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The opioidreceptor mu1 (OPRM1) geneencodesopioid receptors inhumans andis associatedwith
marijuana dependency. Patients with the AA genotype may be at an increased risk for developing
dependencewhencomparedtopatientswiththeGGor AGgenotypeoftheOPRM1gene(PharmGKB,
2016).
MONITORINGPATIENTRESPONSE
There are various dosage forms of cannabis; inhalation results in the fastest onset of action (5–10
minutes)andtheshortestdurationofaction(2–4hours).Thereisdifficultyinfindingthesafetherapeutic
doseforeachpatient;therefore,itisrecommendedthatprescribersstartlowandgoslowwhentitrating
toensurethatthedosegivenissafe.Itisrecommendedthatphysiciansfollowupwithpatientsevery3
monthstomonitorforanycomplicationsorrisksofabuse,diversion,ormisuse.
PATIENTEDUCATION
DrugInformation
Cannabis is a drug that affects most body systems. It produces anxiolytic, sedative, psychedelic, and
analgesicpropertiesandisalsoknowntostimulateappetiteinpatients.Althoughithasawidepanelof
effects,thesideeffectsprofileismild.
Commonadverseeffectsofcannabisincludedizziness,reddenedeyes,drymouth,dysphoria, ataxia,
sedation,changedvisualperceptions,alteredsenseoftime,andbronchitis.
ThebiggesteffectofcannabisisthepsychologicaleffectthatcomesfromTHC.THCisthecompound
thatproducesthe“high,”whichcaneaseanxietyandpainandproducethepsychedelicfeeling.Thehigh
can cause perceptual changes that may make colors seem brighter and music seem louder, and
hallucinationscanoccurwithhigherdosesofcannabis.Theeffectsofcannabisonapatient’scognitionis
similartotheeffectsofalcoholandbenzodiazepines.Itcancauseaslowingofreactiontime,defectsin
short-termmemory, motorincoordination,anda lossofattention.Patientsshouldnotoperateavehicle
whenundertheinfluenceofcannabis.
Tolerance hasbeenstudiedinpatientsand hasbeenshownto develop tothehigh as well as other
effectsthatcannabiscausesinapatient.Increaseintolerancecancausepatientstoincreasethedosage.
Cannabisusedisorder(CUD)canoccurandisdiagnosedasotherusedisorderspertheDiagnosticand
StatisticalManualofMentalDisorders,FifthEdition(DSM-5)criteria(Patel&Marwaha,2020).The
prevalence of dependence peaks in the age group of 20 to 24 and decreases with age. Withdrawal
symptoms of cannabis are similar to those of alcohol and benzodiazepine and can include insomnia,
anxiety,restlessness,andincreasedaggression.
Patient-OrientedInformationSources
Most states with approved medical marijuana programs have a Web site dedicated to providing
additionalinformationforthepatient.MajorreputablehealthWebsitesalsoincludepatientinformation
regarding medical cannabis. One such example is Americans for Safe Access (see
https://www.safeaccessnow.org/resources_for_patients).
NutritionorLifestyleChanges
Cannabisusecanleadtoincreasedappetiteandincreasedsomnolenceandfatigue.C.indicaisknownto
stimulateappetiteandpromoterelaxationandsleep.C.sativaisknowntopromoteamoreeuphoricand
upliftingexperienceandalsoincreaseenergyintheuser.Dronabinol(Marinol)isanoralformofTHC
thatisclinicallyusedforthetreatmentofanorexiaandweightlossinpatientswithHIVinfection.
CASESTUDY1
H.P.isa67-year-oldfemalewithahistoryofhypertension,highcholesterol,andchronicneuropathic
pain.
Shecurrentlytakesthefollowing:
–Atenolol50mgdaily
–Simvastatin40mgdaily
–Tramadol100mgextended-releasetwicedaily
Shereceivesdronabinol(off-labeluse)forchronicneuropathicpainatadoseof5mginthemorning
and2.5mgatlunch.
1.Whatconcernsdoyouhave?
Answer:Theconcernscenteraroundthesideeffectsofthedrug,suchasdizziness,euphoria,and
othercentralnervoussystem (CNS)effectsthatmaybecompoundedwiththeconcomitantuseof
tramadol.
2.Whatarethepotentialdruginteractions?
Answer:DronabinolisprimarilymetabolizedbytheCYP2C9and3A4systems.Theotheragents
H.P.istakingarenotextensivelymetabolizedbyeitherofthesepathways,noraretheyconsidered
inhibitors or inducers of these enzymes; thus, there is not likely a pharmacokinetic interaction.
However, as noted previously, the continued use of tramadol may promote a pharmacodynamic
interactionandcanalterthesystemconcentrationofdronabinol;cautionmustbetakenwhenused
concomitantly.However,dronabinolisnotcurrentlyconsideredaninhibitororinducerofeitherof
theseenzymesystems.
3. H.P. calls4 dayslater and tells you sheis experiencingdrymouth,dysphoria, ataxia, sedation,
changedvisualperceptions,andanalteredsenseoftime.Whatdoyoudo?
Answer:Suggestloweringthedosetoatleast2.5mgtwicedailyorpotentially2.5mgoncedaily
todecrease the adverseeffects. Also, check onhow thepain is beingmanaged.Further,inquire
about external marijuana use-has the patient been using anything in addition to the prescribed
medication,thuspotentiallyincreasingtheTHCequivalent?
CASESTUDY2
A43-year-oldfemalewithahistoryoftraumaticbraininjurysecondarytoamotorvehicleaccidentat
theageof28initiallypresentedwithpaininherneckandshoulder,rated8/10onthevisualanalogue
scale(VAS).Thepainwasalleviatedbyheatandmassageandaggravatedbyincreasedactivityand
sleep. Aregimenoflong-acting morphineandimmediaterelease (total = 160 morphineequivalents
daily)reducedherpainto4/10 ontheVAS.Tofurther reduceherpain,shewasstartedonmedical
cannabis (1:2 tetrahydrocannabinol [THC]: cannabidiol [CBD] ratio) at 2.5 mgTHC daily usinga
vapingsystem.Thisregimenfurtherreducedherpainto2/10.
1.Wouldyouconsiderweaningherofftheopioidnarcotics?Ifso,why?Ifnot,whynot?
Answer:There are pluses andminuses toweaningheroff.Weaningheroffwould decrease her
opioid burden,thusreducingthepossibilityofanopioidusedisorder.However,thepainmaybe
controlledbyacombinationofthetwoagents.Ifsheistobeweaned,closemonitoringforopioid
withdrawalandreboundpainiswarranted.Ifsheisnottobeweaned,thenmonitoringforopioid
usedisorderaswellascannabis-usedisorderisnecessary.
2.Whatconcernsdoyouhavewithkeepingthepatientonmedicalcannabis?
Answer:Medicalcannabisdoeshaveapotentialtohelptreatpatientswithchronicpain.However,
currentfederalandstatelawsmayhinderapatient'saccesstomedicalmarijuanaandusingtheU.S.
Food and Drug Administration (FDA)-approved agents off label may not be an option. State
marijuanalawsarealsoconstantlychanging,andprescribersneedtokeepupwiththemultitudeof
changes.
3.Whatwouldyoudoifthepatient'spainincreasedto4/10again?
Answer: Consider increasing the cannabis dose to 5 mg THC daily, noting the potential for
increasedsideeffects.Donotconsiderincreasingtheopioid,asthismaybemoredetrimentaltothe
patient.
Bibliography
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*Lynch, M. E., & Campbell,F. (2011). Cannabinoids for treatment of chronic noncancer pain: A systematic review of randomized trials.
BritishJournalofClinicalPharmacology,72,735–744.
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PlantScience,9,1969–1976.
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*Sativex.UKPrescribinginfo.(2010).GWPharmaLtd.https://www.medicines.org.uk/emc/product/602/smpc
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DrugandAlcoholDependence,165,181–190.
UNIT
3
PharmacotherapyforSkinDisorders
12
ContactDermatitis
JeffreyTagleandVirginiaP.Arcangelo
LearningObjectives
1. Identify the differences in the causes and the patho-physiology of contact dermatitis and atopic
dermatitis.
2.Differentiatethesymptomsofeachdiseasestatetoappropriatelydiagnoseapatient.
3.Compareavailabletreatmentoptionstotreatdermatitis.
4.Formulateatreatmentplanforapatientwhopresentswithsymptomsofdermatitis.
INTRODUCTION
Contactdermatitis(CD)isdefinedasanyskindisordercausedbyexposuretoasubstancethatelicitsan
allergic or irritant response. This inflammatoryreaction canoccur after a single exposure or multiple
exposurestoanagentorinresponsetoanallergen.AccordingtotheAmericanAcademyofDermatology,
CDisacommonproblem andresultsinapproximately5.7millionvisitstohealthcareproviderseach
year.CDisalsoprevalentinoccupationalsettingsandcanbeasignificantcauseofworkplacedisability.
CDisdividedintoirritantcontactdermatitis(ICD)andallergiccontactdermatitis(ACD).ICDismore
common, especially in the occupational setting. About 80% of cases of occupational dermatitis are
attributedtoICD.ACDisalsoprevalent,affectingabout20%ofthegeneraladultpopulation.
Atopic dermatitis (AD), also knownas eczema, is a formof allergic dermatitis characterized as a
pruritic,chronicinflammatorycondition.ADaffectsabout12%ofchildrenand7%ofadults.
CAUSES
Aspreviouslymentioned,CDoccursafterexposuretoanoffendingagent.ICDresultsfromexposureto
chemicalstimulithathasatoxiceffectontheskin.Examplesofoffendingagentsincludehandsoapand
hydrofluoric acid from chemical plants. ACD results from exposure to an antigen that causes an
immunologicresponse.AprimeexampleofACDisareactionfromexposuretopoisonivy.
ManyfactorsplayaroleinAD,includinggeneric,immunologic,andenvironmentalfactors,whichall
leadtodysfunctionalskinbarrieranddysregulationoftheimmunesystem.
PATHOPHYSIOLOGY
In ICD, exposure to the offending agent results in release of proinflammatory cytokines from the
keratinocytes.Thisleadstoskinbarrierdisruptionandepidermalcellularchanges,causingdamagetothe
water–protein–lipidmatrixoftheouterlayerofskin.
ACD is T-cell mediated and requires initial activation of the innate immune system. This reaction
occursintwophases:thesensitizationphaseandtheelicitationphase.Duringthesensitizationphase,first
contact of the antigen with the skin leads to activation of skin cells, most importantly the epidermal
Langerhanscells anddermaldendritic cells. These cells migratetolocal lymphnodes andpresentthe
antigens to naive T-cells. This leads to proliferation of contact-allergen-specific T-cells and
differentiationintoeffectorT-cells,whichfurther distributethroughouttheblood.Duringtheelicitation
phase,repeatedskinexposuretotheantigeninducesinflammation,andtheseeffectorT-cellsarerecruited
tothesiteofinflammation,whichleadstotheclinicalsymptomsofACD.
The complex pathogenesis of AD involves genetic factors, skin barrier defects, and immune
dysregulation.ThefilaggringeneisresponsibleforencodingFLG(fillagrinprotein),whichisastructural
proteininthestratumcorneum.Mutationsinthisgeneimpairskinbarrierfunction,leadingtoanincreased
risk for AD. This disruption in the epidermis and environmental triggers lead to stimulation of
keratinocytes, which release cytokines (interleukins, chemokines, and lymphopoietins), which in turn
activate dendritic and Langerhans cells. In the acute phase, these play a role in suppression of
antimicrobialpeptide (AMP)productionanditching.In thechronicstagesofAD,otherT-helper cells
releasecertaincytokinesthatresultinepidermalthickeningandabnormalkeratinocyteproliferation.
PHARMACOGENOMICS
There is ongoing research looking into gene expression and proteomics that will assist in the
identificationofbiomarkerstohelpimprovediagnosisandtreatmentofdermatitis,namelyinACDand
AD. Clinical appearance of ACD can be similar for different allergens, but the underlying immune
responses can be different.Inflammationandskin barrier–relatedgenesandproteins are differentially
regulatedinallstudies,butthechallengeistoidentifybiomarkersthatallowforthedifferentiationamong
ACD,ICD,andotherformsofdermatitis.
VariousriskfactorshavebeenidentifiedinAD,butonlyfamilyhistoryofatopyandloss-of-function
mutationsintheFLGgenehavebeenstronglyassociatedwiththedevelopmentofAD.Allergen-specific
serumimmunoglobulinE(IgE)levelsarenonspecific,sincetheyarefoundin55%oftheU.S.population
andmayalsobeelevatedinothernonatopicconditions.Thereisongoingresearchlookingintodifferent
T-lymphocyte subsets, chemokines, and cytokines as reliable biomarkers. Once novel biomarkers are
identified,thismayleadtoidentificationoftargeteddrugtherapy.
DIAGNOSTICCRITERIA
The typical symptomsofICDincludeburning,itching, stinging,soreness, and pain onpresentation.In
contrast,pruritusismorecommonlyassociatedwithACD.InbothtypesofCD,therearethreephasesof
morphologicalpatternsduringwhichthepatientmaypresent:acute,subacute,andchronic. Intheacute
phase,erythema, edema,oozing,crusting,tenderness,vesicles,orpustulesarecommon.Inthesubacute
phase,crusts,scales,andhyperpigmentationareoftenpresent.Inthechronicphase,lichenificationismost
common. Visual symptoms are mostly scattered in appearance or present on the hands or face. It is
importanttoobtaina completehistoryregardingthepatient’soccupation,hobbies, andanytopicalsor
oral medications thatthe patienttakesoruses, includingany cosmetics andjewelrythepatientwears.
Thismayhelpidentifyanypossibleallergensorirritantsthatcontributetothepatient’ssymptoms.Patch
testingisthegoldstandardtoconfirmadiagnosisofACD,wheretheallergensareplacedonthepatient’s
back and the results are interpreted after 48 to 72 hours. The local allergic reaction is graded from
negativetoextremereaction.
FeaturestypicallypresentinADincludepruritusandeczemaandarecommonlyseenatanearlyage,
although patients may develop symptoms later on in life. Dry skin (xerosis) is also fairly common.
Nonspecific symptoms include atypical vascular responses (facial pallor, delayed blanch response),
ocularchanges,andlichenification.Ininfantsandchildren,symptomsarecommonintheface,neck,and
extensorareas.Inadolescentsandadulthood,symptomsappearintheflexuralareas.
Other skin conditions, such as scabies, cutaneous T-cell lymphoma, psoriasis, immune deficiency
diseases,andphotosensitivitydermatoses,shouldbeexcludedfromthedifferentialdiagnosis.
INITIATINGDRUGTHERAPY
Themosteffectiveformoftreatmentisprevention.Oncetheallergenorirritanthasbeenidentified,the
patientmustbecomeaware ofthecausesortriggersandeitheravoidtheallergenand/orirritantoruse
appropriate skin protection. The use of personal protective equipment such as gloves, goggles, or
uniformsintheoccupationalsettingishelpful.
Coolcompressesmayofferrelieffromitching.Colloidaloatmealbaths,calaminelotion,andBurow
solution are effective for drying the vesicles and bullae that may be associated with CD. If these
treatmentsfailorifthedermatitisismoreextensive,drugtherapyisinitiated.
Beforeinitiatingdrugtherapy,deliveryofthedrugtotheskin,protection/barrierfunction,andcosmetic
acceptabilitymustbeconsidered.Ointmentandgelsofferthebestdeliveryandprotectionbarrier.Creams
arelessgreasybutlesseffective.Lotionsaredilutecreams.Solutionsarealcohol-basedliquidsandare
usefulfortreatingthescalpbecausetheydonotcoatthehair.
Lipid-richmoisturizersincreaseskinhydrationandhelpprotectthebarrierfunctionoftheskin.
Barriercreamscontainingdimethiconeorperfluoropolyethers,cottonliners,andsoftenedfabricsalso
helptoprotecttheskinfromirritants.
GoalsofDrugTherapy
Thegoalsofdrugtherapyfordermatitisareasfollows:
•Restorationofanormalepidermalbarrier
•Treatmentofinflammationofskin
•Controlofitching
Topical agentsarethemainstayofAD,althoughtheymaybe consideredfor off-label useinCDas
well.Therefore,manytherapeutic optionsforADandCDoverlap.Topicalcorticosteroids(TCSs) are
used as first-line therapy in ADand are alsoused inthetreatmentof acute and chronic CD.Topical
calcineurininhibitors(TCI),suchastacrolimusorpimecrolimus,areimmunosuppressantsandaremostly
usedforAD.Systemictherapyisrecommendedforwidespreadsymptoms,althoughitshouldnotbeused
longtermduetoadverseeffects.Antihistaminesareusedforrelievingintensepruritus.
NonpharmacologicTherapy
Moisturizersarerecommendedtopreventxerosis(dryskin)andtransepidermalwaterloss.Emollients,
occlusive agents,andhumectantsare ingredientsinmoisturizers thatprovidebenefits.Emollientshelp
lubricateandsoftentheskin,occlusiveagentspreventevaporationofwater,andhumectantsattractand
retainwater.Moisturizersshouldbehelpfulinpatientswithmilddermatitisbutshouldalsobeconsidered
as adjunct therapy in patients with moderate and severe dermatitis. They also should be used as
maintenancetherapyandtopreventflare-upsinAD.Bathingmaybehelpful,althoughnospecificbathing
practicehasbeenshowntobebeneficial.Limiteduseofneutral-lowpH,hypoallergenic,andfragrancefreecleansersisalsorecommended.Thepatientshouldbeinstructedtousemoisturizersafterbathingto
preventwaterloss.
Wet-wrap therapy (WWT) involves using a topical agent that is covered by an initial wet layer,
consistingofeithergauzeorbandages,andasecondarydrylayer.Thismayhelpincreasepenetrationof
thetopicalagentandalsoprovidesprotectiontotheskin.Phototherapycanbeconsideredasanoptionfor
treatmentinADaftertheuseofmoisturizers,TCSs,andTCIs.
TopicalCorticosteroids
TCSs act on immune cells to interfere with antigen processingand suppress the release ofcytokines,
thereby reducinginflammation.TCSs are thefirst-line topical agentsinAD andmaybe considered in
patientswithlocalizedlesionsinCD.TheymayalsobeusedtopreventflaresinAD.Patientswithmore
localizeddiseaseandfailuretorespondtoadequateskincareanduseofmoisturizersmaybenefitfrom
theadditionofTCSs.TheselectionofTCSsisgenerallybasedonage,areaofthebodythatisaffected,
patientpreferenceinthetypeofvehicle,andcost.
Dosage
TCSsareclassifiedaccordingtopotency(Table12.1),fromverylowtoveryhighpotency.Thereisno
recommended dosing strategy to use. Some practitioners utilize a short burst of high-potency TCSs,
followedbyaquicktaperinpotency.Othersutilizelow-potencyTCSstitratedupwardbasedonresponse
totherapy. Low-potencyTCSsshouldbe usedinthefacial andintertriginousregionsbecausemediumandhigh-potencycorticosteroidsappliedtothefacemaycauseatrophyofthetissueortriggersteroidal
rosacea.Higher-potencysteroidsshouldbereservedfortheextremitiesandtorso.TCSsmaybeapplied
onceortwicedailytotheaffectedareaofdermatitis.
InCD,TCSsshouldbeusedfortheshortestpossibleduration.Prolongedperiodsoftheiruseinthe
treatment of CD should be avoided. For acute flares in AD, TCSs are recommended every day until
lesions have improved. Topreventfurther flares, TCSs once or twice a week can reduce the rateof
flares.
Preparations
TCSs are available in creams, ointments, lotions, gels, solutions, or sprays. Creams are the most
desirablebecausetheyarenotasobviouswhenapplied.Theyare,however,waterbased,whichcauses
moreskindrying.Ointmentsandgelsarethemostpotentandthemostlubricating,andtheyhaveocclusive
properties.Inareaswithlargeamountsofhair or widespreaddermatitis, lotions,gels,sprayproducts,
andsolutions are easiest toapply. Occlusionbya dressingof anareaofa TCS application increases
hydrationandhencepenetration,therebyenhancingefficacy.
TABLE12.1
ClassificationofTopicalCorticosteroidsbyPotency
c,cream;f,foam;g,geI;I,Iotion;o,ointment;s,soIution.
Usedwithpermissionfrom“GuideIinesofcareforthemanagementofatopicdermatitis;Managementandtreatmentofatopicdermatitiswith
topicaltherapies,”byEichenfield,L.F.,Tom,W.L.,Berger,T.G.,etaI.(2014a).JournaloftheAmericanAcademyofDermatology,71(1),
116–132.Copyright2014byElsevierInc.
Application
ThereisnostandardamountofTCSthatshouldbeapplied,buttheamountshouldbeindividualizedtothe
patient.Ingeneral,anamountequaltothelengthfrom thefingertiptothedistal interphalangealjointis
sufficient. Penetration ofa TCS is enhanced when the skinis hydrated. This canbeaccomplished by
moisteningtheskinbeforeapplicationorbyusinganocclusivedressingconstructedfromamaterialsuch
as a plastic shower cap (for the scalp), gloves (for hands), or a plastic wrap or a sock (on other
extremities).
AdverseEvents
TCSsaregenerallysaferthansystemiccorticosteroids,althoughsomeadverseeventsmayoccur.Adverse
effectsontheskinincludepurpura,telangiectasia,striae,focalhypertrichosis,androsacea-likeeffects.
Skinatrophycanoccurinolderpatients,throughuseofTCSsonthinskinoruseofhigher-potencyTCSs.
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