INTRODUCTION AND EPIDEMIOLOGY

The American Pet Products Association (APPA) estimates that approximately 70% of Americans keep pets in their household, equating to 90.5 million homes. Dogs and cats are the most popular and live in around 69.0 and 45.3 million United States (U.S.) households, respectively, followed by 11.8 million households for freshwater fish, 9.9 million households for birds, and 3.5 million households for horses.¹ Public, residential, leisure, and specific occupational environments (e.g., farms, laboratories, pet shops) have high concentrations of pet allergens because of the high prevalence of community pet-keeping and Americans’ tendency to live indoors. Allergic reactions to pets have been recognized for at least 100 years.² Risk factors for developing asthma and rhinitis include allergies to furry animals, especially cats and dogs.³ Direct or second-hand pet exposure increases the likelihood of exacerbating disease in pet-sensitive people. However, evidence also shows that early childhood exposure to dogs or cats before one year of age may have protective effects in preventing allergic sensitization.⁴

Notably, allergies to unusual or exotic pets have increased over the last decade.⁵ In many urban areas, apartment complexes prevent owning large pets or charge a fee for owning cats and dogs, leading to the choice of smaller, more unusual animals. Some examples of uncommon pets are rodents (mice, rats [which allegedly make very good pets], guinea pigs, and other mammals like ferrets, pigs), amphibians (axolotl [a Mexican salamander], dart frogs, and fire belly newts), and reptiles (snakes).⁶ The allergic signs and symptoms or diseases associated with uncommon pets are like those manifested in cat and dog allergies. In addition, patients may present with respiratory symptoms induced by bird allergens and gastrointestinal symptoms after consuming bird eggs; this is called a bird-egg syndrome.⁷

Overall, the incidence of specific allergy to exotic or uncommon pets is unknown because literature only includes isolated cases or small series. In the U.S., an estimated 15% to 30% of people are allergic to their pets.⁸ Among people with pet allergies, a fraction is sensitized to more than one animal. Moreover, according to the Asthma and Allergy Foundation of America, cat allergies are reported twice as often as dog allergies. Animals are also recognized as the third leading cause of allergic asthma, after mites and pollens.⁸ Many people adopt ferrets or rabbits, believing they are hypoallergenic. They are not, and pharmacy staff should be aware of that fact.^9,10 The most frequent allergic reactions result from inhalation, contact, or bites.

This continuing education activity summarizes knowledge of pet allergens, including those from uncommon pets; the allergy reaction mechanism and its signs and symptoms; current advances in diagnosis and treatment methods such as immunotherapy; and recommendations for patient education and counseling.

PAUSE AND PONDER: When patients ask about medication for pet allergies, what kinds of questions should you ask?

PET ALLERGENS

Allergy Mechanisms

Compared with other conditions’ mechanisms, allergy mechanisms are simple and encompass three specific paths: allergic sensitization, allergy, and cross-reactivity.¹¹

• Allergic sensitization is the presence of immunoglobulin E (IgE) antibodies to an allergen.
• Allergy is the occurrence of reproducible symptoms or signs initiated by exposure to a defined stimulus at a dose tolerated by nonallergic persons and mediated by specific immunologic mechanisms. If no symptoms develop, a person could be sensitizing to a particular allergen but not be allergic.
• Cross-reactivity is the process of IgE antibodies (originally developed against a given allergen) binding to homologous molecules originating from a different allergen source.

Characterizing Pet Allergens

Allergies to pets are common. Pet allergy is an allergic reaction to proteins (allergens) found in animals’ skin cells (dander), saliva, urine, or sweat on their fur.⁵ Allergens within the same protein family can cause cross-reactivity. Most allergens are spread via airborne particles. Dander contains allergens formed in sebaceous gland secretions and saliva. Secretions containing allergens adhere to the hair and stratum corneum of the skin. When an animal sheds, tiny particles disperse into the air and remain buoyant for an extended period of time. After the particles slowly settle onto the floor, furniture, or other items, they can be easily re-dispersed into the air. As a result, pet-sensitive people could experience allergy symptoms in the nose, eyes, and respiratory tract even if the pet is not present.⁵ Additionally, people can carry pet allergens that settled onto their clothing or hair.

For cats and dogs, the primary allergen sources are dander and saliva. Similarly, the primary allergen source in rabbits is saliva. In contrast, the primary allergen source is urine in rodents (mice and rats) and Mustelidae (ferrets and minks).

Rodents are an interesting case study. Most research laboratories experience a very high rate of staff turnover because lab workers develop allergies to rodents. Children who are exposed to rodent urine can develop this allergy, too. Male rodents produce a larger quantity of and more condensed urine than female rodents. This explains why people who commonly come in contact with male rodents are more likely to develop allergic symptoms. Allergy to rodents acts as an occupational hazard for researchers. Mouse urine is the most concentrated of all urines—far more concentrated than any other species.¹² One study showed that 30% of people exposed to mice and 13.7% of people exposed to rats suffered from allergy symptoms.¹² Symptoms range from conjunctivitis to asthma to skin reactions, which makes working with these animals difficult.

Most animal allergens belong to one of three primary protein families. Within the three families, lipocalin-like proteins and the serum albumin family are the two most widely studied. Other identified allergens are considered minor, including gelatins, immunoglobulins, and transferrins presented in secretions and dandruff. Knowledge of these allergens’ allergenicity and cross-activity is essential to improve treatment and prevent allergic reactions. Table 1 summarizes partially characterized pet allergens, including those generated by exotic pets, because not all allergens are fully characterized.⁵

Table 1. Summary of Characterized Pet Allergens^13-22

Lipocalin Superfamily

More than 50% of allergens identified from furry animals belong to the lipocalin superfamily and are found in animal dander, saliva, and urine.²³ Lipocalins are large proteins and can induce IgE production in a large proportion of atopic individuals (people who have enhanced immune response to common allergens) who are exposed to the allergen source.²⁴

Serum Albumin Family

Serum albumin is a globular protein prone to participation in IgE-mediated cross-reactions.²⁴ Serum albumin is commonly found in pet dander and saliva and causes an allergic reaction by inhalation and ingestion.

Secretoglobin Superfamily

Secretoglobins are the most potent allergens in cats (e.g., Fel d 1) and other pets (e.g., rabbit; Ory c 3). Produced by the skin, salivary and lacrimal glands, these proteins have an unknown function. Dried saliva and dandruff are spread as airborne particles and cause sensitization in susceptible people.²⁵

SIGNS AND SYMPTOMS OF PET ALLERGIES

The most frequently observed pet allergies result from inhalation, contact, and bites. The main allergic symptoms are similar across both common and uncommon pet types. They present as rhinitis, conjunctivitis, urticaria (red, itchy welts that result from a skin reaction), and lower and upper respiratory symptoms, which can be mild to severe and rarely cause anaphylactic shock.⁵

Hypoallergenic Pets

“Hypoallergenic” is defined as possessing decreased risk of causing an allergy in people, which means that hypoallergenic animals could still elicit allergies in humans.⁹ To make hypoallergenic animals, breeders or researchers combine breeds that produce less allergen (in dogs, breeders use breeds that shed less than other breeds, or have hair rather than fur). However, animals often have different mechanisms of allergenicity, so infrequent shedding does not solve all allergy problems.

In a dog allergen study, homes that included hypoallergenic dogs had no statistically significant difference in dog allergen levels compared to homes that included non-hypoallergenic dogs. The common allergen in dogs, Can f 1, was reported at similar levels in all groups.²⁵ The frequency of shedding varies in different dog breeds, but all dogs can elicit allergies in humans.

The main allergen in cats, Fel d 1 protein, comes from their saliva and sweat glands. Because of its small size and adhesiveness, Fel d 1 floats around and sticks to everything, making it almost impossible to remove physically. In fact, Fel d 1 measures in at less than one-tenth the size of ribosome; it’s so small, it easily navigates its way deep into the lungs and can precipitate asthma.²⁶ For this reason, making a completely hypoallergenic cat has proven impossible, however vaccines to decrease the production of Fel d 1 protein have been studied; one vaccine is a combination of recombinant Fel d 1, tetanus toxoid protein, and a snippet of the coat of a plant virus.²⁷ Researchers are unsure as to the purpose of Fel d 1 in cats or why levels of Fel d 1 vary.

Ferrets—which are related to otters, minks, and weasels—are considered hypoallergenic because they are less likely to cause an allergic reaction compared to other animals. However, they can still provoke allergies in people. Allergies to ferrets come from their hair, saliva, and urine. Ferret hair and saliva is usually easy to control because they shed infrequently and do not lick people like dogs and cats often do. However, urine is harder to control and can cause allergies when owners clean crates.⁹

Rabbits produce allergens through dander, hair from shedding, and saliva. They tend to shed more often than ferrets, around every three months, so keeping up with cleaning may be difficult. Rabbit hair isn’t naturally allergenic, but when rabbits lick their fur, they transfer a saliva protein that is contaminated with the protein allergen.¹⁰

DIAGNOSIS

Skin Prick Test

Allergists (allergy specialists) use skin prick tests together with medical history and physical examinations to rule out or confirm a suspected IgE-mediated animal allergy.²⁸ Manufacturers prepare skin prick tests by extracting natural allergens from animal hair, dander, and urine. The doctor or nurse will prick the patient’s skin on the forearm or upper back and determine if an allergic reaction occurs within 15 minutes. If a patient develops a red, itchy bump where the pet allergen extract is pricked into the skin, the patient is allergic to that pet allergen. Diagnosticians should first use a skin prick test as it is inexpensive, easy to use, and quick to perform. However, allergen concentrations and components are inconsistent, varying among similar commercial tests from different manufacturers. Healthcare providers should be aware that patients’ test results may be inconsistent if they use different skin prick tests at different times.²⁸

Serum-specific IgE Test

Allergists can use a serum-specific IgE (blood) test when patients’ symptoms and skin test results are contradictory or when patients’ skin conditions prevent a skin test. Serum-specific IgE tests can only determine if a patient is sensitized to a specific pet allergen, but it cannot determine if a patient is allergic to that allergen. Serum-specific IgE tests are highly sensitive, but prone to false-positive results. From this perspective, serum-specific IgE tests may be less accurate than skin prick tests.²⁹

Molecular Diagnosis

Recent scientific advances have allowed molecular diagnosis to differentiate patients who are allergic to a single species or sensitized due to cross-reactivity. This method can aid targeted recommendations for avoidance and assess the choice and composition of immunotherapy.²⁸

PET ALLERGY MANAGEMENT

Pet allergies cannot currently be cured. The treatment goal is to control symptoms and improve patients’ functional status and well-being.

Nonpharmacologic Treatment – Avoid & Minimize Allergen Exposure

Current recommendations for managing pet allergy symptoms start with exposure avoidance. Starting when animals are young, bathing them at least once weekly can reduce allergens and eliminate reactions in humans who are exposed to them (see SIDEBAR).³⁰ Immediate removal of animals from the household will not alleviate symptoms if the owner has carpeting and other pieces of furniture/items that the pet slept or sat on. Mammalian allergens are stable and can persist in house dust for up to six months.³² Additionally, using high-efficiency particulate air (HEPA) filters and mattress encasement, vacuuming, and chemically treating carpet are alternative methods for reducing exposure to contaminated materials, but may not reduce disease severity.³³

PAUSE AND PONDER: When patients have pet allergies, which symptoms are best treated with antihistamines?

SIDEBAR: To Bathe or Not to Bathe…^26,31

Bathing a cat or dog regularly appears to reduce the quantity of allergen harbored by the pet. To effectively lower Can f 1 concentrations, owners need to bathe the animal at least twice every week because Can f 1 concentrations rise rapidly, approaching baseline concentrations within three days after washing. Twice-weekly bathing can reduce the amount of recoverable Can f 1 on dogs by more than 80%, but researchers note that ideally, one would bathe the dog two to three times every week. Airborne Can f levels can fall by ruff-ly 40% but will quickly escalate.

However, the beneficial effects of reducing allergen levels by regular bathing are more likely associated with dogs, because their allergen burden returns faster than that of cats. So, bathing animals reduces the amount of allergen far better than vacuuming.

But should companion animals be bathed so often?

Most cats are notoriously averse to bathing, although some breeds like water (i.e., the Bengal). Dogs vary in the response to bathing—some like it, others do not. People who plan to bathe their cats or dogs regularly should do three things:

1. Check with a veterinarian or a breed advocacy group. The American Kennel Club indicates that how often an owner should bathe a dog depends on the dog’s coat type and presence or absence of an undercoat (in the latter case, frequent bathing can affect a dog’s temperature regulation). Bathing an animal is not just about a human’s allergies, the animal’s health and welfare should be a primary concern.
2. Consider the labor and time involved in bathing a pet often, safely, and well.
3. Start when the animal is young.

An allergen reducing cat food (Pro Plan LiveClear) is now available, and its manufacturer indicates it reduces the number of allergens in cat hair and dander by 47% after three weeks of feeding.³⁴ It is produced using eggs that contain an anti-Fel d1 antibody. When cats consume the food, the egg powder binds to and neutralizes Fel d1 in the cat’s saliva.³⁴

Pharmacologic Treatment

When avoidance and reducing allergens are not enough, depending on the severity of signs, over the counter (OTC) medications like antihistamines or local/topical steroids may provide temporary relief of allergy symptoms.³⁵ Those symptoms include runny/itchy nose or throat, sneezing, and itchy, red or watery eyes. Combination products that contain both an antihistamine and a decongestant or an analgesic are available but should be used with caution due to the increased risk of adverse effects. Other allergy medications, besides the ones mentioned, are used less often, including mast cell stabilizers and leukotriene antagonists. Table 2 summarizes common medications (both OTC and prescription) for treating mild to moderate allergy symptoms.³⁵

Table 2. Medications to Treat Allergy Symptoms³⁶

In general, for conditions eligible for self-care (e.g., allergic rhinitis) patients should start taking OTC allergy medications one week before they expect symptoms from a predictable exposure or as soon as possible before allergen exposure (for episodic exposure).³⁵ Prescribers should tailor the pharmacologic therapy and length of treatment based on symptoms and severity. Usually, complete relief takes two to four weeks. Intranasal steroids control nasal symptoms more effectively than antihistamines, as they inhibit multiple cell types and mediators, and should be recommended for moderate or persistent allergic rhinitis. Decongestants are effective in nasal congestion but have little effect on other symptoms. Intranasal and ocular preparations are available for nasal and eye symptoms. Intranasal cromolyn is the preferred initial choice for pregnant or lactating patients, as the body does not absorb it based on the route of administration. As mentioned in the table, fluticasone and triamcinolone nasal sprays are available OTC.³⁵

If a patient has persistent allergies, allergy medication is more effective when taken regularly.³⁵ For example, if a patient with moderate or severe persistent allergic rhinitis has completed two to four weeks of treatment with intranasal corticosteroids or oral antihistamines and achieved symptomatic control, healthcare providers can optimize the treatment’s effect by reducing the dose and continuing treatment for one additional month. If a patient’s symptoms are uncontrolled after two to four weeks of OTC treatment, pharmacists should assess the patient’s adherence and refer for prescription therapy if necessary.³⁵

PAUSE AND PONDER: Which providers in your area provide allergen-specific immunotherapy? What should patients expect if they take this route?

Allergy Immunotherapy

Allergen-specific immunotherapy has been used in pet allergies for years and has proven efficacy to help control symptoms and prevent disease progression. Allergists will consider allergy-specific immunotherapy when symptoms are uncontrolled by medications and/or avoidance measures, when adverse drug effects are intolerable, or when patients want to reduce long-term use of allergy medications.³⁷

The basis for allergen-specific immunotherapy is gradual reprogramming of the immune system to build a tolerance to allergens. The U.S. Food and Drug Administration (FDA) characterizes allergen-specific immunotherapies as biologics because they are produced from living cells, not synthesized by chemists, and regulated under the Center for Biologics Evaluation and Research (CBER).³⁸ This class comes in three forms:

• Sublingual allergy immunotherapy (SLIT) tablets
• SLIT drops, and
• subcutaneous allergy immunotherapy (SCIT)

As of 2022, the FDA has approved four SLIT tablets to treat allergic rhinitis with or without allergic conjunctivitis caused by ragweed, northern pasture grasses, and dust mites in susceptible individuals; the FDA has not approved SLIT tablets for pet allergies.²²

SLIT drops are made from FDA-approved allergy extracts used to make SCIT shots. However, these extracts are only FDA-approved for injection use under the skin, and they are not approved for use under the tongue. Therefore, SLIT drops are not FDA-approved and are off-label in the U.S., and Medicare or Medicaid does not cover these treatments in most cases. Despite not having FDA approval, patients can still receive SLIT drops from some prescribers who prepare a custom-mixed formulation but must pay out of pocket. Research indicates SLIT is safe and effective.³⁹

The FDA has approved SCIT for cat allergies, but not for other pet allergies. Patients who receive SCIT usually call it “allergy shots.” One systemic review evaluated 88 trials that enrolled 3,459 asthmatic patients and exposed them to SCIT. One case of deterioration in asthma symptoms was avoided for every three patients treated with SCIT (95% CI, 3-5), and one patient would avoid increasing symptomatic medication use for every four patients treated (95% CI, 3-6).⁴⁰ Another study found that SCIT can reduce the need for systemic steroids in allergic rhinitis patients.⁴¹ Usually, the patient receives a solution for injection with 10,000 bioequivalent allergy units (BAUs) per milliliter (standardized extract) of lyophilized cat hair and dander added to glycerol and human serum albumin (0.03%). A clinician administers one to two subcutaneous injections every week starting at low doses (1:10,000 dilution) and titrating up to a seemingly effective maintenance dose. Then, the prescriber extends the injection interval gradually to every 2 weeks to 4 weeks. For cat allergens, the effective maintenance dose usually falls within the 1,000 to 4,000 BAU range.⁴²

S'CIT sometimes can cause treatment-related systemic allergic reactions; however, near-fatal or severe reactions are rare, and most reactions are local and mild (swelling, pruritis, and redness at injection site).⁴³ SCIT should not be recommended to patients who have severe uncontrolled heart problems or asthma if they take beta-blockers, which are associated with more frequent reactions, more severe reactions, and reactions that are refractory to epinephrine. Additionally, allergy shots should not be recommended for pregnant women unless discussed with their obstetricians.⁴³

Both SCIT and SLIT require gradual up-titration of dosages with ongoing and multiple treatments and may take three to five years to reach desensitization. Also, for SCIT, based on its route of administration (subcutaneous injections are invasive), patients will need to visit the doctor's office more frequently and may experience the treatment-associated side effects.

SLIT has been increasingly recommended because of its ability to modify the immune system for the long term while reducing allergy symptoms. SLIT also showed a safer profile, only associated with mild mouth symptoms, and improved adherence compared to SCIT.⁴⁴ When compared to traditional allergy treatments, SLIT tablets showed similar clinical efficacy to nasal corticosteroids and greater clinical efficacy than second-generation antihistamines and montelukast.⁴⁵

What About Cost?

In adherent patients, SCIT and SLIT have proven to be an economically viable option. The annual cost of using SCIT depends on patients’ insurance: Medicare ($1021.70), Medicaid ($758.16), and the commercial average ($1722.24). Yearly treatment costs for SLIT are self-pay because treatment is not FDA approved and costs around $679.25.⁴⁶ Because SLIT drops are administered at home by patients, they tend to be more affordable than the cost of SCIT. Patient preference might be for a once monthly administration, rather than taking oral antihistamines daily.

OTC medications are less expensive than immunotherapy, but costs vary. In a comparison of second-generation antihistamines versus montelukast, levocetirizine (Xyzal) had the best efficacy per cost value. Generic fexofenadine (Allegra), although similar in efficacy, was more expensive than levocetirizine.⁴⁴

CONCLUSION

Healthcare providers should counsel patients about reducing allergen exposure and help patients to choose OTC medications for self-care based on individual patient needs and conditions to optimize treatment effects. Pharmacy staff should refer patients to allergists when necessary to identify the cause of their allergy symptoms. If a patient's allergy does not allow him or her to have pets at home and the patient owns a pet, suggest that the patient ask family members or friends about placement before contacting the local animal shelters.

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INTRODUCTION

Let’s start this continuing education (CE) activity with a case. Bob is a 63-year-old who has had lifelong exacerbations of disabling psychosis. In addition to his psychiatric diagnosis, Bob also struggles to control concomitant medical conditions. These conditions include urinary incontinence, benign prostatic hyperplasia (BPH), and severe constipation that persists from a previous gastrointestinal obstruction and surgical perforation. He has been experiencing breakthrough psychotic symptoms on his current antipsychotic and arrives at the pharmacy today to pick up his new antipsychotic, xanomeline combined with trospium chloride (Cobenfy). Bob mentions to the pharmacy technician he is also having pain and trouble sleeping. He would like to purchase a bottle of over-the-counter (OTC) Tylenol PM (acetaminophen with diphenhydramine). The pharmacy technician recognizes diphenhydramine’s potential conflict with his new prescription and alerts the pharmacist. Staying current with new medications is key to providing optimal care and safety for patients. The pharmacist contacts the prescriber to discuss less complicating anticholinergic options for Bob.

Acetylcholine (ACh) is a neurotransmitter found in the brain and peripheral nervous system. Pharmacologic manipulation of this neurotransmitter has resulted in the advancement of novel pathways to treat conditions ranging from anaphylaxis rescue to treatment of dementia. Unintentional consequences of ACh manipulation include adverse effects associated with anticholinergic burden (ACB). The magnitude of ACB increases with the number of medications with anticholinergic characteristics added to the prescribed regimen. Often overlooked is the added burden of a patient’s OTC medications ranging from sleep aids to antidiarrheals.¹ It is also important to differentiate anticholinergic action from drug-induced fluid depletion, like that expected with diuretics, which have no hallmark muscarinic effects.

Increased ACB results in short-term adverse effects like dry mouth, blurred vision, and urinary retention. It can also cause or contribute to long-term effects including dementia, worsening physical function, and increased risk of falls.¹ The characteristics of anticholinergic reactions are easier to remember when understanding the normal function of muscarinic receptors at different sites in the body. The following symbolic descriptions can help you recall these effects²:

• Mad as a hatter (delirium, cognitive deficits)
• Blind as a bat (eye symptoms, blurry vision)
• Dry as a bone (decreased sweating/dry mouth/dry skin)
• Hot as a hare (elevated body temperature)
• Bloated as a toad (constipation)
• The heart runs alone (tachycardia)
• Full as a flask (urinary retention)
• Red as a beet (cutaneous vasodilation)

Clinicians (including pharmacists and technicians) can rank medications according to their ACB contribution and predict their cumulative effects.

PAUSE AND PONDER: What diagnoses and conditions may be worsened if patients are exposed to anticholinergic medications?

What Does the Beers Criteria Have to Say?
The American Geriatrics Society (AGS) Beers Criteria warns of diminished medication elimination as we age. Using highly anticholinergic medications is riskier in older adults, resulting in exaggerated adverse effects such as confusion, xerostomia (dry mouth), and anticholinergic toxicity. Even younger adults are at risk of long-term cumulative exposure to anticholinergic drugs that can lead to delirium (an acute, fluctuating disturbance in attention and awareness) and dementia (a chronic, progressive cognitive decline).¹ In addition to central nervous system anticholinergics, Beers also recommends avoiding anticholinergic gastrointestinal antispasmodics and skeletal muscle relaxants because of questionable efficacy (Table 1).¹

Table 1. Illustrative List of Potentially Inappropriate Medication Use in Older Adults¹

The Beers Criteria also includes potentially inappropriate medications (PIMS) for older adults that can worsen a condition or syndrome. Anticholinergic medication can exacerbate lower urinary tract symptoms, BPH, and glaucoma. Therefore, prescribers should avoid them in patients with these conditions.¹ Peripheral effects of ACB include constipation, dry mouth, tachycardia, and urinary retention. Central adverse effects include agitation, confusion, delirium, and cognitive impairment. Individuals with serious mental illnesses (SMI) are in a state of chronic cerebral cholinergic depletion and exposure to high ACB can worsen negative symptoms (a reduction or absence of normal behaviors and functions related to motivation and interest, or verbal/emotional expression) leading to further functional and cognitive impairment.³

Anticholinergic medications frequently cause dry mouth, and medication-induced xerostomia can result in discomfort and oral health complications.⁴ Saliva not only facilitates swallowing and digestion, but also promotes the removal of harmful microorganisms.⁵ Medication-induced xerostomia has been reported in twice the number of patients taking anticholinergic medications compared to non-medicated individuals (30% as opposed to 16%, respectively).⁶ Data suggests that patients with dry mouth are 11.5% more likely to develop oral candidiasis, also called thrush, than those without xerostomia.^7,8 More than 95% of dry mouth cases reported in residential long-term care settings for older adults were attributed to medication use and not a natural consequence of aging.^4,9

The development of dementia with long-term anticholinergic use has been well researched. Numerous studies have investigated the potential cognitive impacts of prolonged chronic anticholinergic exposure.^10-14 Epidemiological research has demonstrated that anticholinergic medications’ impact on the development of dementia is significant, with an increased risk of up to 50% among those with high ACB. Researchers have been able to detect risk associated with anticholinergic use up to 20 years before diagnosis.^10-14

PAUSE AND PONDER: What diagnoses and conditions may be affected when using anticholinergic medications? What OTC medications may pose anticholinergic risk?

ESTABLISHING AN ACB ACTION PLAN

Establishing an ACB action plan is as easy as following five steps.

First, the Beers Criteria expert panel recommends routine medication reviews that include consideration of total ACB. Clinicians should calculate ACB risk scores to determine ACB magnitude. Numerous published scales are available to measure ACB. Expert consensus groups develop scales using clinical experience along with research evaluating anticholinergic properties of medications. One calculator that is available is the ACB Calculator, which combines the Anticholinergic Cognitive Burden Scale (ACBS)¹⁵ and the German Anticholinergic Burden Scale (GABS).¹⁶ This calculator is available at https://www.acbcalc.com/.¹⁷ The developers report their source calculators are valid, reliable, and have been used as a pharmacology standard to measure ACB. A score of 3 or greater on the ACBS is associated with significant cognitive impairment and increased mortality.

The second step is to use direct observation and consider patient self-reported adverse effects.

• Clinicians should inquire about physical symptoms associated with anticholinergic toxicity at each patient encounter. They should evaluate ACB in individuals with new or worsening urinary retention, significant constipation, dry mouth, or any of the symptoms described earlier.
• Clinicians should evaluate individuals who report confusion or new or worsening memory impairment for ACB.

Third, the clinical team needs to evaluate the patient’s regimen to determine whether pharmacologic substitution to medications with less ACB is possible.

• Diphenhydramine (Benadryl) or sedating antihistamines for allergies? Individuals seeking relief of allergic symptoms may find less sedating options such as loratadine (Claritin) adequate. For others requiring greater control, exploring intranasal steroids (like fluticasone) used along with loratadine may provide better symptom relief.
• Ask the question, “Can the patient use antipsychotics or antidepressants with less ACB?” Individuals taking antipsychotics report a spectrum of adverse effects and symptom improvement. Clozapine is ranked among the most anticholinergic antipsychotics currently available, however its position also as the most superior antipsychotic prevails for many patients who need it.¹⁸ Clinicians can evaluate potential ACB using established rankings when prescribing antipsychotics. Odds ratios reveal that quetiapine (Seroquel) has one of the highest odds ratios of 4.53, meaning a 4.53 times higher chance of experiencing anticholinergic effects (see Figure 1).¹⁸ While not all antipsychotics are entirely interchangeable, evidence supports relative equivalency for most when given for an adequate duration and at optimal doses. Antidepressants can be ranked for ACB more efficiently by their class effects, with the tricyclic antidepressant class contributing high ACB and selective serotonin reuptake inhibitors (SSRI)/serotonin norepinephrine reuptake inhibitors (SNRI) with low ACB contribution potential. The SSRI paroxetine (Paxil), however, is an exception to the SSRI class benefit because Beers cautions against its use for those at risk of high ACB.¹

Figure 1. Anticholinergic Effects of Commonly Prescribed Second Generation Antipsychotics Ranked by Odds Ratio¹⁸

Fourth, it’s essential to educate patients about OTC medications for sleep and allergies that have anticholinergic properties.^1,19

• Using diphenhydramine in situations such as acute treatment of severe allergic reactions is appropriate, even for older adults. Having diphenhydramine on hand for many families is critical to emergency planning.
• Diphenhydramine and other sedating antihistamines are limited by tolerance that develops when used chronically as a sleep aid. Melatonin is a popular alternative; however the Food and Drug Administration (FDA) regulates it less strictly than other medications, and some formulations contain inconsistent amounts of melatonin. In fact, analysts have found melatonin supplements to contain almost 3.5 times more melatonin than reported on the label. Prescription melatonin agonists like ramelteon (Rozerem), are an option for individuals who prefer a non-controlled, FDA approved intervention for sleep onset insomnia.
• Patients with sleep complaints can try nonpharmacologic interventions before exploring medications that can cause further complications. Interventions include developing a consistent schedule for sleep-wake times, controlling the environment (decreasing noise and temperature), and avoiding vigorous physical activity and caffeine consumption before bedtime. Avoiding blue light from cell phones and other devices is also essential to promote natural melatonin release and facilitate decreased sleep latency.
• Pharmacy technicians can be a great to deliver educational materials with pharmacist review. These materials can include symptom checklists prepared by healthcare professionals. Pharmacists should calculate scores when a patient presents with possible ACB or when conducting a routine medication review. Pharmacists can also check ACB scores technicians calculate for them before they share them with patients. Pharmacy technicians be sure to include OTC purchases and all prescription medications because burden scores should consider the total medication regimen.

Finally, all healthcare providers need to stay current with newly approved medications because these may not be available in an ACB calculator.^1,20

• The AGS Beers Criteria is scheduled for updates every three years. Pharmacists and pharmacy technicians should review the summary tables that highlight anticholinergic agents newly included in the List.
• ACB calculators are limited by the medications they include for ranking. New medications are often not readily available until expert update the calculator.
• Cobenfy’s prescribing information, for example, is not available in the ACBS yet. This “first in class” antipsychotic is a muscarinic combination of xanomeline and trospium chloride. The prominent precautions provided in its labeling are associated with its anticholinergic adverse effects and risks, as reflected in Table 2.

Table 2. Highlights of Xanomeline/Trospium Chloride’s Anticholinergic Warnings²⁰

So, what about Bob? Clinicians skilled in developing ACB action plans determined that with some small changes, as described in Table 3, they could minimize his anticholinergic risks. They continued some of Bob’s current medications that did not contribute to the ACB. More options could be considered in the future if Bob’s symptoms continue or require further intervention. For example, the clinical team chose brexpiprazole because it had the least ACB of available options, but many others could be explored. What changes would you have made?

Table 3. Reducing Bob’s Anticholinergic Burden

CONCLUSION

Clinicians should consider using a calculator, such as the Anticholinergic Burden Calculator, as a clinical support tool for determination during a routine medication review. Many medications with anticholinergic properties are prescribed out of clinical necessity and without an appropriate alternative for certain patients. Calculating ACB is also advisable if the patient presents with symptoms that suggest possible anticholinergic toxicity.

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INTRODUCTION

Imagine you’re working a late shift at your local pharmacy when a mother rushes in with her child, whose hands are red and covered in small, weeping lesions. The child says they itch constantly, and the mother explains the pediatrician mentioned “contact dermatitis,” but mom’s unsure how to help. She didn’t know who else to turn to but hopes you could provide some suggestions on what products can help her child.

While skin conditions aren’t necessarily the pharmacy staff’s bread and butter, your expertise can still make a difference. You can scrutinize the affected area and ask some guided questions to decide what products may help the child.

PAUSE AND PONDER: What questions may help determine the best remedy for this child?

Before recommending products, it’s important to first understand what contact dermatitis is, how it develops, and the most effective treatment options.

WHAT IS CONTACT DERMATITIS?

Contact dermatitis is a form of eczema (a group of inflammatory skin conditions that cause dry skin, itchiness, rashes, scaly patches, blisters, and skin infections) that occurs when a substance comes into contact with the skin and causes irritation or an allergic reaction.^1,2 Contact dermatitis occurs in 15% to 20% of people. Contact dermatitis is the most common form of reported occupational skin disease accounting for approximately 90% to 95% of cases.^1,3 Although contact dermatitis has no cure, patients can manage symptoms effectively with topical treatments and by identifying and avoiding the triggering substance.

It's important to note many different clinical patterns of contact dermatitis exist. Some common patterns include^4-10

• Erythema multiforme—lesions present as macules (flat, distinct spot on the skin that's a different color than the surrounding area but doesn't impact the skin's texture or thickness), papules (red bumps), bullae (blisters filled with clear fluid), or urticarial eruptions (itchy welts), often demonstrating a characteristic 'target lesion' pattern predominantly affecting the extremities
• Urticarial papular plaques—skin lesions that appear as itchy papules and raised patches, often appearing in lines or clusters
• Lichen-planus—presents as shiny red, purple, gray, or brown bumps that may merge into plaques, commonly on wrists, arms, legs, or lower back; may cause mild to intense itching
• Purpuric petechial reactions—skin or mucous membrane discoloration as a result of hemorrhage from small blood vessels. Lesions are often 1 mm to 2 mm across
• Pustular reactions—a rash consisting of small pustules (bumps) less than 5 mm to 10 mm that are filled with pus
• Pigmentation disturbances
• Pemphigoid—present as large fluid-filled blisters that rupture and form crusted erosions

Types of Contact Dermatitis

Contact dermatitis has two main presentations: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). Table 1 provides more information on these two presentations.

PAUSE AND PONDER: How does ICD differ from ACD?

Table 1. The Main Types of Contact Dermatitis and their Characteristics.^1,2-4,11-14

Apart from these two main types of contact dermatitis, other less common presentations can develop. Photoallergic and photoirritant contact dermatitis are reactions primarily affecting sun-exposed areas including the face, back of the hands, arms, upper chest, and lower legs.¹¹

Photoallergic contact dermatitis requires ultraviolet radiation to activate the allergic agent to trigger an allergic reaction. The most common causative agents are chemicals found in sunscreens. Benzophenones (most commonly oxybenzone) are common sunscreen components and chemical triggers. Other agents include ethylhexyl methoxycinnamate (octinoxate), butyl methoxydibenzoylmethane (avobenzone), ethylhexyl dimethyl (padimate O), and octocrylene. A less common cause implicated in photoallergic contact dermatitis reactions is ketoprofen, a topical nonsteroidal anti-inflammatory drug.¹¹

Photoirritant (phototoxic) contact dermatitis requires ultraviolet radiation to activate the irritant and cause cellular damage. It occurs after contact with plants that contain furocoumarins or psoralens (e.g., lime, lemon, parsnips, parsley, celery, hogweed, rue [Ruta graveolens], meadow-grass, fig tree). Due to its association with limes and sunlight, photoirritant contact dermatitis is commonly referred to as “Margarita dermatitis.”¹¹

Protein contact dermatitis is caused by exposure to high-molecular-weight proteins often found in foods, latex, and other biologic material. Common foods involved include vegetables, animal proteins, spices, wheat, and milk. Most cases are occupation-related with food handlers frequently developing this form of dermatitis.¹¹

Systemic allergic contact dermatitis, also known as hematogenous contact dermatitis, occurs when an individual who has been previously sensitized to an allergen through skin contact later encounters the same substance through a systemic route (e.g., ingestion, injection, inhalation, implantation, or suppository use). Common triggers include metals (most commonly nickel); medications (e.g., aminoglycoside antibacterials, corticosteroids, and aminophylline); chemicals (e.g., parabens, formaldehyde, and propylene glycol); certain foods (e.g., soy, chocolate, nuts, and spices); and plants. Common plant sources include those in the Compositae family (known as the “daisy” family such as dandelions, sunflowers, and ragweed) and Anacardiaceae family (known as the “cashew” family and such as cashews, mango, and sumac), garlic, and balsam of Peru.^11,13,15-17

Pathogenesis of Allergic Contact Dermatitis

The difference in mechanism between ACD and ICD results in their distinct pathogenic pathways. See the SIDEBAR for definitions on the immune cells involved in contact dermatitis’ pathogenesis.

SIDEBAR: Overview of Immunomodulatory Cells Involved in the Pathogenesis of Contact Dermatitis^18-22

• T-effector cells: Activated T-cells that migrate to infection sites to eliminate pathogens. These cells develop through antigen recognition (following presentation by antigen-presenting cells), leading to T-cell proliferation and differentiation to effector cells.
• T-memory cells: Form of activated T-cells that become long-lived memory cells. These cells rapidly expand and mount a stronger immune response upon re-exposure to the same antigen.
• Interleukin-1 alpha (IL-1α): A pro-inflammatory cytokine found in most cell types, especially barrier tissues. It’s released during cell injury or stress to trigger local inflammation, recruit immune cells, and promote tissue repair.
• Interleukin-1 beta (IL-1β): A pro-inflammatory cytokine produced by activated immune cells that requires inflammasome processing (enzymatic activation of an inactive precursor by intracellular immune complexes) to become active. It mediates systemic inflammation, fever, and leukocyte recruitment.
• Interleukin-1 receptor antagonist (IL-1RA): A natural inhibitor that blocks IL-1α and IL-1β from receptor binding, preventing excessive inflammation and maintaining immune balance.
• Interleukin-10 (IL-10): An anti-inflammatory cytokine that suppresses pro-inflammatory cytokine production and limits tissue damage by controlling immune cell activation.
• Interleukin-6 (IL-6): A multifunctional cytokine produced during infection or stress that activates immune cells, induces acute-phase responses, and contributes to systemic inflammation and metabolic changes.
• Tumor necrosis factor-alpha (TNF-α): A key inflammatory cytokine—secreted mainly by macrophages—that regulates immune responses, promotes inflammation, and influences metabolism and tissue repair.
• Chemokine ligand 20 (CCL20): A chemokine that binds CCR6 (C-C chemokine receptor type 6) to attract lymphocytes and dendritic cells to inflamed or infected tissues. It plays a central role in Th17-driven inflammation and autoimmune disease.
• Chemokine ligand 21 (CCL21): A chemokine that binds CCR7 (C-C chemokine receptor type 7) to direct T-cells and dendritic cells to lymphoid organs, supporting immune cell organization and adaptive immune responses.
• Chemokine ligand 8 (CXCL8)/Interleukin-8 (IL-8): A chemokine that binds CXCR1 (C-X-C motif chemokine receptor 1) and CXCR2 (C-X-C motif chemokine receptor 2) to recruit neutrophils to infection sites, contributing to inflammation, angiogenesis, and tissue remodeling.
• Intercellular adhesion molecule 1 (ICAM-1): An adhesion molecule on endothelial cells and leukocytes that mediates immune cell attachment and migration during inflammation and supports T-cell activation.

Pathogenesis of ACD can be broken down into three stages: sensitization, elicitation, and resolution.¹³

Sensitization occurs during initial allergen exposure. The skin absorbs the allergen (antigen) which then binds to dendritic cells (immune cells that present antigens to T-cells and help drive adaptive immunity) and migrate to lymph nodes.²³ In the lymph nodes, these allergens trigger the development of allergen-specific T-cells. The T-cells then differentiate into T-effector cells and T-memory cells and recirculate into the blood and skin. This process may take up to 15 days. Patients may not develop active dermatitis during this phase.¹³

Elicitation occurs upon allergen re-exposure. The allergen binds to the dendritic cells and is presented to the antigen-specific T-cells. This triggers a rapid inflammatory response cascade that releases pro-inflammatory cytokines and recruits inflammatory cells. This process occurs hours to days after the exposure and manifests as an itchy rash at the contact site. The dermatitis response can last days to weeks following exposure.¹³

Resolution occurs post-exposure. A large population of T-memory cells replace T-effector cells. This ensures that if individuals experience subsequent exposures, the immune reaction to the allergen is of increasing intensity. As a result, patients may experience a worsening severity of symptoms with repeated exposures due to the increasing population of T-memory cells in the skin.¹³

Pathogenesis of Irritant Contact Dermatitis

ICD’s pathogenesis is less clearly understood than ACD’s pathogenesis; however, experts have determined a few key mechanisms involved. These mechanisms include disruption of the epidermal barrier (the stratum corneum) and the loss of lipids, damage to keratinocyte cell membranes, cytotoxic effect on keratinocytes, inflammatory cytokine release from keratinocytes, and activation of innate immunity.¹²

Previous experimental studies show that disruption of the epidermal barrier  by occlusion or by physical/chemical irritation results in increased skin permeability, transepidermal water loss, and reduced natural moisturizing factor. These steps are considered the initiation event of ICD. ICD’s pathogenesis also varies depending on whether the condition is acute or chronic.¹²

In acute ICD, studies using both human and animal models show that acute damage to the epidermal barrier (such as that caused by sodium lauryl sulfate, a surfactant used in many cleaning and hygiene products) triggers the release of preformed cytokines from keratinocytes, including interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor (TNF)-α. IL-1α and TNF-α serve as key mediators, initiating the release of additional pro-inflammatory cytokines (e.g., CCL20, CCL21, CXCL8) that recruit mononuclear and polymorphonuclear cells to the irritation site. TNF-α stimulates the expression of ICAM-1 on keratinocytes, facilitating leukocyte migration to the epidermis. Concurrently, the body produces anti-inflammatory mediators such as IL-10 and IL-1RA in response to irritant exposure, helping to regulate and resolve the inflammatory process.¹²

Researchers don’t fully understand the underlying mechanisms of chronic ICD yet. One proposed theory suggests repeated exposure to mild irritants or persistent wet work (occupations that involve frequent or prolonged contact with water or other liquids; e.g., healthcare, hairdressing, or construction). Continuous exposure leads to downregulation of the inflammatory response while promoting keratinocyte proliferation and differentiation. Studies comparing normal skin with areas repeatedly exposed to irritants, such as sodium lauryl sulfate, have shown decreased levels of pro-inflammatory cytokines (IL-1 and TNF-α) and increased levels of IL-1RA in chronically affected skin.¹²

Additionally, ICD appears to involve unique gene expression changes within the skin that distinguish it from ACD. Some individuals develop a tolerance to chronic irritant exposure, a process referred to as the “hardening phenomenon.” Although the exact mechanisms remain unclear, structural and biochemical adaptations—such as epidermal thickening (acanthosis [patches of thickened, velvety, darkened skin that appear within body folds and creases] and hyperkeratosis), alterations in stratum corneum lipid composition, changes in barrier permeability, and modulation of inflammatory mediator expression may contribute to this adaptive response.^12,24

Risk Factors

Risk factors for contact dermatitis are a mix of circumstantial and inherent traits. For example, a circumstantial trait is cosmetic preference. A woman partial to perfumes or jewelry has a greater risk of contact dermatitis than a woman who is not. An example of inherent risk is skin type; individuals with thin skin, for instance, are at an increased risk of contact dermatitis. Table 2 describes additional risk factors.

Table 2. Common Risk Factors of Contact Dermatitis.^4,11,25

In addition to these risk factors, higher dermal absorption may increase an individual’s risk for contact dermatitis.²⁶ Factors that impact dermal absorption include skin integrity, absorption location, the chemical’s physical and chemical properties, chemical concentration, absorption time of the chemical, and the surface area of skin that absorbs the chemical.¹

Signs and Symptoms

Signs and symptoms of contact dermatitis depend on whether the reaction is acute or chronic. An acute reaction, such as contact with poison ivy, can cause the skin to appear red and swollen and may have small vesicles. However, a chronic reaction caused by repeated reactions is more akin to a presentation of eczema with a rash that appears to thicken, scale, or crack.^3,13

The symptom location will also vary depending on the substance’s contact location. For example³

• A reaction to a skin care product’s ingredient may be localized to the face or eyes
• A reaction to poison ivy may be localized to the legs or hands
• A reaction to jewelry may be centralized around the neck or wrists

Common symptoms of contact dermatitis include^1,2

• Dry, flaking, scaly skin (may crack, ooze clear fluid, or crust)
• Inflamed skin (may look pink, red, brown, purple, or gray depending on skin tone)
• Itching (may lead to intense scratching and even bleeding)
• Pain
• Redness
• Small blisters or wheals (itchy, red circles that have a white center)
• Swelling

PAUSE AND PONDER: What over-the-counter products are appropriate to suggest to a patient with a poison ivy rash?

Diagnosis

Contact dermatitis often resolves once patients identify the trigger and avoid the substance going forward. With acute examples such as poison ivy, symptoms may resolve prior to a doctor’s visit.

However, for persistent symptoms that warrant an office visit, clinicians diagnose contact dermatitis by evaluating symptoms based on appearance and duration. They consider factors such as occupation and hobbies and use patch testing to confirm allergens.²⁶ Clinicians can perform skin biopsies to rule out additional skin conditions such as psoriasis and seborrheic dermatitis among others.²

During testing, clinicians apply small amounts of diluted allergens to the patient’s back under paper tape patches. After 48 hours, they remove the patches and evaluate the skin for signs of a reaction; the evaluation is repeated 72 to 96 hours later. A patch test helps identify chemicals or substances a patient is allergic to so they can be avoided in the future. The baseline patch test (baseline patch testing panels vary by geographic location, depending on the allergens available in each region ) finds approximately 70% of allergens.^2,3,28

The American Contact Dermatitis Society (ACDS) updated their “Core Allergen

Series” in 2020 to increase the chances of finding the responsible agent in contact dermatitis cases. This series is a patch-test panel designed to provide clinicians a tool to identify clinically relevant allergens beyond the standard baseline series.²⁹

Since job-specific allergies are common, patch testing is available for certain industries. For example, dermatologists and allergy specialists can use patches specific for florists or dental technicians. This expanded patch testing finds approximately 80% of allergens. Additional series may be applied based on the site of dermatitis, the suspected allergen exposure, and if patients bring their own products to be tested (may require dilution).^27,28

Reactions to patch testing are graded for each allergen on a spectrum as seen in Table 3.

Table 3. Grading and Interpreting Results to a Patch Test^28,30,31

Positive reactions can be further classified based on their relevance or potential risk. A current relevance reaction indicates the identified allergen explains the patient’s present dermatitis. A past relevance reaction reflects an allergen responsible for a previous episode but not the current one. A future relevance reaction suggests sensitization to an allergen the patient is likely to encounter again. An uncertain relevance reaction identifies an allergen whose significance remains unclear until further investigation or inspection of the patient’s personal care or occupational exposures. Finally, a potential cross-reaction indicates that sensitivity to one allergen may cause a reaction to related substances.²⁸

TREATMENT OF CONTACT DERMATITIS

Pharmacologic Treatment

Currently, no cure for contact dermatitis exists. However, a variety of over-the-counter (OTC) and prescription products can provide patients with symptom relief.

Clinicians tailor treatment based on contact dermatitis type, location, severity, and classification (acute versus chronic). Clinicians classify cases as extensive, severe, or disabling if they involve over 20% of the total body surface area or involve the face, hands, feet, or genitalia.³²

While pharmacologic treatment provides rapid symptom control, prevention is the mainstay of management for both ACD and ICD. ACD treatment usually involves topical corticosteroids or tacrolimus with added emollients, while ICD treatment focuses on consistent emollient use and topical corticosteroids (when necessary to control irritation).^12,32

Providers must recognize that while topical corticosteroids may be used in ICD, evidence supporting their ability to restore the epithelial barrier remains limited. However, they may be prescribed for their anti-inflammatory properties. In ICD, ointments are generally preferred over creams as they are more occlusive. Formulations of products ordered from most to least occlusive are ointment, creams, lotions, and oils.^12,33 See the SIDEBAR for information on the uses and products that fall under each corticosteroid group.

SIDEBAR: Groups of Corticosteroids³⁴

Topical corticosteroids are grouped into seven classes based on their potency, ranging from superpotent (Group I) to least potent (Group VII). Potency affects both therapeutic efficacy and risk of adverse effects, making appropriate selection essential for safe and effective treatment.

• Group I (superpotent): used for thick, resistant plaques (e.g., clobetasol propionate 0.05%, halobetasol propionate 0.05%).
• Group II to III (high to medium-high potency): commonly used for less severe lesions or shorter treatment courses (e.g., betamethasone dipropionate 0.05%, fluocinonide 0.05%, triamcinolone acetonide 0.5%).
• Group IV to V (medium potency): appropriate for most body areas and moderate conditions (e.g., triamcinolone acetonide 0.1%, mometasone furoate 0.1%).
• Group VI to VII (low to least potent): preferred for sensitive areas such as the face, groin, or intertriginous areas (e.g., hydrocortisone 1%, desonide 0.05%).

For acute, localized ACD affecting the hands, feet, and nonflexural areas (areas of the body that do not naturally bend; e.g., the torso), treatment is a group I to III corticosteroid used once or twice daily for two to four weeks (treatment may be shorter if symptoms resolve).³²

For acute, localized ACD affecting the face or flexural areas (areas of the body that naturally form folds; e.g., the elbow or knee joints), treatment is a group IV to VI corticosteroid used once or twice daily for one to two weeks and then tapered off over two weeks. If treatment duration must be longer than two weeks, topical tacrolimus is used twice daily until improvement and is then tapered off. If the contact dermatitis is resistant to other treatments, topical ruxolitinib is used once daily until symptom resolution.³²

For extensive, severe, or disabling ACD, treatment is systemic corticosteroids. Prednisone is dosed at 0.5 mg/kg per day (or an equivalent dose, with a max daily dose of 60 mg/kg) for seven days. This dose is then reduced by 50% for five to seven days and then tapered off over two weeks.³²

For chronic ACD localized to the hands, feet, and nonflexural areas, treatment is a group I to III corticosteroid once daily for seven to 10 days, then once every other day.

For chronic ACD localized to the face and intertriginous (area where two skin areas may touch or rub together e.g., between digits or the armpit) areas and resistant to topical corticosteroids, treatment is topical tacrolimus used once or twice daily until symptom resolution. If it is resistant to other therapies, topical ruxolitinib is used once daily until symptom resolution.³²

Last, for chronic ACD that is resistant to topical treatments, phototherapy (bath psoralen plus ultraviolet A photochemotherapy or narrowband ultraviolet B has demonstrated clinical improvement in chronic hand eczema cases), or systemic immunosuppressive medication (such as oral methotrexate, cyclosporine, mofetil, azathioprine, mycophenolate) are used.³²

For mild, non-facial ICD, treatment is a group II or III corticosteroid that is used once or twice daily for two to four weeks. For severe, non-facial ICD, treatment is a group I corticosteroid used once or twice daily for two to four weeks. For facial or flexural ICD, treatment is a group IV to VI corticosteroid used once or twice daily for one to two weeks. Last, for chronic ICD with lichenification, treatment is petroleum jelly with or without a medium potency (group IV to V) corticosteroid overnight (under occlusion) for a few days.¹²

Over-the-Counter Treatment

In addition to prescription products, patients can use several OTC options to manage ACD or ICD. OTC products are chosen based on the symptoms the patient wants to treat.

Cold compresses or antihistamines (such as cetirizine, diphenhydramine, or loratadine) may reduce itching. Pharmacists and pharmacy technicians can recommend calamine lotion or aluminum acetate to dry oozing lesions. Alternatively, patients can take oatmeal baths; this is helpful in cases where the lesions are widespread over the body. Emollients and moisturizers effectively reduce irritation and improve the skin barrier. Additionally, hydrocortisone cream or ointment can decrease inflammation.^3,4,12

While people use the terms emollients and moisturizers interchangeably, knowing the distinction can prove useful when recommending products. Moisturizers help hydrate and maintain the skin’s moisture balance. Emollients help soften and smooth the skin by forming a protective layer that reduces water loss. Often, emollients can be used as an ingredient in the formulation of a moisturizer.³³

The two main types of emollients are occlusives and humectants. Occlusives create a lipophilic (“water-repelling”) film on the skin’s surface that acts as a barrier, helping to prevent moisture from evaporating from the outermost layer of the epidermis. Occlusives help skin retain moisture, but don’t provide additional moisture. Examples of occlusives include petroleum jelly, lanolin, oil (mineral or vegetable), beeswax, ceramides, and liquid paraffin.^12,33,35 However, some patients may experience “lanolin allergy,” which is a separate condition from contact dermatitis. Lanolin was the ACDS’s 2023 “Allergen of the Year” and some patients should avoid this ingredient.³⁶

Humectants are hydrophilic (“water-attracting”) and draw in and hold moisture within the stratum corneum, functioning in a way similar to the skin’s natural moisturizing factors found in corneocytes. Examples of humectants include glycerin, hyaluronic acid, urea, sorbitol, and propylene glycol.^12,33,35

Consistent application throughout the day improves the efficacy of emollients. Reapplication after handwashing and before bedtime especially help maintain the skin barrier and prevent flare-ups.¹²

Moisturizers reduce skin dryness, scaling, and transepithelial water loss which helps maintain skin integrity, flexibility, and barrier function.³³ Moisturizers are primarily comprised of emollients, occlusives, and humectants but may contain additional ingredients such as fragrances, surfactants (cleansers), and preservatives. Some special formulations may include ingredients with antimicrobial, anti-itch, and anti-inflammatory functions.

Choosing the ideal product for a patient depends on the target allergies, the skin’s condition and characteristics (inherent risk factors), and personal preference. Patients using a combination of prescription and OTC products may see symptom resolution within as early as one to two weeks.

Prevention

Prevention is the mainstay treatment for both ACD and ICD. Patients can take several actions to help prevent contact dermatitis.

First, patients should identify and avoid known allergens and irritants to prevent possible reactions. Making lifestyle choices such as selecting hypoallergenic jewelry, changing hair or skin care products, and putting cloth covers on metal fasteners (e.g., a jean button) can minimize reactions.^13,37

Patients can also improve and protect their skin barrier by continuously moisturizing and hydrating their skin. Various OTC products with different formulations allow patients to find a regimen that works best for their skin.^12,37

Patients should wash skin exposed to the allergen or irritant immediately after exposure to remove the irritant (e.g., poison ivy, poison oak) that cause the reaction. Products like Tecnu cleanser, Zanfel cleanser, and Cutter scrub effectively remove urushiol oil (the component of poison ivy and poison oak that causes the red, itchy rash patients experience). Urushiol oil binds to skin proteins within 10 to 15 minutes so immediate use of these products is vital.^13,37,38

Patients should also be mindful of pets. Sometimes, allergens can be carried from outside into the house by clinging to a pet’s fur. If patients suspect their pet encountered an allergen (such as poison ivy), they should bathe the animal to reduce the risk of spreading it to people.^13,37

Wearing gloves or protective clothing provides an excellent alternative for patients to avoid contact with irritants. This is especially vital for many occupational contact dermatitis cases. Barrier creams are another alternative that function to protect skin from irritants. Barrier creams prevent penetration of hazardous materials into the skin. These products contain compounds such as glycerin, silicones, ceramides, squalene, petrolatum, and other water repelling compounds. Barrier creams should be applied to exposed skin two to three times per day.^12,37

ALLERGENS IN CONTACT DERMATITIS

Common Causes of Allergic Contact Dermatitis

ACD is caused by a variety of common chemicals and substances. Common causes include^{11,13,32,37,39-43}

• Excipients (propylene glycol, lanolin)
• Fragrances (limonene, linalool, fragrance mix 1, fragrance mix 2)
• Glues (acrylates)
• Hair dyes and hair care products (toluene-2,5-diamine sulfate, para-phenylenediamine, cetrimonium chloride, cetrimonium bromide)
• Latex (balloons)
• Medications (antibiotics, glucocorticoids, topical antihistamines)
• Metals (nickel, cobalt, and gold); commonly used in jewelry, buckles, claps, buttons, etc.
• Personal care products such as body washes, cosmetics, and skin care products (panthenol, chlorphenesin, parabens, balsam of Peru, colophony [rosin])
• Plants (Toxicodendron genus is the most common; includes poison ivy, poison oak, and poison sumac)
• Preservatives (benzisothiazolinone, formaldehyde, methylisothiazolinone, quaternium-15)
• Surfactants (cocamidopropyl betadine, decyl glucosides)

This list is not exhaustive but serves as a strong starting point for identifying products or substances that may trigger ACD. As new cases are reported, experts continue to identify potential allergens, reflecting evolving exposure patterns and improving diagnostic awareness. Notably, toluene-2,5-diamine sulfate, a chemical commonly used in hair dye, was named the 2025 Allergen of the Year, highlighting its emerging significance in contact dermatitis.³⁹

Common Causes of Irritant Contact Dermatitis

ICD can be caused by a range of common chemicals and substances. Common causes include^11,12,37,40

• Acids and alkalizing agents (sulfuric acid, sodium hydroxide, ammonia)
• Adhesives
• Bleach, detergents, and solvents (benzene, toluene)
• Cosmetics
• Dust
• Fertilizers and pesticides
• Hair products
• Oxidizing agents (sodium hypochloride)
• Paints and varnishes
• Perfumes
• Personal care products
• Plant parts (thorns)
• Plastics
• Rubber gloves
• Soap
• Water

Pharmacy staff should recognize that certain products, such as hair and personal care items, can cause both ACD and ICD reactions. However, the underlying mechanisms and nature of the reactions differ between the two conditions.

ALLERGEN ALTERNATIVES

Once an allergen has been identified, the most effective management strategy is avoidance. Because many ingredients appear under multiple names, careful review of product labels is essential. For example, balsam of Peru has several names including, but not limited to, Balsamum peruvianim, Black balsam, China oil, Indian balsam, Myroxylon pereirae Klotzsch resin, Myroxylon pereirae Klotzsch oil, and Toluifera Pereira balsam.⁴⁴

Patients may need guidance selecting products that provide the desired symptom relief while avoiding their allergens. Many items contain suitable substitute ingredients and pharmacy staff can support patients by reviewing product labels for potential allergens.

For example, toluene-2,5-diamine sulfate is frequently used in hair dyes as a primary intermediate (main reactive dye precursor).⁴⁵ An alternative to this chemical is paraphenylenediamine.³⁹ Other strategies include replacing nickel-containing jewelry with sterling silver or titanium; selecting products preserved with phenoxyethanol or benzyl alcohol instead of chlorphenesin or parabens; choosing formulations that minimize preservatives through plant-derived alternatives or hydrosols; and opting for fragrance-free products to avoid balsam of Peru.^46,47

It is also important that pharmacy staff understand various terminology used to describe products that would be better suited for patients with allergies. Currently, no Food and Drug Administration regulated definition for the term “hypoallergenic” exists.⁴⁸ Therefore, terms such as “fragrance-free,” “noncomedogenic,” and “dermatologist-tested” are indicators of products that may be better suited for patients with allergies. Pharmacists and pharmacy technicians should notify patients that products with these terms may be more expensive. These products are often placed on lower shelves as they tend to sell slower compared to other popular, branded items.

Additionally, pharmacy staff can recommend swatch testing new products before use to minimize risk of a reaction. Patients can apply a quarter-sized amount of the new product on a spot of their skin where the product won’t be washed away or rubbed off, such as the underside of the arm or the bend of the elbow. Patients should follow the instructions of the product to determine how long the product would normally stay on the skin (if the product [e.g., a cleanser] has no specific instructions, leave on the skin for five minutes). The product should be applied to this test spot twice daily for seven to ten days. If there is no reaction after this period, the patient can safely use the new product.⁴⁹

Common Allergen-Free Over-the-Counter Products

Finding allergen-free products or brands can be tricky, however online resources can alleviate this burden.

One helpful resource is the Contact Allergen Management Program (CAMP) created by the ACDS. CAMP is a web-based tool designed to help patients manage ACD and find personal care products that are safe for them to use. However, CAMP is an exclusive tool for ACDS members and their patients, so access may be limited for some healthcare providers.

In addition to using this resource, pharmacists and pharmacy technicians should counsel patients to always read and scrutinize product labels. One tool to navigate product labels and ingredients is skinsafeproducts.com. This website allows patients, providers, and pharmacy teams to scan barcodes or search products to determine if they contain ingredients a patient would react to. It’s important to note this website does not have a filter for every possible allergen.

For example, consider Alvin, a 35-year-old man allergic to parabens and various fragrance mixes. He asks for help finding an aftershave and body lotion. Using the SkinSAFE website (skinsafeproducts.com) you identify that “Clubman Pinaud Reserve Aftershave, Whiskey Woods” is paraben-free and “Minimalist Body Lotion, Niacinamide 0.5%” is fragrance-free.

Pharmacy staff should always consider recommending a switch in product. For instance, if a patient has a small cut, pharmacists and pharmacy technicians can recommend petrolatum over bacitracin. Bacitracin was named the Contact Allergen of the Year for 2003 by the ACDS and patients have an increased risk of reaction with this product.⁵⁰ Pharmacy staff have the unique opportunity to help patients make safe and informed product changes.

One thing to keep in mind is that formulations change! A product may be safe the first time a person uses it, but it may not be safe the next time. It’s essential to ensure healthcare providers and pharmacy staff always verify the accuracy of all information they provide to each unique patient!

CONCLUSION

Now that you’ve reviewed the key concepts of contact dermatitis, let’s revisit our opening case.

To start, ask the patient clarifying questions such as, “When did the rash appear?”, “Have you done anything out of the ordinary recently?”, and “Has the child started any new products?” You then discover the family went camping over the weekend. When this information is combined with the child’s current symptoms, poison ivy is the likely culprit. Suggesting OTC products such as calamine lotion (for lesions) and a cold compress or antihistamine (for itching) can help the manage the patient’s symptoms. However, it’s important to advise the mother to bring her child to the pediatrician if symptoms persist or worsen.

By identifying likely triggers, recommending appropriate symptomatic relief, and knowing when to refer the patient to seek additional medical attention, pharmacy staff can improve outcomes for patients with contact dermatitis.

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