TREATMENT OF PSORIASIS Topical therapy Phototherapy Systemic therapy Climatotherapy

4. • Assurance.
• Avoidance of psoriasis triggers.
• Daily baths Helps to remove scales and calm inflammation. Avoid
harsh soaps preferably use medicated soap.

5. FACTORS INFLUENCING SELECTION OF TREATMENT:
1. Age: childhood, adolescence, young adulthood, middle age, >60 years.
2. Type of psoriasis: guttate, plaque, palmoplantar pustular psoriasis,
generalized pustular psoriasis, erythrodermic psoriasis.
3. Site: localized to palms and soles, scalp, anogenital area, scattered
plaques.
4. Severity of psoriasis: mild, moderate or sever.
5. Previous treatment: ionizing radiation, systemic glucocorticoids,
photochemotherapy (PUVA), cyclosporine A (CsA), and methotrexate
(MTX) & their responsiveness.
6. The impairment of quality of life. The visibility of the lesions and symptoms
such as pruritus.
7. Associated medical disorders (e.g., HIV) that exist or might develop.

6. • To date, no treatment has been shown to cure psoriasis.
• The management of psoriasis requires individualization of therapy,
• Treatments that are given as either mono—or combined—or rotational
therapy.
• Combination therapy denotes the combination of two or more
modalities, while rotational therapy denotes switching the patient after
clearing and a subsequent relapse to another different treatment.
• In practice most patients receive combination therapy.

7. Several key points in the cascade of events that lead to psoriasis can be
targeted for interventional therapy. These include:
1. Disruption of lymphocyte trafficking that leads to migration of activated
T cells from endothelial cells into the epidermis and dermis.
2. Inhibition of APC presentation and subsequent T-cell activation and
proliferation.
3. Prevention of Th1 cytokine production and release following T-cell
activation.
4. Direct antagonism of Th1 cytokine responses.
5. Augmentation of Th2 cytokine responses.
6. Anti-Hyperproliferative effect of epidermal cells.

8. A.Topical
B. Phototherapy
C.Systemic
D.Climatotherapy

12. INDICATIONS OF TOPICAL THERAPY:
1. Mild to moderate involvement, topical treatments are the first choice.
2. Widespread involvement may also be treated with a topical agent;
however, a high degree of compliance is required and this can be
difficult to achieve.
3. Combination therapy is advised for the vast majority of patients, thereby
 efficacy and  side effects.
4. Long-term form of maintenance Daily use of a topical vitamin D3
analogue (below the maximum allowed weekly dosage) provides a safe
therapy (if needed). If the therapeutic response is insufficient,
intermittent application of a topical corticosteroid (once or twice
weekly) is helpful.

13. 1. Vitamin D3 analogues
2. Local corticosteroids
3. Anthralin (Dithranol)
4. Topical retinoids
5. Salicylic acid
6. Coal tar
7. Calcineurin inhibitors
8. Emollients

14. • Vitamin D3 analogues inhibits epidermal proliferation,
and it induces normal differentiation by enhancing
cornified envelope formation and activating
transglutaminase; it also inhibits several neutrophil
functions.
• Potent topical corticosteroids are superior to
calcipotriene. But calcipotriene was more effective
than coal tar or Anthralin.
• Due to their therapeutic efficacy, cosmetic acceptability and limited toxicity,
calcipotriene (calcipotriol) and other vitamin D3 analogues have become a
first-line therapy of mild to moderate psoriasis. Also first-line therapy for mild to
moderate juvenile psoriasis.
• The efficacy of calcipotriene is not reduced with long-term treatment.

16. • Calcipotriene is applied twice daily.
• Salicylic acid inactivates calcipotriene.
• When the amount used does not exceed the
recommended, calcipotriene can be used
with a great margin of safety.
• It is often used in combination with or in rotation with topical
corticosteroids in an effort to maximize therapeutic
effectiveness while minimizing steroid-related skin atrophy.
• When calcipotriene and betamethasone dipropionate are
combined, an ~70% reduction in PASI has been observed
(ointment formulation) bas has clearing/minimal disease in
~70% of patients with scalp psoriasis (gel formulation).
• Other vitamin D analogues are tacalcitol and maxacalcitol.

17. • They are commonly first-line therapy in mild to
moderate psoriasis and in sites such as the flexures and
genitalia (need low potency products to avoid SE),
where other topical treatments can induce irritation.
• Maximum improvement usually achieved within 2 wks.
• Improvement is usually achieved within 2 to 4 weeks,
then maintenance is achieved by use in the weekends
only.
• Topical steroids under occlusion do have a limited
place in the management of recalcitrant psoriasis of
the scalp, hands, feet and other areas.
• Potent preparations are likely to be needed on the
scalp and knuckles particularly.

19. • Tachyphylaxis (decrease in efficacy with time) and/or
rebound of topical steroids in psoriasis is well-established.
• Long-term topical steroids may cause adrenal suppression.
• Intensive treatment with the most potent preparations
can induce generalized pustular or erythrodermic psoriasis.
• Because of these side effects potent topical steroids
e.g. clobetasol may be used on alternate day basis.
• Intermittent treatment schedules (e.g. once every
2 or 3 days or on weekends) are advised for more prolonged treatment courses.
• To avoid systemic effects of class I glucocorticoid, a maximum of 50 g oit. may be used /w.
• Corticosteroids are manufactured in various vehicles, from ointments, creams and lotions
to gels, foams and shampoos. Ointment formulations, in general, have the highest efficacy.
• For small plaques (< 4 cm) or nail matrix in cases of severe psoriatic nails, triamcinolone
acetonide aqueous suspension 3-10 mg/mL diluted with normal saline is injected into the
lesion intradermally.

20. • It is a anthracene derivative which is extracted from
coal tar.
• It is made up in a cream, ointment, or paste.
• It has an anti-hyperproliferative effect, also inhibits
mitogen-induced T-lymphocyte proliferation and
neutrophil chemotaxis.
• It is mainly used on plaques resistant to other therapies.
• Anthralin can be combined with UVB phototherapy with
good results using the INGRAM REGIMEN.
• Treatment usually in an inpatient setting or day-care
center. If the anthralin treatment is performed at home,
the efficacy is substantially less.

22. • Classic anthralin therapy starts with low concentrations (0.05 to 0.1 %)
incorporated in petrolatum or zinc paste combined with salicylic acid 1% and
given once daily. The concentration is  weekly in individually adjusted
increments up to 4 % until the lesions resolve.
• Most common side effects are: 1. Irritant contact dermatitis
2. Staining of clothing, skin, hair, and nails.

23. • It is a third-generation retinoid.
• It is available in 0.05 % and 0.1 % gels, and a
cream.
• Selectively binds Retinoic Acid Receptor (RAR)-β
and RAR-γ.
• Tazarotene has been shown to  epidermal
hyper-proliferation and it inhibits psoriasis-associated
differentiation (e.g. transglutaminase
expression and keratin 16 expression).
• It reduces mainly scaling and plaque thickness, with
limited effectiveness on erythema.

25. • When used as a monotherapy, a significant proportion of patients
develop local irritation, burning & erythema (especially with the 0.1%
formulations).
• Efficacy can be enhanced by combination with mid- to high-potency
steroids or UVB phototherapy but it has been recommended that UV
doses be reduced by at least one-third if tazarotene is added in the
middle of a course of phototherapy.

26. • If the psoriatic plaques have thick scale, this needs to
be reduced to enhance penetration of topical
medications and ultraviolet (UV) light.
• Salicylic acid 5–10% has a substantial keratolytic effect
and, in the case of scalp psoriasis,
• Salicylic acid can be formulated in an lotion, shampoo,
oil or ointment base.
• Application of salicylic acid to localized areas can be
done daily, but, for more widespread areas, two to
three times per week is preferred. This is to prevent
systemic intoxication especially in infants or those with
reduced renal function.

27. • The use of tar to treat skin diseases dates back nearly
2000 years.
• Tar is the dry distillation product of organic matter heated
in the absence of oxygen.
• Exactly how coal tar works to treat these conditions is not
completely understood. It appears to have antimicrobial,
anti-inflammatory, photosensitizing actions and is
effective as an antipruritic.
• Coal tar, in concentrations 5- 33% can be compounded
in creams, ointments, shampoos and pastes.
• Although crude coal tar may be the most effective tar
available for the treatment of psoriasis, a distilled
products are also used.

29. • It is often combined with salicylic acid (2-5%) 
keratolytic action leads to better absorption of the
coal tar.
• In 1925, Goeckerman introduced “THE GOECKERMAN
TECHNIQUE” which uses crude coal tar and UV light
for the treatment of psoriasis.

30. DISADVANTAGES OF COAL TAR:
1. Allergic reactions.
2. Folliculitis.
3. Unwelcome smell and appearance.
4. Stain clothing and other items.
5. Carcinogenic (controversy).
6. It has mutagenic potential, tar is contraindicated in pregnant or
lactating women.

31. • Agents: Tacrolimus & Pimecrolimus.
• They inhibit calcineurin, thus blocking both T-lymphocyte
signal transduction and IL-2 transcription.
• They are not effective in plaque psoriasis. However,
pimecrolimus for treatment of inverse and seborrheic
dermatitis-like psoriasis of the face and ear canals.
• The main side effect of these medications is a burning
sensation at application site.
• Anecdotal reports of lymph node or skin malignancy
require further evaluation in controlled studies, and
these drugs have a U.S. Food and Drug Administration
(FDA) “black box warning”.

32. • Between treatment periods, skin care with
emollients should be performed to avoid
dryness.
• Emollients reduce scaling, may limit painful
fissuring, and can help control pruritus.
• They are best applied immediately after
bathing or showering.
• The use emollients in combination with
topical treatments improves hydration while
minimizing treatment costs.

34. • Photo(chemo)therapy represents a mainstay in the treatment of
psoriasis.
• Phototherapy with broadband or narrowband ultraviolet B (UVB) and
photochemotherapy with ultraviolet A (UVA) following ingestion of or
topical application of a psoralen are classic treatment options.
• INDICATIONS: Moderate to severe psoriasis: first-line treatment as
monotherapy or in combination.
• The investigators also developed practice guidelines and
recommended the following sequence of therapies: UVB, PUVA,
methotrexate, acitretin and then cyclosporine.

35. 1. NB-UVB
2. PUVA
3. Excimer Laser

36. NB-UVB PUVA Excimer laser
•2-6 MED twice
weekly
•Initial dose 0.5-2.0
J/cm2, depending on
skin type followed by
twice weekly
•Increase dose by 40%
per week until
erythema, then
maximum 20% per
week until a maximum
of 15 J/cm2
•Initial dose at 70%
of MED followed by
3 treatments /w
•Lubricate before
session
•Increase dose
by at least 10-20%
of the MED

37. Excimer
laser
NB-UVB PUVA
1. Genetic disorders characterized by increased photosensitivity or an  •As NB-UVB
risk of skin cancer.
2. Melanoma, and nonmelanoma skin cancers
ABSOLUTE
CONTRAINDI-CATIONS
3. High cumulative number of PUVA
treatments, i.e. >200-300 individual
treatments (PUVA)
4. Pregnancy or lactation
5. Impaired liver function or
hepatotoxic medication
6. Treatment with cyclosporine
1. Skin type I •As NB-UVB
2. Photosensitive dermatoses
3. Unavoidable phototoxic systemic or topical medications
4. Immunosuppressive medication
5. Previous history of arsenic exposure, ionizing irradiation
6. Age < 10 yr,
7. Seizure disorder (risk of fall/injury)
RELATIVE
CONTRAINDI-CATIONS
8. Cataracts
9. Men and women in reproductive
years without contraception

40. The 308 nm excimer laser can be used to treat a limited
number of plaques in patients with localized disease.

42. • Can be used when other modalities fail to achieve desirable response.
• The concept of rotational therapies is valuable.
• Cyclosporine should not be used as a maintenance treatment, whereas
methotrexate, acitretin and fumarates can be employed for long-term
control of psoriasis.
• However, long-term use of these systemic treatments is restricted by their
cumulative toxicity potential.
• If neither photo(chemo)therapy nor classic systemic medications provide
adequate improvement, treatment with a biologic agent is indicated.

46. • Structure
• Pharmacodynamics
• Mechanism of action
• Dosage
• Indications
• Side effects
• Monitoring
• Contraindication
• Drug Interactions
• Toxicity & antidote

47. • Is an Antimetabolite.
• MTX is a first-line systemic therapy for psoriasis as it is highly efficacious for
severe disease and all clinical variants of psoriasis.
• In chronic plaque psoriasis, initial improvement is observed 1-7 weeks
and maximum improvement can be expected after 8–12 weeks of
treatment.
• Potential side effects restrict its use to moderate to severe disease resistant
to topical treatments and photo(chemo)therapy and/or situations in
which these are contraindicated.
• Of the systemic medications, methotrexate is regarded as the treatment
of choice in childhood psoriasis.

48. • Folic acid analogue

49. • MTX is not difficult to use and oral administration achieves reliable blood
levels unaffected by food intake.
• MTX is widely distributed throughout the body, but penetrates the blood–
brain barrier poorly.
• Within 1 hour of ingestion, distribution and active cellular uptake is
complete.
• Plasma MTX is 50% protein-bound, and irreversibly bound to dihydrofolate
reductase, the enzyme it inhibits.
• By 4 hours, the kidneys have excreted the plasma portion of the drug.
• Over the next 10–27 hours, the drug is slowly released from body tissues.

50. DHFR
Thymidylate
synthetase

51. 1. Dihydrofolate reductase (DHFR) converts dihydrofolate to
tetrahydrofolate (fully reduced folic acid), which is a
necessary cofactor in the de novo synthesis of
thymidylate and purine nucleotides, which, in turn, are
required for DNA/RNA synthesis. MTX competitively inhibits
DHFR, although this inhibition can be at least partially
reduced by concomitant folic acid administration.
Although originally believed to suppress keratinocyte
proliferation, it is more likely that MTX inhibits DNA synthesis
in immunologically active cells especially lymphocytes,
circulating and cutaneous.
2. Forms polyglutamyl-MTX which traps MTX inside cell also
exerts partially reversible inhibition downstream on
thymidylate synthetase, inhibiting cell division in S phase.
Decreases THF intracellular which decreases conversion
of Deoxyuridine monophosphate (dUMP) to dTMP.

52. 3. MTX decreases inflammation
through other mechanisms as well.
By inhibiting amino-imido-carboxy-amido-
ribonucleotide
transformylase (AICAR
transformylase), MTX increases
local tissue concentrations of the
potent anti-inflammatory mediator
adenosine.
4. By inhibiting methionine synthase
(MS), MTX reduces production of
the proinflammatory mediator S-adenyl
methionine (SAM).

53. • Once-weekly dose of up to 30 mg.
• Oral, IM, SC.
• The starting dose 2.5–7.5 mg may be gradually increased
by 2.5 to 5 mg every 2–4 weeks until satisfactory results are
obtained with minimal toxicity.
• The usual weekly dose 10–15 mg, although doses up to
25 mg per week are not uncommonly used, except in
patients with renal insufficiency.
• Once disease control has been attained for at least 1–2
months, the MTX can be tapered by 2.5 mg every 1–2
weeks to the lowest dose that still maintains disease control.
• 2.5 mg tab & 25 mg/ml vial are the most commonly
available forms.

54. • Historically; The triple-Dose (Weinstein) Regimen over 24 hours (8 a.m. and 8
p.m. day 1, and 8 a.m. day 2). There were theoretical advantages for the
divided dosing regimen from a cell cycle kinetics standpoint.
• However, since the clinical result is the same, a single dose, which is easier
and less confusing (for the patient and the pharmacist), is currently
recommended.

56. 1. CTCL
2. Dermatomyositis
3. Pityriasis rubra pilaris
4. Lupus erythematosus
5. Langerhan’s cell histiocytosis
6. Lymphomatoid papulosis
7. Localized scleroderma (morphea) & systemic scleroderma
8. PLEVA
9. Pompholx
10.Bullous Pemphigoids

58. • Pancytopenia typically develops early, compared to liver fibrosis and
cirrhosis, which take years to develop.
• The higher the cumulative dose of MTX, the greater the risk of significant
liver damage.
• Photosensitivity may occur and patients should take appropriate sun
precautions.
• Gastrointestinal intolerance & megaloblastic anemia is often reduced
with concomitant folic acid therapy (1–5 mg orally daily except on day
MTX administered, based on symptoms) without diminishing the
efficacy of antipsoriatic treatment.

59. • Baseline & Repeat baseline tests weekly during dose escalation, then every
2 wk and later at intervals of perhaps 3 months.
• It's best to do blood tests at least 5 d. after a dose & just prior to next dose.
1. Liver enzymes
2. Complete blood count
3. kidney function tests (creatinine)
4. Pregnancy test
5. liver biopsy: In the most recent guidelines, patients with normal liver
function tests and without a history of liver disease or alcoholism are
not asked to undergo liver biopsy until they have been treated with a
cumulative MTX dose of 1.0 to 1.5 g. Repeat biopsies are done
approximately 1.0 to 1.5 g thereafter if liver function test and biopsy
findings are normal.

60. • Drugs that elevate MTX blood levels include:
1. NSAIDs
2. Salicylates
3. Sulfonamides
4. Chloramphenicol
5. Phenothiazines
6. Phenytoin
7. Tetracyclines
• Drugs also inhibit the folate metabolic pathway and markedly
increase the risk for pancytopenia with concomitant use:
1. Trimethoprim
2. Sulfonamides
3. Dapsone
• Systemic retinoids and alcohol may cause synergistic liver damage.

61. • Leucovorin calcium (folinic acid) is the only
antidote for the hematologic toxicity of MTX.
• When an overdose is suspected, an immediate
leucovorin dose of 20 mg should be given
parenterally or orally as early as possible, and
subsequent doses should be given every 6 hours.
• Alkalinize urine & hydrate patient to dilute &
increase solubility of metabolites.

63. • It is the free metabolite of etretinate.
• Acitretin is an effective treatment for psoriasis as well as disorders of
keratinization.
• May contribute to improvement by normalizing keratinization and
hyperproliferation of the epidermis.

64. • In patients with chronic plaque psoriasis, 0.5 mg/kg/day is the initial
dosage, which can be increased depending upon the clinical response
and side effects.
• For erythrodermic psoriasis, the initial dosage is 0.25 mg/kg/day, and in
pustular psoriasis, the dose should be maximized up to 1 mg/kg/day (25-50
mg daily).
• In patients with chronic plaque psoriasis, mild cheilitis (just perceived by
the patient) is the goal, whereas in patients with pustular psoriasis, a dose
that causes a clinically apparent but tolerable cheilitis is an endpoint.

65. • The efficacy of acitretin monotherapy in chronic plaque psoriasis is limited,
with approximately 70% of patients achieving a moderate or better
response.
• Treatment with photo(chemo)-therapy and/or vitamin D3 analogues results in
a substantial improvement in clinical response. Maximal therapeutic efficacy
is reached after 2–3 months.
• Acitretin has been shown to be an effective maintenance therapy.
• As monotherapy, acitretin is highly effective in erythrodermic and pustular
psoriasis. Its efficacy in nail psoriasis and psoriatic arthritis is only modest.
• The drug is category X thus teratogenicity, makes contraception mandatory
in women of childbearing age during treatment and (depending on the
drug half-life) for a period of 2 months to 3 years after discontinuing therapy.
• Most patients relapse within 2 months after discontinuing acitretin.

68. • Is a natural cyclic polypeptide
immunosuppressant isolated from a
certain type of fungi.
• Highly effective treatment for the severe
manifestations of psoriasis.
• Up to 90% of patients achieve clearance
or marked improvement.

69. • It is a calcineurin inhibitor.
• Indicated in Severe psoriasis Conventional therapies (topical treatments,
photo(chemo)therapy, acitretin, methotrexate) ineffective or
inappropriate.
• Efficacy of cyclosporine has been demonstrated in all variants of psoriasis
(including nail psoriasis), but less so for psoriatic arthropathy.
• High-dose method: 5 mg/kg daily, then tapered
Low-dose method: 2 mg/kg daily, increased every 2-4 wk up to 5 mg/kg
daily, then tapered.
• The improvement is observed within a few weeks.
• During longterm treatment, there are no signs of tachyphylaxis.

72. • In view of its nephrotoxic effects (e.g. reduced glomerular filtration rate,
tubular atrophy), cyclosporine should be given for several-month courses.
In elderly patients and patients with a history of hypertension, the risks of
renal impairment and hypertension are increased.
• Cyclosporine can produce dramatic rapid improvement of psoriasis, but
this must be balanced by the requirement for an appropriate
replacement therapy, given the need to ultimately stop cyclosporine
therapy.
• Cyclosporine treatment in psoriatic patients has been reported to
increase the frequency of SCCs, especially in those previously treated
with PUVA due to  in immunosurveillance of the skin.

74. i. Sulfasalazine
ii. Mycophenolate mofetil
iii. Fumarates
iv. Oral calcitriol
v. Hydroxyurea
vi. 6-thioguanine
vii.Apremilast (Otezla) [PDE-4i]

76. • They are bioengineered molecules that target specific proteins involved in
the pathogenesis of immune-mediated disorders.
• For the treatment of moderate to severe psoriasis and/or psoriatic arthritis.
• Safety concerns, lack of efficacy, and inconveniences are important
restrictions, in particular for long-term use of other medications. For such
patients, biologic agents can provide benefit for their skin disease as well
as psoriatic arthritis.
• Currently available biologics for psoriasis target either the T-cells or block
the inflammatory action of cytokines.

77. 1. Etanercept (Enbrel®)
2. Infliximab (Remicade®)
3. Adalimumab (Humira®)
4. Ustekinumab (Stelara®)
5. Alefacept (Amevive®)
6. Efalizumab (Raptiva®)

84. Some tests that should be done before starting treatment with
biologics:
1. Liver function tests
2. CBC with differential
3. Hepatitis panel (B & C)
4. HIV testing
5. TB testing: PPD/interferon-γ release assay (IGRA) and/or chest X-ray
During treatment
1. TB testing: Annually
2. Others: every 3–12 months (or as clinically indicated)

85. 1. Etanercept (Enbrel®)

86. 2. Infliximab (Remicade®)

87. 3. Adalimumab (Humira®)

88. 4. Ustekinumab (Stelara®)

92. Etanercept Infliximab Adalimumab Ustekinumab
• Fully human IgG1
monoclonal antibody that
binds with high affinity and
specificity to the p40 subunit
that is shared by the
heterodimeric IL-12 and IL-23
cytokines
• IL-12 has a critical role in
the development of Th1 cells
and NK cell activation,
whereas IL-23 is necessary for
the generation of Th17
• Fully human
recombinant IgG1
monoclonal
antibody that
specifically targets
TNF-α
• Chimeric IgG1
monoclonal
antibody that
has high
specificity,
affinity, and
avidity for TNF-α
• Human
recombinant,
soluble fusion
protein TNF-α
receptor. Binds
soluble TNF-α
and neutralizes its
activity. • By interacting with membrane-bound
TNF-α, the IgG1 monoclonal
antibodies can also activate
complement-dependent cytotoxicity
(ADCC) and induce cellular apoptosis

93. Etanercept Infliximab Adalimumab Ustekinumab
• Subcutaneous
injection
• 45 mg (if weight
is ≤100 kg) or 90 mg
(if weight is >100
kg) at weeks 0 and
4, then every 12
weeks.
• Subcutaneous
injection
• An initial loading
dose of 80 mg is
typically given,
followed by 40 mg on
day 8 and then 40 mg
every other week.
• Only slow
intravenous infusions
over 2 h.
• 5-10 mg/kg at
weeks 0, 2, and 6
then every 8 weeks
• Faster onset of
action
• Subcutaneous
injection
• 25 to 50 mg twice
weekly for the first 3
months followed by
50 mg weekly
• Recommended
intermittent courses
no longer than 24
week

94. Etanercept Infliximab Adalimumab Ustekinumab
Highly variable Unknown Variable
between
individuals and
may depend on
the initial dose
given
Variable and
dose-related
ranging from 70-
90 days

98. Etanercept Infliximab Adalimumab Ustekinumab
Category B Ctegory B Ctegory B Category B

99. Etanercept Infliximab Adalimumab Ustekinumab
STELARA®
• Prefilled syringes
available in 45 &
90 mg strengths
• 45 mg multiple-use
vials.
HUMIRA ®
• 40 mg prefilled
syringe or
autoinjector
REMICADE ®
• Vial contains 100
mg lyophilized
powder
ENBREL®
• Prefilled syringes
available in 25 &
50 mg strengths
• 25 mg multiple-use
vials.
• 50 mg
autoinjectors,

100. 1. Rheumatoid arthritis
2. Ankylosing spondylitis
3. Juvenile idiopathic arthritis (JIA)
4. Dermatomyositis
5. Neutrophilic dermatoses: Sweet
syndrome/pyoderma
gangrenosum
6. IBD: Crohon’s disease/ulcerative
colitis
7. Behcet syndrome
8. Cutaneous lupus
erythematosus
9. Autoimmune bullous diseases
10.Lichen planus
11.Hidradenitis suppurativa,
12.Multicentric
reticulohistiocytosis
13.Relapsing polychondritis
14.GVHD
15.Sarcoidosis

101. • Etanercept should be considered the first choice for patients with
significant uncontrolled psoriatic arthritis.
• Infliximab is useful in clinical circumstances requiring rapid disease control
e.g. in unstable erythrodermic or pustular psoriasis due to it very rapid
onset of action and high response rate.

102. 1. Topical corticosteroids–other antipsoriatic treatments:  in the duration of
subsequent remission periods.
2. Calcipotriene–superpotent topical corticosteroids.
3. Calcipotriene–cyclosporine.
4. Calcipotriene–acitretin.
5. Calcipotriene–PUVA: marked  in the cumulative dose of UVA required.
6. Etanercept (25 mg subcutaneously once weekly)–acitretin has been shown to
be as effective as etanercept 25 mg subcutaneously twice weekly.
7. Phototherapy–anthralin or tar is a time-honored therapy. However, if
phototherapy is optimized by using near-erythematogenic doses, the
additive benefit of anthralin or tar above that of phototherapy alone has
not been substantiated, although remission periods following the combination
of anthralin and optimized phototherapy are prolonged.
8. Etanercept–narrowband UVB.

103. 1. Cyclosporine–acitretin: accumulation of cyclosporine, because
cyclosporine is inactivated by the cytochrome P450 system, which
is inhibited by acitretin.
2. Cyclosporine–PUVA:  occurrence of SCCs either simultaneously or
sequentially.
3. Coal tar–PUVA: may induce significant phototoxic responses.

105. • Mild (no thick plaques): Tar or ketoconazole shampoos
followed by betamethasone valerate, 1% lotion; if
refractory, clobetasol propionate, 0.05% scalp
application.
• Severe (Thick, adherent plaques): Removal of scales
from plaques before active treatment by 10-20%
salicylic acid in mineral oil, covered with a plastic cap
and left on overnight.

106. • After shedding of scales, Intermittent use of potent and
ultrapotent topical corticosteroids in combination with
calcipotriene lotion with the scalp covered with plastic
or a shower cap, left on overnight or for 6 h.
• When the thickness of the plaques is reduced,
clobetasol propionate, 0.05% lotion, can be used for
maintenance. If unsuccessful or rapid recurrence or if
associated with generalized psoriasis, consider systemic
treatment.
• Some formulations such as foams and solutions are
easier to use in the scalp than either creams or
ointments.

107. • Injection of the nail fold with intradermal triamcinolone acetonide (3
mg/mL) is effective but painful and impractical when all nails are involved.
• PUVA is somewhat effective when administered in special hand-and-foot
lighting units providing high-intensity UVA.
• Long-term systemic retinoids (acitretin, 0.5 mg/kg) are also effective, as are
systemic MTX.

108. • Initiate therapy with topical steroids but as these are atrophy-prone
regions, steroids should be applied for only limited periods of time;then
switch to topical vitamin D3 derivatives or tazarotene or topical tacrolimus
or pimecrolimus. If resistant or recurrent, consider systemic therapy.
• In these sensitive areas, tacalcitol and calcitriol tend to result in less irritation
as compared to calcipotriene; the use of ultrapotent corticosteroids should
be avoided.

109. • Treat streptococcal infection with antibiotics.
• Narrow-band UVB irradiation is the most effective. If it fails, try PUVA

110. • Patients should be hospitalized and treated in the same manner as
patients with extensive burns.
• Rapid suppression and resolution of lesions is achieved by oral retinoids
(acitretin, 50 mg/d). Supportive measures should include fluid intake, IV
antibiotics to prevent septicemia, cardiac support, temperature control,
topical lubricants, and antiseptic baths.
• Systemic steroids to be used only as rescue intervention as rapid
tachyphylaxis occurs.

111. • MTX, once-a-week schedule as outlined above.
• Infliximab or etanercept are highly effective.

113. • Combination of graded solar
exposure and the application of
mud (pelotherapy) or crude coal
tar along with a spa-like
experience.

116. • Psoriasis and psoriatic arthritis: Dr Arvind Kaul, Royal Free Hospital
• Bolognia 3rd ed
• http://dermnetnz.org
• Google images