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Psoriasis: A Seminar

Conducted at Le Meridian Hotel, Dubai on 2nd Jan 2001.

Moderator: Dr.S.M.S.Pillai, Dubai
Editor: Dr.V.S.Hanish Babu, Ajman


vDefinition, Incidence andPrevalence




vBiochemical Aspects

vProvocation Factors


vClinical Features and Complications

vTopical Therapy Other Than Steroids

vSteroids in Psoriasis

vMethotrexate in Psoriasis

vRetinoids in Psoriasis

vPhoto therapy

vOther Immunosuppressive Therapy

vDefinition, Incidence and Prevalence

Contributed by Dr.S.C.Bose, Sharjah

Introduction: Psoriasis derives its name from the Greek word for 'itch'. It is a comparatively easier skin disease to diagnose but very difficult to treat causing frustration to patient and clinician alike.

Definition: Psoriasis is a common, chronic and non-infectious skin disease characterized by well defined erythematous slightly raised plaques and papules with silvery scales and typical extensor distribution

Incidence and Prevalence: Psoriasis is universal in occurence. Genetic and environmental factors greatly influence the clinical development of the disease. Occurence varies from 0.1% to 3 % in different parts of the world.

Americas: 1-2 %. Rare in American blacks and absent in Red Indians.

South America: 0.97%

Germany: 1.3%

Great Britain: 1.6%

Denmark: 1.7%


West Africa-Rare


Eskimos: Very Low

No studies have been done in general population in India, but a study of patients attending clinics and hospitals showed a prevalence of 0.8% to 5.6%.

Age of onset: Even though it can appear at birth as well as very old age, the most common onset is in 2nd to 4th decades of life.

Familial Occurrence: Approximately 1/3rd of the patients with psoriasis has a relative similarly afflicted.

Sex: Occurs with almost equal frequency in males and females, but a slightly higher prevalence noticed in males. 

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Contributed by Dr.R.Soman, Dubai

Genetic Predisposition: The evidence that psoriasis may be inherited is based on population surveys and family analysis. Controversy exists on the mode of transmission. More evidence is in favour of single gene autosomal dominant inheritance with reduced penetrance.

The incidence of psoriasis in siblings appears to be as high as 50% when both parents are affected.

HLA Systems: The relationship of psoriasis to HLA system was studied by many researchers. Many have confirmed association with B13, B17 and CW6. In GPP strong association with HLA B8 and in GPP association with B27 was found.

Provocative and exacerbating Factors:See below.

Endocrine Factors: Peaks of psoriasis has been reported during puberty and menopause. Psoriasis remains unaltered in about 40% of pregnancies, improved in 40% and worsened in 15 %. GPP may be provoked by pregnancy and may get exacerbated premenstrually and with high dose estrogen therapy.

Metabolic Factors: Hypocalcaemia following parathyroidectomy and dialysis has precipitated psoriasis.

AIDS: The prognosis of Psoriasis in AIDS patients and AIDS in psoriatic patients appears to be poor due to the decrease in T helper cells.

Also see Pathogenesis, immunology, biochemical aspects and provocative factors below for a full review of aetiopathogenesis of psoriasis. 

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Contributed by Dr.T.C.Satish, Dubai

It is a complex interaction between alteredkeratinocytic proliferation & differentiation, inflammation & immune dysregulation.

The earliest changes are vascular. There is swelling & intercellular widening of endothelial cells followed by deregulation of mast cells around post-capillary venules. Hours later activated macrophages appear in the lower epidermis where there is loss of desmosome tonofilament complexes. Finally lymphocytes & neutrophils appear.

Electron Microscopic studies shows psoriatic keratinocytes have significant abnormalities. Tonofilaments are decreased in number and diameter and lack normal aggregation. Keratohyaline granules are decreased in size and number. The cornified cells retain organelles and nucleus as parakeratotic cells. The basal keratinocytes show cytoplasmic processes protruding into dermis through gaps in the basal lamina and they correlate with disease activity. The intercellular spaces between all epidermal cells are widened because of deficiency in the glycoprotein rich cell surface coat. The spongiform pustule of Kogoj, one of the most characteristic features of psoriasis is located in the uppermost portion of spinous and granular layers. Here neutrophils lie intercellular in a multilocular pustule in which sponge like network is composed of degenerated and flattened keratinocytes. The capillary loops in dermal papillae in psoriasis show wider lumen, bridged fenestrations & gaps between endothelial cells, extravasation of RBCs and inflammatory cells & thickened basement membrane. They may be due to deposition of amorphous substances & accumulation of collagen fibrils in the BMZ.


The rate of epidermal cell replication is markedly increased as suggested by the higher number of basal and suprabasal mitotic figures. The mitotic activity varies in different lesions & even within the same lesion. It correlates with degree of parakeratosis.Early investigations suggested that the transit time of cells from basal cell layer to uppermost row is shortened to 7 days in psoriasis from 53 days in normal epidermis. Further investigations showed the germinative cell cycle shortened from 311 to 36 hrs i.e. 8 fold faster proliferation in psoriasis, doubling of proliferative cell proliferation in psoriasis from 27000 to 52000 cells/sq mm of epidermal surface area, 100% of germinative cells of epidermis enter growth fraction instead of only 60% for normal subjects. However another study showed that the germinative cell cycle time in normal epidermis is 200 hrs while in psoriasis it is only 2 fold faster i.e. 100 hrs. The source of cycling cells in suprabasal layers is not yet well defined. It could be expanded population of basal keratinocytes or could be recruited from transit amplifying cells (TAC) which are suprabasal keratinocytes committed to terminal differentiation that undergo rounds of amplifying divisions above basal layer. Keratin studies suggest TAC since they express K1/K10 & K6/K16 keratins and not K5/k14 as basal keratinocytes do.


Keratinocytes undergo a process of differentiation as they migrate upward through the epidermis from basal layer to cornified layer when several structural proteins are synthesized. One such protein family is keratins, which are intermediate filaments, found in the cytoplasm of all epithelial cells. Studies show that in normal epidermis K5/K14 are expressed in basal keratinocytes and K1/K10 are expressed in suprabasal keratinocytes. Involucrin, one of the major precursor proteins of cornified cell envelope are detected higher in granular & cornified layers. In psoriatic skin basal keratinocytes continue to expressK5/K14. However keratins K1/K10 are replaced by so called hyper proliferation associated keratins K5/K16.Also involucrin expressed prematurely in lower suprabasal layers. K17 also found in upper suprabasal keratinocytes while normally they are found in deep outer root sheath of hair follicle.

Immuno pathological factors also play a very important role in the pathogenesis of psoriasis.

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Contributed by Mammen Jacob, Sharjah

Many different hypotheses have been put forward for the role of the immune process in psoriasis. It is believed that the inflammatory infiltrate results in epidermal hyper proliferation and abnormal differentiation of keratinocytes. Some of the factors responsible for the inflammatory process are: A gene defect which results in the absence of a clone of suppressor T cells that are supposed to prevent the 'recognition' of basal cell nuclear antigens. This results in the formation of antibasal cell nuclear antibody under appropriate conditions e.g. environment, stress or other triggers. This cell-mediated immune response disturbs the epidermal basal cells causing an altered maturation and keratinisation of the keratinocytes. It also causes the release of more basal cell nuclear antigen resulting in a self-perpetuating inflammatory process.
Normal serum contains stratum corneum antibody (SCab). SCab does not bind to normal skin but does so in psoriatic skin because SC antigen is hidden in normal skin but is available in psoriatic skin. It is also available in koebnerised skin. This antigen antibody reaction activates complement with the resultant release of leucotactic factors and a migration of leucocytes into the epidermis. The inflammatory infiltrate in psoriases consists of neutrophils, lymphocytes and monocytes. These cells produce cytokines, which pass into the epidermis and stimulate the proliferation of keratinocytes. Interleukin 1 beta is seen in very high concentrations in the psoriatic plaque, especially at the advancing edge. The HLA genes associated with psoriases are HLA- B13, B17, B39, B57, Cw6, Cw7, DR4 and DR7. The HLA gene clusters contain several genes whose products are involved in the psoriatic process: C2, C4, Tumour Necrosis Factors alpha and beta. These clusters also contain genes whose products are involved in antigen presentation i.e. peptide transports and proteasomes. All these and other factors may be responsible for the inflammatory infiltrate and antigen antibody reaction resulting in epidermal hyper proliferation and abnormal differentiation of keratinoctes and thus the psoriatic plaque or pustule.
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vBiochemical Aspects

Contributed by Dr.Lilly Jose,Sharjah

Since the aetiopathogenesis of psoriasis is still not well established, there are several postulations.

The biochemical aspects of psoriasis are mainly related to the arachidonic acid metabolism. The release of arachidonic acid is increased by the enhanced activity of phospholipase A2.The cycloxygenase pathway is inhibited in psoriatic skin so this acid is diverted to the lipoxygenase pathway leading to increase in concentration of many human peripheral leucocytes attractants like leukotrene B4, eicosatetraenoic acid, interleukines, peptides, platelet activating factors etc.

Another important factor implicated is the complement C5a (des arg) derivative. This is produced due to compliment activation by complexes formed between stratum corneum antigens and antistratum corneum antibodies.

All the above factors as well as increase in the epidermal growth factor, increase in IL6 and LTB4 etc increases the mitogenic potential. The alterations in the cyclic AMP, cGMP ratio also contributes to this. CGMP is increased and cAMP is decreased in psoriatic skin.

There are controversial reports about a decrease in Protein Kinase C, metabolite of phosphotidyl inositol. Protein Kinase C deficiency leads to increase in mitosis.

Calcium andits binding protein calmodulin modulate growth and differentiation of cells. Increase in calcium binding protein is seen in psoriatic skin leading to increase in epidermal proliferation

Ornithidine decarboxylase is the rate-limiting enzyme in the synthesis of polyamines (spermidine, spermine and putrescine), which in turn increase DNA synthesis and cell proliferation. Some reports are showing an enhanced production of polyamines in the causation of increased epidermal proliferation.

Most of the changes are not specific for psoriasis. To some extent these alterations are seen in contact dermatitis, atopic dermatitis etc also.

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vProvocation Factors

Contributed by Dr.Hanish Babu, Ajman

Psoriasis is marked by periods of remissions and exacerbations. Remissions usually last a few weeks to many years. Both local and systemic provocation factors bring in exacerbations.

Local Factors: Local injury to the skin produces psoriatic lesions, the well-known Koebner Phenomenon.

Trauma involving the papillary dermis could be physical, chemical, mechanical, allergic or burns, drug eruptions, dermatitis, lichen planus, miliaria, herpes zoster, chickenpox etc. Koebner phenomenon occurs usually within 7-14 days (ranging from 3 days to 3 weeks)

Seasonal variations: In most patients, psoriasis worsens during cold weather. High humidity is usually beneficial, whereas sunlight worsens in some but improves in many.

Pregnancy:In most cases pregnancy induces remissions, though raised levels of progesterone in the latter half of pregnancy can precipitate generalized pustular psoriasis in some.

Emotional Stress: Psoriasis is well known to be induced, exacerbated, or sustained due to emotional stress. The mechanism is not yet well understood, but neuropsychoimmunological mechanisms are hypothesized. The disease itself could produce a reactive depression, which could further exacerbate the disease.

Infections:Streptococcal URTI has been shown to exacerbate existing psoriasis and precipitate an attack of acute guttate psoriasis mainly in children. Koebner phenomenon also produces psoriatic lesions in certain bacterial, fungal and mycotic skin infections. Other hidden infective foci from sinus, tonsil, gall bladder, appendix, urogenital tract, and oral cavity also may be the cause for exacerbation of psoriasis in certain individuals.

Drugs:Many drugs are known to precipitate or exacerbate psoriasis.

Beta-blockers like propranalol, practalol, and metapralol may induce or exacerbate psoriatic eruption by depressing the cyclic AMP levels. The eruption usually disappears within 2 to 6 weeks of cessation of the drugs.

Almost all NSAIDS affect psoriasis adversely. Anti depressants like lithium compounds and Trazodone may precipitate generalized pustular psoriasis. 

Too rapid withdrawal of corticosteroid therapy may precipitate pustular or erythrodermic exacerbations of psoriasis. 

Alcoholic beverages affect psoriasis adversely.

Chloroquine, clonidine, iodides, glibenclamide, and tetracycline are a few other drugs known to exacerbate psoriasis.

Very harsh or overenthusiastic topical therapy is also a culprit.

The role of food visa viz psoriasis is controversial. Red meats are generally considered to exacerbate psoriasis. A few shellfish may stimulate an acute exacerbation while, as a whole fish is considered beneficial in psoriasis. Fish oils containing essential fatty acids have been found to be effective in many patients, though conclusive evidence is still awaited.

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Contributed by Dr.George Jacob, Ras al Khaima

In the EPIDERMIS, the characteristic changes consist of acanthosis and elongation of the rete ridges, a reduced or absent granular layer, parakertosis, oedema of the papillae and thinning of the super papillary plate, and the presence of micro pustules in the upper epidermis. The early changes: The first histopathological change is invasion of the epidermis by neutrophil polymorphs (and maybe a small micro abscess). The changes in established psoriasis:are essentially epidermal. The horny layer shows considerable hyper & parakeratosis, often alternating. The granular layer is reduced or absent in active lesions.

The rete ridges are greatly elongated & often clubbed. They are separated by oedematous papillae, also club shaped, above which the spinous layer is thinned. Mitotic activity is the basal and suprabasal cells are greatly increased. Cellular invasion takes place, particularly in the suprapapillary region to form the Munro 'micro abscess' which are extruded in the horny layer or they may collect in disintegrated malphigian cells, the cytoplasm of which had been lysed to form the multilocular or spongiform pustule of


In the DERMIS the main changes consist of papillary oedema, dilatation and tortuosity of the papillary capillaries and a mild to moderate infiltrate of lymphocytes with occasional histiocytes.

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vClinical Features and Complications

Contributed by Dr.Balachandran,Dubai

Development of erythematous well-defined, dry, scaly papules and plaques of varying sizes characterize psoriasis. The scales are abundant, loose, dry (sometimes greasy) and silvery white. On scrapping, characteristic adherence of scales can be seen as if one scratches on a wax candle. When the scales are completely scrapped of, a moist, pinpoint bleeding surface is seen. Development of isomorphic lesions at the site of local trauma is more common during the acute or eruptive stage (Koebner phenomenon).

In some patients, raindrop like erythematous papules erupt abruptly with a bilaterally symmetrical distribution. This type of guttate lesions may also occur in patients with chronic plaque psoriasis when they are exacerbated or become eruptive. Chronic plaque psoriasis is common type. If palm sized lesions predominate, it is called psoriasis geographical and if coin shaped lesions predominate, it is called nummular psoriasis. 

Sudden withdrawal of corticosteroids or application of irritants can cause erythema and scaling. This condition is called exfoliative psoriasis. Patients may have hyperpyrexia, hypoalbuminaemia, eneteropathy and generalized lymphadenopathy.

Sometimes over treatment with tar, anthralene or potent steroids or by systemic therapy with progesterone or corticosteroids may lead to development of superficial pustules on the surface. It is called pustular psoriasis. This may be localized or generalized. Impetigo herpetiformis that occurs in last trimester of pregnancy is considered to be a variant of generalized pustular psoriasis. 

Psoriasis of nails can manifest as pitting of nail plate, subungual keratosis, crumbling of nail plates and onycholysis. Yellowish discoloration, ridges, grooves and splinter hemorrhages may also occur.

In addition to annular migrans that occur on tongue and cheek in GPP, scaly well-defined papules may occur on glans penis.

Arthritis may occur in 5-10% of psoriatics. HLA studies revealed that B23, DR3, A26 and B38 are significantly associated with psoriatic arthritis. It is customary to divide psoriatic arthritis into classic type, rheumatoid type, mutilating type, oligoarticular type and psoriatic spondylitis.

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vTopical Therapy Other Than Steroids

Contributed by Dr.Smruti, Sharjah

A. Tar Therapy:

Tar has been used in topical therapy for more than a century. It is assumed to have an antimitotic effect.

Types of Tar: Coal tar, wool tar and pine tar. The cruder the tar extract, the more effective it is. Coal tar is a mixture of thousands of substances produced by primary condensation during the carbonization of coal; while pine tar is oil from cade (birch tree).

Concentration of crude coal tar upto 10% are incorporatedin various vehicles for local treatment of psoriasis.

Adverse reactions: 

1. Staining and odour of the tar, lessened in newer preparations

2. Folliculitis (Commonest)

3.Primary irritant reaction if used in areas like face, genitalia and flexures.

4. Carcinogenecity: In cases of prolonged usage with UV light therapy.


1. Erythrodermic Psoriasis

2. Generalized Pustular Psoriasis

3. Pre-existing folliculitis/ severe acne

B. Dithranol/Anthralin:

It is a synthetic derivative of chrysarobin, a tree bark extract. Since it is an unstable product, combining with salicylic acid stabilizes it.

Dithranol paste is of unquestionable effectiveness but is highly irritant especially on the head and neck areas and stains linen irreversibly. Kinetic studies showing penetration of full epidermis in 100 minutes or less have encouraged the notion of short contact therapy, which is effective and less irritant. A concentration of 0.05-0.5% is applied for 10 minutes to one hour under occlusion.

C. Salicylic Acid:

It is a keratolytic agent. It is used in a concentration of 3-5% incorporated into cold cream or hydrophilic ointment.

D. UV Light:

Artificial UV light B is frequently used. In recurring cases, patient may be advised to own an ultraviolet lamp and expose himself daily to it. A fixed treatment distance of about 3 feet should be used and time of exposure gradually increased by a few seconds daily starting with 2 minutes.

Tar applications or baths prior to UVB have been credited with enhancing its effect.

For widespread and recalcitrant psoriasis, ultraviolet therapy combined with tar or anthralin is the basis for Goeckerman and Ingram regimens.

Goeckerman: - 2-5% tar preparation is applied daily several times and a tar bath is taken daily. Excess tar is removed with mineral oil and UV light exposure is done.

Ingram:- Daily a coal tar bath in a solution of 120 ml liquor carbonis detergens to 80 liters of water is followedby exposure to ultraviolet light for daily increasing periods. An anthralin paste is then applied to each plaque. Talcum powder is sprinkled over the lesions and stockinet dressings applied.

E.Iodochlor hydroxyquine (vioform):

It has been used frequently in a formula of 3% ointment/cream.

F. Retinoic Acid as 0.5% ointment base: It induces a moderately severe reaction at local site and is contraindicated in generalized psoriasis.

G. Vitamin D3 (Calcipotriol):

1a, 24-dihidroxy vit D3, a synthetic analogue of 1a, 25 dihydroxy vit D3 (calcitriol)

Mechanism of action is through induction of terminal differentiation of keratinocytes and inhibition of T cell proliferation.

It is widely used in chronic, plaque psoriasis alone or in combination with potent steroids. It is available as 50mg/gm. Weekly dosage should not exceed 100gms per week, after which serum calcium levels increase.

A drug under trial is maxacalcitol, which is 1a, 25 dihydroxy 22 oxacalcitriol which displays approximately 10 times greater efficacy at suppressing keratinocyte proliferation in vitro than calcipotriol. It is being used as 25mg/gm.

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vSteroids in Psoriasis

Contributed by Dr.SMS Pillai,Dubai

Topical steroids are the most widely used medications for psoriasis. They are effective, convenient to use and affordable.

Corticosteroid ointments are greasy and messy, but are more effective than cream.

Most common side effect is cutaneous atrophy. But the atrophy is reversible in most cases if medication is discontinued early. Other side effects are telangiectasia, folliculitis, perioral dermatitis etc.

Many dermatologists believe that tachyphylaxis and steroid rebound are major limitations of long-term therapy with steroids in psoriasis.

In the absence of any maintenance therapy, the relapse is estimated to occur in 60% of cases within one month and 93% of patients in one year. Even with maintenance corticosteroid therapy, relapse is estimated to occur in 51% of patients within one month and 71% of patients within 1 year.

Application of clobetasol propionate 0.05% ointment has been shown to cause a rapid and statistically significant reduction of plasma cortisol levels within 24 hours. Suppression of HPA axis is indeed the most serious adverse effect of treatment with super potent steroids. Hence a pulse therapy is advisable when such topical therapy is attempted.

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vMethotrexate in Psoriasis

Contributed by Dr.Bindu, Sharjah

In 1951,amethopterin (or methotrexate as it is more commonly known), a folic acid antagonist, was found to be excellent in the control of psoriasis. 20 years later, FDA approved it in psoriasis.

Methotrexate is structurally similar to folic acid and is a potent inhibitor of the enzyme dihydrofolate. It binds to it within 60 minutes competitively and irreversibly, preventing the conversion of dihydrofolate to tetrahydrofolate, which is necessary for the DNA and RNA synthesis. It acts on 's' phase of cell cycle.2 agents can reverse the actions of methotrexate, viz leucovorin and thymidine and can be used in toxicity.

Methotrexate can be administered oral/IV/IM. Concurrent food intake, especially milk products may reduce bioavailability in oral dosage.

A methotrexate candidate should have a debilitating state that either is uncontrolled by more conventional methods or is not amenable to such therapies.


Absolute: Pregnancy, Lactation

Relative: Decreased renal function, hepatic disease, severe hematological abnormalities, alcoholism, child bearing age (12weeks before conception: should be stopped in both sexes), active infectious diseases, h/o potentially serious infection that could be reactivated, immunodeficiency syndromes, unreliable patient.

Monitoring Guidelines:

Baseline: Careful history and physical examination, identification of patients with increased risk of toxicity, recording concomitant medication to rule out drug interactions eg, salicylates, NSAID, sulfa, tetracycline, chloramphenicol, phenytoin, phenothiazines, probenicid, dipyridamole.

Follow-up: CBC, Platelet, LFT- every week for 4 weeks, 7 days after each dose escalation

CBC, Platelet, LFT- every 3-4 months after dosage stabilization.

Liver Biopsy: after every 1.5-2.0 gm total dose for low risk patients.

After every 1.0 gm total dose for high risk patients

After every 6 months for IIIA liver changes.

Well, now liver biopsy is outdated as blood analysis of amino terminal propeptide of type 3 procollagen is sufficient for evaluation of LF.

Therapeutic Guidelines:

Occasional IM if nausea from oral dose.

Oral dose: single, or more commonly 3 divided doses at 8 am, 8 pm, 8 am once a week (Rationale: Presumed cell kinetics in psoriasis cell cycle shortened from 19 days in normal to 37.5 hours in psoriatic epidermis.)

Initial dose-5-10 mg stat: CBC, LFT after 7 days.

If Okay, escalate dose to 2.5-5mg per week to get reasonable benefit without toxicity.

10-12.5 mg/week on an average gives maximum benefit.

IM: 0.2-0.4mg/kg every 7-14 days

Adverse Effects: 

Hepatotoxicity: Regular monitoring to detect 

Pulmonary Toxicity: Pneumonitis, Pulmonary Fibrosis

Hematological Effects: Myelosupression

Gastrointestinal: Nausea, diarrhoea, ulcerative stomatitis, anorexia, vomiting

Potent Teratogen

Renal Toxicity only in high dosage

Other: alopecia, fatigue, phototoxicity, headache, and dizziness.

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vRetinoids in Psoriasis

Contributed by Dr.M.J.Cyriac, Dubai

Retinoids are synthetic or natural analogues of vitamin A.

The 3 main ones are: 

1. Isotretinoin (13 cis retinoic acid) 

2. Etretinate

3. Acitretin

Acitretin is an active metabolite of Etretinate. Etretinate is an ester and acitretin a corresponding free acid. Its great advantage over etretinate is its decreased lipophilicity, which results in elimination half-life of 50 hours as opposed to more than 80 days for etretinate. However the clinical efficacy and side effects are similar to etretinate.

The mode of action of retinoids is not fully established. It seems to induce a better maturation in keratinocytes and to reduce the neutrophil chemo taxis in pustular psoriasis.


1. Generalized Pustular Psoriasis: Considered to be the drug of choice.

2. Psoriatic erythroderma.

3.Severe psoriasis vulgaris, where other modalities have either failed or are contraindicated.

4.Palmo-plantar pustular psoriasis.


0.5-1 mg/kg/day is the usual initial dose of etretinate. Maintenance dose of 0.5 to 0.75mg/kg/day. Remission may take anywhere from 12-24 weeks. Relapses are very common following discontinuation of treatment.

Acitretin- an optimum dose of 50mg daily (mean 0.66mg/kg/day) is recommended.


1.Women of child bearing age, unless the psoriasis is unresponsive to other therapies or where clinical condition contraindicates the use of other regimens.

In such cases the following precautions are to be strictly adhered to:

a. Has received both oral and written warning of hazards of taking acitretin

b. Should be on reliable form of contraception

c. Should have negative serum and urine pregnancy test done at least 1 week prior to beginning treatment.

d. Treatment should be started on the 2nd or 3rd day of next normal menstrual period.

2. Pregnancy

3. Children

4. Active liver disease

5. Pre-existing hyperlipidemia

Side Effects:

- Almost 99% of patients receiving retinoids develop some sort of side effect. 

- It is highly teratogenic.

- The retinoids are lipophilic and are retained in the body for a considerably longer period of time. Sowomen receiving the drug should avoid pregnancy for a period of 3 years.

- It does not have any significant efect on the semen.

- Lipid abnormalities in the form of increased serum triglycerides and cholesterol may necessitate discontinuation of therapy. In mild cases, the abnormality may be alleviated by concomitant administration of fish oils.

- Liver enzyme elevation, hepatitis and jaundice

- Radiological spinal changes including anterior spinal ligament calcification, osteophytes, disc abnormality, DISH (diffuse idiopathic skeletal hyperosteosis) can occur

- In children, premature closure of epiphyses, growth retardation andhyperosteosis can occur

- Dryness of the lip, nose, mouth, eyes, throat with peeling of skin, exfoliative cheilitis, uveitis, balanitis, gingivitis, corneal ulceration, burning sensation of skin, atrophy of skin, alopecia, epistaxis, increased bruising, generalized erythema

- Purulent paronychia may necessitate stopping of therapy.

- Pseudotumour cerebri is not uncommon

Drug Interactions:

1. Do not give tetracyclines along with retinoids (pseudotumour cerebri)

2. No supplementation with vitamin A

3.Concommitant methotrexate increases hepatotoxicity

4. Ethanol should not be given along with acitretin because it is converted to etretin

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vPhoto therapy

Contributed by Dr. Sathish Kumar, Dubai

Parrish et al first reported this mode of therapy in 1974. It consists of ingestion of Psoralen in the dose of 0.6-mg/kg body weight on alternate days and followed in 2-3 hours later by UV radiation for graded periods.

The commonly used psoralens are 8-methoxy psoralen and 4,5,8 trimethoxy psoralen.

PUVA therapy affects DNA synthesis and proliferation of cells in psoriatics by 2 mechanisms:

a. An anoxic reaction that affects cellular DNA with the formation of photo adducts.

b. An oxygen dependent reaction where free radicals and reactive oxygen formed may damage the membrane of lipid per oxidation and induce activation of mediators of the eicosanoid system.

PUVA therapy also reduces the chemo tactic activity of the psoriatic leukotactic factor.

Topical PUVA has been tried in the form of PUVA bath. Trimethoxy psoralen 50mg in 100ml ethanol is added to a 150-litre bath. Patient is allowed to bath for 15 minutes and then exposed to UVA at 290-320 nm. Photosensitivity is achieved immediately after this bath is 15 times greater than after oral psoralen and side effects like nausea, headache can be minimized by PUVA bath.

Side effects of PUVA therapy:

- Nausea, vomiting, headache, vertigo, erythema, pruritus, blistering

- Koebner phenomenon

- Hypertrichosis, hyper pigmentation

- Lichenoid eruption

- Photo-onycholysis

- Premature ageing of skin, Cataract formation

- Increased incidence of skin cancers etc.

Taking steps to minimize the total dose of PUVA, by combination therapy with topical PUVA, oral retinoids and methotrexate, can reduce these side effects.

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vOther Immunosuppressive Therapy

Contributed by Dr.S.M.S.Pillai, Dubai

Cyclosporine (Cy A) is a cyclic undecapeptide derived from fungus Toylypocladium inflatum gams. It is indicated for the treatment of adult non immuno-compromised patients with severe recalcitrant psoriasis who have failed to respond to at least one systemic therapy or in patients for whom other systemic therapies are contraindicated or cannot be tolerated.

To start with it is given in the dose of 3 mg/Kg body weight in two divided doses, which can be gradually increased to 5mg/Kg/day depending upon the therapeutic response. The effects of Cy A are evident within weeks; they are dose dependent.

The exact mechanism by which Cy A acts in psoriasis is not clear. It possibly down modulates proinflammatory cytokines that are increased in psoriatic lesions

Cy A is contraindicated in renal diseases, past or present malignancy, and uncontrolled hypertension. It is not safe for pregnant women and during lactation. Adverse effects include hypertension with raised serum creatinine level, IT comlicationss, hirsutism, headache and haemorrhagic gingivitis.

TACROLIMUS a macrolide immunosuppressive isolated from streptomyces tsukubaensis act by inhibiting the keratonocyte receptor pathway, an endogenous regulator of the cell cycle. Topical application of the drug is promising in the initial pilot studies.

ASCOMYCIN another immunosuppressant macrolide is effective in the concentration of 0.1 to 0.5%.


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