesses.

The advanced stage is characterized by regular acanthosis (thickening of stratum spinosum) and epidermal “psoriasiform hyperplasia” with regular elongation of the rete ridges and thinning of suprapapillary plates . Mitotic activity is often quite marked, a further indicator of the hyperproliferative nature of this condition. Parakeratosis become confluent, with loss of granular layer. There is transmigration of inflammatory cells through epidermis into parakeratotic scale resulting in intracorneal collections of neutrophils, the so called “Munro microabscesses” . Similar accumulation in the stratum spinosum are defined as “spongiform pustule of Kogoj”. When subcorneal abscesses are prominent the disease is designated as pustular psoriasis .

Munro microabscesses and Kogoj micropustoles are diagnostic clues of psoriasis, but they are notalways present. All other features can be found in numerous eczematous dermatitis, such as allergic contact dermatitis and atopic dermatitis. However, in these lesions spongiosis and “oozing” (presence of coagulated serum in cornified layer) are marked. Moreover, in allergic contact dermatitis there is a characteristic eosinophilic infiltrate which is normally absent in psoriasis.

 Dermal inflammatory infiltrate is heavier than in early lesions, it is composed by T lymphocytes, containg a few Langherhan cells with occasional neutrophils. Under the epidermal basement membrane, macrophages CD11c positive are present. In addition to neutrophils, T lymphocytes are also found interspersed between keratinocytes throughout the epidermis and in larger quantities in the dermis. With immunohistochemical analysis it has been shown that epidermal lymphocytes are chiefly CD8+ T cells, while dermic lymphocytes are a mixture of CD4+ and CD8+ T cells, with a CD4+ predominance, similar to that seen in peripheral blood. Later lesions there is orthokeratosis, an intact granular layer and mild exocytosis of inflammatory cells .