Sunday, October 28, 2007

Psoriasis, by Dr. Azar Rasheed

PSORIASIS

The familiar pink or red lesions with a scaling surface and well defined edge are easily recognized. These changes can be related to the histological appearance:

1. The increased thickness of the epidermis, presence of nuclei above the basal layer, and thick keratin are related to increased epidermal turnover.

2. Because the epidermis is dividing it does not differentiate adequately into normal keratin scales. These are readily removed to reveal the tortuous blood vessels beneath – clinically, “Auspitz sign”. The psoriatic plaque can be likened to a brick wall badly built by a workman in too much of a hurry – it may be high but it is easily knocked down.

3. The polymorphs that migrate into the epidermis from sterile pustules in pustular psoriasis. These are most commonly seen on the palms and soles.

4. The dilated blood vessels can be a main feature, giving the clinical picture of intense erythem.

The equivalent changes in the nail cause thickening and “pits” 0.5 – 1.0 mm in diameter on the upper nail plate that then fall out. Onycholysis, in which the nail plate is raised up, also occurs in psoriasis.

While still considering the individual lesion remember the following points.

The size or the lesion varies from a few millimeters to very extensive plaques.

Scaling may predominate, giving a thick plaue, which is sometimes hence the name “rupioid.” Scratching the surface produces a waxy appearance – the “tache de bougie” (literally “a line of candle wax”).

Erythema may be conspicuous, especially in lesions on the trunk and flexures.

Pustules are rare on the trunk and limbs, but deep seated pustules on the palms and soles are fairly common.

Psoriasis usually occur in early adult life, but the onset can be at any time from infancy to old age, when the appearance is often atypical. The following factors in the history may help in making a diagnosis:

· There may be a family history – if one parent has psoriasis 16% of the children will have it, if both parents the figure is 50%.
· The onset can occur after any type of stress, including infection, trauma, or childbirth.
· The lesions may first appear at sites of minor trauma – Köebner’s and toes or phenomenon
· The lesions usually clear on exposure to the sun
· Typically, psoriasis does not itch
· There may be associated arthropathy – affecting either the fingers and toes or a single large joint.

Clinical Presentation

Patients usually present with plaques and sometimes annular lesions on the elbows, Köbner’s phenomenon with lesions developing in areas of skin trauma such as scars or minor scratches. Normal everyday trauma such as handling heavy machinery may produce hyperkeratotic lesions on the palms. In the scalp there is scaling, sometimes producing very thick accretions. Erythema often extends beyond the hair margin. The nails show “pits” and also thickening with separation of the nail from the nail bed (oncholysis).

Guttate psoriasis – from the Latin gutta, a drop – consists of widespread small pink macules that look like drops of paint. It usually occurs in adolescents and often follows an acute ß haemolytic streptococcal infection. There may be much distress to both parent and child when a previously healthy adolescent erupts in apparent leprous spots.

Pustular lesions occur as chronic deep seated lesions on the palms and soles with surrounding Erythema which develop a brown colour and scaling. In clinics north of the border these pustules make the patient ask whether the condition is “smitten’ – that is, infectious. It is important always to explain that it is not.

Flexural psoriasis produces well defined erythematous areas in the axillae and groins and beneath the breasts. Scaling is minimal or absent.

Napkin psoriasis in children may present with typical psoriatic lesions or a more diffuse erythematous eruption with exudative rather than scaling lesions.

Generalised pustular psoriasis is uncommon. Superficial pustules develop in an area of intense erythema

Erythrodermic psoriasis is a serious, even life threatening, condition with erythema affecting nearly the whole of the skin. Diagnosis may not be easy as the characteristic scaling of psoriasis is absent, although this usually precedes the erythroderma. Less commonly the erythema develops suddenly without the erythema develops suddently without preceding lesions. There is a considerable increase in cutaneous blood flow, heat loss, metabolism, and water loss.

It is important to distinguish between the stable, chronic, plaque type of psoriasis, which is unlikely to develop exacerbations and responds to tar, dithranol, and ultraviolet treatment, and the more acute erythematous type, which is unstable and likely to spread rapidly, particularly when irritated by tar, dithranol, or ultraviolet light.

Patients with seronegative arthropathy of the non-rheumatoid type show double the normal (2%) incidence of psoriasis. Psoriatic arthropathy commonly affects the distal interphalangeal joints, sparing the metacarpophalangeal joints, and is usually asymmetrical. Rheumatoid nodules are absent. The sex ratio is equal but a few patients develop a “rheumatoid like” arthropathy, which is more common in women than in men. There is a third rare group who suffer bones.

Other members of the families of those with psoriatic arthropathy are affected in 40% of cases. There may be severe pustular psoriasis of the fingers and toes associated with arthropathy. One patient was so severely affected that she was immobilized until her condition cleared on treatment with methotrexate.

The cause is unknown but there is an inherited predisposition. Local trauma, acute illness, and stress may be factors in causing the appearance of clinical lesions. ß haemolytic streptococcal throat infection is a common precipitating factor in guttate psoriasis. Antimalarial drugs, lithium, and ß blockers can make psoriasis worse. There is evidence that psoriasis occurs more radily and is more intractable in patients with a high intake of alcohol. Smoking is associated with palmo-plantar pustulosis.

There is evidence that both hormonal and immunological mechanisms are involved at a cellular level. The raised concentrations of metabolites of arachodonic acid in the affected skin of people with psoriasis are related to the clinical changes. Prostaglandins cause erythema, while leukotrienes (LTB4 and 12 HETE) cause neutrophils to accumulate. The common precursor of these factors is phospholipase A2, which is influenced by calmodulin, a cellular receptor protein for calcium. Both phospholipase A2 and calmodulin concentrations are raised in psoriatic lesions.

T helper lymphocytes have been found in the dermis as well as antibodies to the basal cell nuclei of psoriatic skin. There are also dermal factors that contribute to the development of psoriatic lesions. The detailed treatment of psoriasis is covered in the next lesions. The only point to be made here is the importance of encouraging a positive attitude with expectation of improvement but not a permanent cure, since psoriasis can recur at any time. Some patients are minor lesions are a catastrophe.

Abnormalities found in psoriatic skin with possible explanations

Abnormalities
Comment
Accelerated transit time of keratinocytes through the epidermis
The most consistent observation in psoriatic skin.
Increased mitotic activity
Increased rate of DNA synthesis
Not only the basal layer keratinocytes, but also cells two or three layer above
Increased levels of phospholipase A2 activity
Availability of fee arachidonic acid High levels LTB4 may explain pustules in psoriatic lesions
Elevated levels of polyamine synthesis
May well be secondary to rapid cell proliferation
Increased levels of plasminogen activator
May explain Koebner phenomenon
Presence of keratins 6 and 16 in epidermis
Probably secondary to accelerated transit time.
Increased cGMP levels leading to high ration Cgmp/Camp

High levels of calcium binding protein calmodulin
Both cyclosporine and dithranol are calmodulin antagonists

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