Retinoids in dermatology seminar

DR.AARYA.S
MODERATOR-DR .JAYASHREE NAYAK
RETINOIDS IN DERMATOLOGY

DISCUSSIONS
• HISTORY
• STRUCTURE
• NATURAL RETINOIDS AND CAROTENOIDS
• MECHANISM OF ACTION
• CLASSIFICATION
• EFFECT OF RETINOIDS ON HUMAN BODY
• INDIVIDUAL DRUGS
• SIDE EFFECTS,DRUG INTERACTION
• NEWER RETINOIDS

RETINOIDS
• All synthetic and natural compounds that have
biological activity similar to Vitamin A.

HISTORY
• First dermatological use 1943 by Straumford for
acne vulgaris
• 1962Stuttgen –Therapeutic effectiveness of topical
tretinoin for keratinisation disorders.
• 1969Kligman and colleguestopical tretinoin for
Acne vulgaris.
• 1955Isotretinoin first synthesised in Europefirst
used for disorder of keratinisationacne vulgaris.
• 1982FDA approved isotretinoin for severe
nodulocystic acne

• 1972Bollag discovered etretinate and Acitretin
• 1986 Etretinate used for PSORIASIS
• 1988Etretinate phased out ,replaced by
ACITRTETIN.
• 1999Bexarotene approved for CTCL
• 1999Alitretinoin approved for KAPOSI SARCOMA

STRUCTURE
Cyclohex
enyl Ring
Conjugat
ed Side
Chain
Polar
Terminal
Group

 All classes of Retinoids : basic sructure of Vit A with
modifications
1st gen. Retinoids 2nd gen. Retinoids 3rd gen
Retinoids
Change of Polar end
group & polyene
side chain
Replacing cyclic end group of
Vit A with subsituted & non
subsituted ring systems.
Cyclization of
polyene side chain.

NATURAL RETINOIDS
 Daily requirement: 0.8-1mg/ 2400-3000IU
 FUNCTIONS :
Retinal(as 11-cis &11-trans isomer) : in Visual
function
Retinol : in Reproduction
Retinoic acid : in Epithelial differentiation &
normal growth

CAROTENOIDS
 Organic pigments : Naturally occurring in chlorophyll &
chromoplast of plants .
 They are not biologically active until converted to one of
the retinoids in the body .
 1 mol. Of β carotenes = 2 mol. of retinal.
 Found in vegetables and fruits.
 Ex : Carotene α, Carotene β, Lutein, Lycopene,
Zeaxanthin

ABSORBTION AND DISTRIBUTION
• BA fatty foodmax Acitretin and Bexarotene
• Serum transporter albumin .
• Storge ito cells hepatocytes
• Cytosolic transporter CRABP1Modulates level of
RA in tissues.
• CRABP 2 Human epidermisepidermal
differentiation.
• RA predominantly all trans RA (ATRA)

ISOTRTINOIN and ACITRETIN water soluble,less deposition
ETRETINATE -LIPOPHILIC

• 1. Isotretinoin
•
oxidation
4 oxo isotretinoin
2. Etretinate
Hydrolysis
Acitretin
Isomerization
Cis isomer
• β-glucoronide derivatives (13 trans and 13 cis acitretin)
Demethoxylation

RETINOID RECEPTORS
 Belongs to Steroid thyroid hormone receptor
superfamily
 Exists as α, β, γ types
 Human skin mainly contains RXRγ & RARα

BASIC PRINCIPLES: RETINOID
RECEPTORS
RARs and RXRs are ligand-dependent transcription factors
that regulate gene expression in two ways:
 Upregulate expression of genes by binding to RARE
located in the promoter region of target genes
 Downregulate expression of transcription factors
such as AP1.

 Non-Aromatic Retinoids
Tretinoin (all-trans retinoic acid)
Isotretinoin (13-cis retinoic acid)
Alitretinoin (9-cis retinoic acid)
All-trans Retinoyl B-glucornide
Fenretinide
Ist GENERATION

 Monoaromatic Retinoids
Etretinate
Acitretin
Motretinide
2nd GENERATION

• POLYAROMATIC RETINOIDS
BEXAROTENE
TAZOROTENE
TAMIBAROTENE(Am-80)
AROTINOID SULFONES
Adapalene:- naphtoic acid derivative have properties of
retinoids,not in 3 generations
3rd GENERATIONS

Newer retinoids
• Seletinoid –G :-4th generation
• Arotinoids
The effects of a novel synthetic retinoid, seletinoid G, on the
expression of extracellular matrix proteins in aged human skin
in vivo,2005

1.Epithelial differentiation
2.Sebolytic
3.Synthesis of dermal matrix
4.Anti inflammatory
5.Angiogenesis
6.Immunomodulation
7.Melanotrophism
8.Morphogenesis

EFFECTS ON EPIDERMAL GROWTH AND
DIFFERENTIATION
• Modulate the growth and differentiation.
• Have actions on cultured keratinocytes and invivo
human skin.
• Promote cell proliferation in normal epidermis
• Normalisation of hyperkeratotic skin.
• TGF –α,EGF,c AMP mediated cell growth,TGF-β2
mediated cell growth.

• Reduction of tonofilaments, corneocyte
cohesiveness,impaired function of the permeability
barrier, TEWL
NORMALISE HYPERPROLIFERATIVE EPIDERMIS,DESQUAMATION AND
PEELING

EFFECTS ON SEBACEOUS GLANDS
• ISO>>ACI>ETRETINATE
• Reduce gland size by 90% decr proliferation of
sebocytes and suppressing sebum production.
• Oral isodecr TAG , free sterols and ceramide in
sebum.
• 80% in local DHT pdn and 2x androgen binding
capacity
• Mechanism unknown-not receptor mediated.

IMMUNOMODULATORY AND ANTI INFLAMMATORY
• Inhibits Proinflammatory cytokines and enzymes of
Phagocytosis
• ￪ cell surface antigens of T cells and NK cells
• Inhibition of Transcription factor AP-1
• ￬ Neutrophil migration, leukotriene B4 mediated
chemotaxis, NO, TNFα levels
• Psoriasis : ￪ IL6, IL8, ICAM1

ANTI PSORIATIC ACTION
• Reduce the proliferation rate by downregulating the
no of cycling cells
• Promote terminal differentiation and filaggrin
synthesis
• Regulate desquamation of corneocytenormalise
TG Levels.
• Modulation of lymphocyte functions and inhibition
of neutrophilic migration.
• Effects seen over 6-12 weeks

ANTI TUMOR EFFECTS
• Retinoid induced apoptosis :
• Regulation of expression of apoptosis linked gene
products: BCL-2, tissue transglutaminase
• Activation of tumour suppressor genes, viz. p21,
p38, p53
• ￪ Caspase proteolytic activity
• Inhibition of AP-1
• SPHINGOMYELINcontrol proli n differentiation
• intracellular ceramideinhibit
proliferation,induction of differentiation and
apoptosis

EFFECTS ON INTERCELLULAR MATRIX COMPONENTS
• Physiological conc : promote wound healing
• ￪ MPS, collagen, fibronectin & GAG, ￬ collagenase
• Supraphysiologic conc: inhibit wound healing
• ￬ fibroblast prolif, ￬ collagen 1 & 3, ￬ GAG

EFFECTS ON EMBRYONIC DEVELOPMENT
• Vit A & retinoids needed for formation of face, heart,
eye, limb & nervous system
• All RAR agonists – strong teratogens
• All RXR agonists – low to absent teratogenic
response
• Retinoids not binding to RAR/RXR – likely non
teratogenic

CLINICAL USES –TOPICAL
FDA APPROVED TOPICAL RETINOIDS
ALL TRANS RETINOIC ACIDAcne vulgaris,fine
rytids,mottled pigmentation,tactile roughness of facial skin
ADAPALENEAcne vulgaris
TAZOROTENEAcne vulgaris,Psoriasis (<20%)
ALITRETINOINAIDS related kaposi sarcoma
BEXAROTENECTCL (Stage 1A & 1B)

CLINICAL USES –ORAL RETINOIDS

OTHER USES-NON FDA
FOLLICULAR DISORDERS
1.Acne related conditionGram neg
follicuitis,HIV associated eosinophilic
folliculitis,Acne with solid facial edema
2.rosacea papulopustular,granulomatous
3.HIDRADENITIS SUPPURATIVA
4.DISSECTING CELLULITIS OF SCALP

CHEMOPREVENTION OF MALIGNANCY
1. Organ transplantation
2. Syn with risk of cutaneous malignancy
a) Bazex syndrome
b) Nevoid BCC
c) Kaposi sarcoma
d) Frequent BCC/SCC

DISORDERS OF
KERATINISATION
1. DARIER’S DISEASE
2.ICHTHYOSIS SPECTRUM
3.PRP
4.KERATODERMA
INFLAMMATORY
DERMATOSIS
1. SLE
2.LP-ORAL
EROSIVE,PALMOPLANTAR
3.LSEA

TRETINOIN
• ALL TRANS RETINOIC ACID
• 1st retinoid introduced in clinical use.
• MOA:-Gene transcription affects growth and
differentiation of cells
• Decreasing cohesiveness of follicular corneocyte.
• Effects :-Comedolysis
• Palliative effects on fine wrinkling,Mottled
hyperpigmentation

• Available topically as 0.01% to 0.1% cream,gel,solutn
• New microsphere formation in 0.1% and 0.04%
• 4*more potent,less irritation,better tolerated
• Enhance efficacy by target delivery system
• Preg C

ACNE SKIN
• ACTIONS->
1. Inhibit abn proli of keratinocyte
2. Decr infl lesions
3. Improve differentiation
4. Inhibit TLR-2anti infl
5. No direct role on sebum /P.acne
Aerobic environmentnon compatable to P.acne
First line non-infl acne
Not used in severe nodular acne vulgaris

Photodamaged skin
• Inc Basal and granular layer thickness
• melanocytic activity, dispersion of melanin
• glycosaminoglycan secretion into intracellular space.
• synthesis of collagen and elastin
• comedolysis

1. Smoothness of skin(4-6
weeks)
2. Lightening of
hyperpigmentation(8-16
wk)
3. Diminished fine
wrinkle(16 wk)

• FDA approved 2 topical retinoidtretinoin 0.05%
&0.02%, tazorotene 0.1% cream
• Photolabile, bedtime
• S/Eskin irritation,erythema and peeling,RETINOID
DERMATITIS
• Avoid astringents,harsh soaps,irritating agents
traumatise epidermis
• Antiaging creamfine wrinkles
• +hyaluronic acid+GA
Rx wrinkles &scarring

ISOTRETINOIN
• 13-cis-retinoic acid
• No affinity for RAR/RXR
• First retinoid for systemic use
• Initially evaluated for ichthyotic disorder,later very
effective in nodulocystic acne.

 Best agent for acne vulgaris : targets all pathogenic factors of acne
 Rapid and early improvement in the inflammatory lesions (pustules)
 Closed comedonal acne & microcystic acne are less responsive

IMPORTANT INDICATIONS
1. Nodulocystic acne
2. Inflammatory acne with scarring
3. Acne with psychological distress
4. Gram negative folliculitis
5. Pyoderma faciale
6. Severe rosacea
7. Hidradenitis suppurativa and dissecting cellulitis of
the scalp
8. Darier’s disease
9. PRP,LE,LP

STANDARD DOSING
• 1mg/kg/day for 4-5 months.
• Start with 0.5mg/kg/day gradually to 1mg/kg for 4-5
months.
• Total cumulative dose120mg-150mg/kg
• Acne fulminans0.5-1mg/kg/day with prednisolone.
• Rosacea10mg/dayRx
telengiectasia,erythema,papules and pustules
• Hidradenitis suppurativa1-2mg/kg/day
• DSOSIso+rifamp more effective

• Lichen planuswidespread,hypertrophic or oral
erosive LPIso+low dose CS

High dose Isotretinoin in acne vulgaris:Improved
treatment outcomes and quality of life
 80 participants
 Three year study period

Isotretinoin therapy for acne: Results of a multicentre dose response
study
John S,Ronald P JAAD 10:490-496,1984
• 150 patients nodulocystic acne
• Double blinded study with 0.1,0.5,1mg/kg/day
• Comparing clinical response,s/e,lab abnormalities and
duration of induced remission.
• Results no significant difference in the clinical response
between dosages.
• 42% patients with 0.1mg/kg/dayrelapse.
• 10% relapsed in 1mg/kg/day

• Minor effects in s/e and lab abnormalities
• CONCLUSIONHIGHER DOSES ARE INDICATED

 To compare the efficacy and tolerability
 Daily,alternate,pulse,low dose regime
 120 patients
 30 group each
 1mg/kg/day,A/D,1mg/kg/day*1week/4week,20
mg A/D 16 weeks and follow up 8 weeks.
 Conventional dose for 8 weeks and maintain
with low dose-nodulocystic acne

Key points
• Max sebosuppression
• Alter VEGF incidence of pyogenic granuloma
• Failure on microcystic acne and closed comedones
• Total cumulative dose 120mg/kg150mg/kg with no
better benefit

ACITRETIN
• Acid metabolite of etretinate.
• Retinoids as monotherapy in psoriasis
• Effects thickness,scaling,itching
• Initial effects4-6 weeks
• Full effects3-4 months
• Maintenance dose z needed
• Re –esterification
• Contraception 2 years in Europe and 3 years in USA

STANDARD DOSING
• PSORIASIS
CHRONIC PLAQUE POSORIASIS 0.3-1 mg/kg/day for 4-12 weeks
Combination with
PUVA/NBUVB
25mg stat 2 weeks prior to the therapy.
0.3-0.5mg/kg/day for 6 weeks.
If pt on stable dose of UV,reduce by 30-70%
7days after acitretin therapy
Erythrodermic psoriasis Start with 0.3mg/kg/day ,inc to 0.5-
0.6mg/kg/day for 3 months.maintenance to
6 months
Pustular psoriasis Start with 1mg/kg/day,dec to 0.5-
0.6mg/kg/day for 3-6 months,maintenance
to 6-12 months

• Not combined with MTX/Ciclosporin
• Sequential therapy z preferred
• Combination therapytopical/PUVA/NBUVB
Preferred

PRECAUTIONS ON ACITRETIN
• NOT donate blood for 1 year after stoppage
• Not recommed in childrenbone changes
• Effects of UV radiation enhanced,avoid excessive
exposure to sunlight
• Refrain from waxingskin fragility
• Greater insulin sensitivityinduce hypoglycaemia on
OHA.Serum BS should check
• Avoid excess intake of vit A

Keratinisation disorders
• Lamellar ichthyosisgood
• BCIE,CIEModerate
• Rapid response,long term treatment
• Low dose in BCIE,Darier’s prevent relapses
• <1mg/kg/day preferrable
OthersPRP,chemoprevention of non-melanoma skin
cancer in solid organ transplant receipients

BEXAROTENE
• Modulation of RXR receptors
• apoptosis through redn of anti-apoptotic
protein,activates capsase 3
• effects;induces tumor regression by PPAR
Incre cellular differentiation and decreased cellular
growth
• Inhibit G1,G2,M phase of cell cycle
• 99%plasma bound,mets by CYP450.
• Central hypothyroidism

• Sun protection ,preg X
• FDAEarly stage I A&I B persistant or refractory
CTCL.
• Dose300mg/m2
• Application A/D
*1wkOD*1wkbd*1wktidqid*1wk
• Response early as 4 week
• Relapse rate 28%
• Effective in lymphamatoid papulosis,chronic severe
hand dermatitis,psoriasis,Alopecia
• S/Esite reaction,rash,pruritis,icd,pain
• fre of appl /+steroid.
• Unlike other retinoids, very little renal elimination –
extreme caution in liver insuff.

TAZOROTENE
• Prodrugtazorotenic acid
• High affinity RAR gammaregulate cell pro n diff
• inflammation and proliferation throu AP-1 in
psoriasis
• Highest cutaneous conc,rapidly metabolised
• T1/2 <20 min
• Preg X
• USES1st topical approved in C/C Psoriasis
• Photo damaged skinclinical and histological
improvement

• USES1st topical approved in C/C Psoriasis
as mono/combination therapy1st line.
• Photo damaged skinclinical and histological
improvement
• Early stage of CTCL
• Genodermatosis (LI,EKV)
• Doses 0.05% and 0.1%

ALITRETINOIN
• Naturally occuring
• Binds to all retinoid receptor
• Down regulate IL-6,alter the expression of oncogen
• Dose0.1% gel.
• FDAAIDS related kaposi sarcoma
• Other usesnon AIDS Kaposi
sarcoma,photoaging,hand dermatitis.
• Preg D
• Expensive,long term Rx

ADAPALENE
• Derivative of napthoic acid
• Affinity to RAR
• More stable,less photoliable,more lipophilic
• Not binding to CRABP I and II
• Less systemic exposure
• Anti inflammatory action LT,PG,Anti AP-1 action
• Immunomodulatory action TLR-2,Cytokine
inhibition

• Comedolysis, microcomedone formation
• Not carcinogenic,mutagenic
• Not teratogenic,genotoxic
• More photostable
• Used for acne,hyperpigmentation,AK,Photoaging
• S/Eerythema, scaling
• Available in 0.1%gel,cream

SERIOUS ADVERSE EFFECTS
I)TERATOGENICITY
• Retinoic acid embryopathy
• Spontaneous abortion
• IPLEDGE
• PREGNANCY CAT X

EXTERNAL ABNORMALITIES
• AUDITORY ABNORMALITIES
Microtia
Absent auditory canals
Conductive hearing loss
Sensorineural hearing loss
Vestibular dysfunction
• OCULAR ABNORMALITIES
Micropthalmia
Optic nerve atrophy

Agenesis of
Cerebellar
Vermis
Abnormal
Cortical Tracts
CNS
ABNORMALI
TIES

INTERNAL ABNORMALITIES
• CVS Abnormalities
• CNS abnormalities
• Parathyroid hypoplasia
• Thymic hypoplasia
• BONE abnormalities

 CARDIOVASCULAR ABNORMALITIES
ASD
VSD
Hypoplastic or
Interrupted Aortic
Arch
Septum

• BONE ABNORMALITIES
Absent clavicle and scapula
Aplasia/hypoplasia of long bones
Short sternum
Sternoumbilical raphe
Absent thumb
• OTHER ABNORMALITIES
Thymic aplasia or hypoplasia
Anal and vaginal atresia

• Lipids
Hypercholestrelemia
hyperTAG
GIT

• OCCULAR
Persistent dry eyes
 night vision
Staph aureus infection
• Endocrine effects
Hypothyroidism
DM
• HEMATOLOGIC
Leukopenia,agranulocytosis
• Neurologic
Pseudotumor cerebri
depression

• hepatic
Transaminases,toxic hepatitis

Bone changes
DISH
Osteophyte formation
Premature epiphyseal closure
Osteoporotic changes
osteophyte

MC MINOR SIDE EFFECTS
• CUTANEOUS

• NASAL
Nasal mucosa dryness, dec mucus secretion,epistaxis
• Msk
Myalgia
Tendinitis
Arthralgia and fatigue

Uses and complications of Isotretinoin therapy.
Charles N Ellis,Kent J krach J Am Acad Dermatol
2001
• Mucocutaneous side effects
• Cheilitis90-100%
• Hair fall20%
• Dry eyes33%
• Spontaneous abortion15%
• Teratogenicity 25%
• Myalgia15%
• transaminases15%(normal within 2-4 wks)
• Photosensitivity 1-5%

VITAMIN E(alpha –tocopherol),800IU daily,may reduce retinoid toxicity.
Lebowohl M,J Am Acad Dermatol 1999;41:260

Concomitant administration of vitamen E does not change the
side effects of isotretinoin as used in acne vulgaris: a random-
ized trial.
Strauss JS, Gottlieb AB, Jones T et al
J Am Acad Dermatol 2000;43:777-84
• Strauss et al, however, found that vitamin E at
dose 800 IU/d provided no significant improvement
when used in acne patients on isotretinoin.

Isotretinoin & Depression : A controversy

Jacobs DG, Deutsch NL, Brewer M. Suicide, depression and
isotretinoin is there a causal link?
J Am Acad Dermatol 2001;45:S168-75.
• Systematic review article 19 articles
• found no biologic basis for depression and
isotretinoin usage.
• further stated that no evidence for a causal
connection existed between isotretinoin and
depression or suicide.
• the authors do recommend the physician monitor for
signs of these symptoms.

Jick SS, Kremers HM, Vasilakis-Scaramozza C. Isotretinoin use and
risk of depression, psychotic symptoms, suicide, and attempted
suicide. Arch Dermatol 2000;136:1231-6
• Cohort study
• found no significant difference in depression or
suicide rates between patients that took oral
antibiotics and patients that took isotretinoin for
acne

An analysis of reports of depression and suicide in patients treated with isotretinoin.
Wysowski DK, Pitts M, Beitz J. J Am Acad Dermatol 2001;45:515-9
• found in an analysis of depression,suicide or suicidal
thoughts a temporal association between depression
by positive de-challenges (improvement upon
medication stoppage), and positive re-challenges
(recurrence of symptoms on re-starting) with
isotretinoin.
• The study called for further research to establish a
causal relationship and to elucidate a possible
synergistic interaction between individuals
predisposed to depression and isotretinoin usage.

Isotretinointreatment for acne and risk of depression: A systematic reviewandmeta-
analysis
Yu-Chen Huang, MD, Ying-Chih Cheng, MD,J Am Acad Dermatol july 2017,volume
76
• A systematic review and meta-analysis of the literature
published from inception to September 30, 2016, was
conducted.
• change in depression scores from baseline was not
significantly different between patients receiving
isotretinoin treatment and those receiving an alternative
treatment (95% confidence interval [CI] −0.680 to 0.011).
•

• The prevalence of depression after isotretinoin
treatment significantly declined (relative risk [RR] 0.588,
95% CI 0.382–0.904).
• The mean depression scores significantly decreased from
baseline (SMD −0.335, 95% CI −0.498 to −0.172).
• Conclusions:
Isotretinoin treatment for acne does not appear to be
associated with an increased risk for depression.
The treatment of acne appears to ameliorate depressive
symptoms.

BAD GUIDELINES 2010 FOR ISO & ACITRETIN
Clinical
LAB
 SERUM PREGNANCY
TEST
 CBC
 LFT
 RFT
 FLP
 URE
 RBS
Before the treatment and every
2-4 weeks for 2 months,then
every 3months

BAD GUIDELINES 2010 FOR ISO & ACITRETIN
• Special tests
X-ray of wrist,ankles,thoracic spine(long term
therapy)
All symptomatic joint should be evaluated
Ophthal examination

BEXAROTENE
• Free T3,T4 and TSH and FLP
• Highest TAGStatin or fenofibrate prior Rx.
• >300-500mg/dllife style n diet
• >500-800mg/dl dose/add a LLA,freq monitoring
• >800-1000mgdldrug discontinue(pancreatitis)
• Ophthal
• Follow up
• Every 2 weeks*1-2 months
• Monthly *next 3 months
• Every 2-3 months

GUIDELINESS FOR PREGNANCY
MONITORING
• 2 Urine/serum preg test
• One 2 weeks before of initiation of isotretinoin
• 2nd during first 5 days of the menstruation/11 days
after the last act of unprotected sexual intercourse.
• Each month –ve UPT
• Therapy start on 2nd or 3rd day of next cycle
• 2 forms of contraception for atleast 1 month
prior,during and 3 years after discontinuation.
• Written consent

DRUG INTERACTION
• Drug
Increase the level(toxicity)
 VIT A
 Tetracyclin,doxycyclin,mi
nocyclin
 Gemfibrozil
 Macrolides,Azoles
Decrease the retinoid
 ATT
 Anticonvulsantph
enytoin,pheno,carb
amazepine

• RETINOIDS
INCRESES THE
DRUG
CICLOSPORIN
CORTICOSTEROID
DECREASES ANTI
OVULATORY
EFFECTS OF MINI
PILLS
ACITRETINMTx hepatotoxicity.
ALCOHOLRE -ESTERIFICATION

INVESTIGATIONAL RETINOIDS
 LGD -1069
RXR panagonist,in clinical trial
 TAMIBAROTENE
Topical antipsoriatic agent
 CD 437
Induction of apoptosiscutaneous carcinoma
 MOFAROTENE
Used in chemotherapy
Augment activity of Doxorubicin,5FU,IL

• AROTINOID SULPHONES
• Used in AK
• Do not bind RAR.
LESS SIDE EFFECTS ,MORE EFFICACY

TAKE HOME MESSAGE
• Retinoids are biologically and structurally related to
VIT A
• TretinoinMultifunctional from acne to
pigmentation to photodamaging.
• Adapalenesimilar efficacy with less side effects
and photostable.
• Isotretinoinhighly effective in nodulocystic acne
;max sebosuppression.long term for severe and
resistant acne

• Acitretinbest in keratinisation disorder.
long term use
recurrence after discontinuation
contraception from 2-3 years.
• Etretinate best for psoriasis
• phased out due to side effects.
• Bexaroteneeffective for early stages of CTCL.
Max s/ecareful monitoring
hypothyroidism
• Investigational retinoidslesser side effects

Retinoids in dermatology seminar

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