Mixed Topics

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

The genus of flowering plants commonly known as prickly pear cacti (Opuntia) or sabra are native to the Americas but are naturalized in many parts of the world, particularly southwest Asia and Sicily, Italy, where they are grown commercially and commonly are seen growing on rocky hillsides. (Figure 1). A prickly pear cactus has paddles that represent modified stems, and the spines are modified leaves (Figure 2). Its bright red or yellow flowers, dark-red fruit, low water requirement, and adaptability to poor-quality soil make it an attractive plant for landscaping and an important agricultural crop in many parts of the world, including the United States, Mexico, and Southern Europe. The prickly pear fruit is tasty but loaded with seeds and often is eaten fresh or used to make jam. The paddles are sometimes cut into strips, breaded or battered, and fried. The spines are easily embedded in skin and are an important cause of dermatitis.

Identifying Features

Opuntia species are found in both warm and temperate zones and grow well in arid climates. Like other cacti, they are distinguished by their water-hoarding stems and glochids (needlelike modified leaves). In prickly pears, the stems flatten to leaflike paddles that alternate in direction. Photosynthesis occurs in the stem tissues, while modified leaves (spines) are purely for defense against predators and unsuspecting humans. Opuntia species are easily identified by their broad flattened stems and dark-red fruits, both of which bear glochids (Figures 3-5).

Dermatologic Implications of Prickly Pear Injury

Prickly pear spines are very small, sharp, and difficult to see. They embed in the skin in great numbers when the plant or its fruit are handled by unsuspecting humans and have a tendency to burrow into soft tissue and underlying structures. It is very difficult to remove prickly pear spines with forceps, and attempts to do so often drive them deeper into the skin.¹ Better results are obtained by tape stripping or using water-activated cosmetic pore strips.

Cactus spine injuries may lead to mucoceles of the oral mucosa and sinuses, especially in individuals who attempt to bite into the fruit without first scorching the spines with a blow torch.² Inflammatory responses to the embedded spines are common and often result in prolonged erythematous inflammatory papules at sites of injury. Recalcitrant dermatitis and edema of underlying tissues typically occur near the point of entry of a prickly pear spine and extend to areas where the spine migrates.^3,4 Individuals who casually brush up against the plant may not be aware that they have been inoculated with the spines and may not relate the prior accidental contact with the onset of erythematous papules and edema that occurs days later. Biopsy may reveal the prickly pear spines or a granulomatous reaction pattern within the dermis. Linear patterns of necrosis surrounded by palisading histiocytes may be noted, representing the tract of the inoculation injury.

If identified in tissue, glochids are variably refractile and measure 40 to 70 µm in diameter. Glochids initiate a delayed-type hypersensitivity and foreign body response. A T-helper 1 cytokine signal is typical, and there may be a secondary influx of neutrophils, but tissue eosinophilia is uncommon. Systemic inflammation also has been reported, including eosinophilic cholangitis without biliary stricture⁵ and septic and aseptic arthritis near the site of leaf puncture and at distant sites.^6,7 Allergic contact dermatitis has been reported due to contact with the fruit of the plant and can be confirmed by patch testing.^8,9

Potential Medicinal Benefits

Prickly pear cacti have shown potential medicinal properties. While the spines may produce intense inflammation when embedded in the skin, extracts of the fruit and leaf juices have shown anti-inflammatory properties. Various vesicle and polysaccharide extracts of Opuntia cacti have been shown to reduce environmental and chemical stressors associated with open wounds.^10-12 Preclinical studies also have suggested that they could be helpful in speeding the wound-healing process when applied topically. Opuntia species also have shown promise in reducing hyperpigmentation after topical application.¹³ Preliminary data in animals also have suggested that oral administration of the fruit may slow kidney deterioration in patients with diabetes.¹⁴ Following tissue penetration by the spines, Opuntia extracts have demonstrated the ability to prevent calcium deposition in soft tissue.¹⁵ Similar preliminary data also have suggested that Opuntia extracts may reduce toxicity from cadmium, chromium, methotrexate, and acetaminophen.^16-19 Extracts from the peel of the red pitaya (Hylocereus polyrhizus), a closely related cactus, have been studied for their potential to prevent the advance of alcohol-associated liver disease, suggesting that studies evaluating the benefits of prickly pear cacti and related species may be worth pursuing.²⁰

Final Thoughts

Prickly pear cacti have the potential to act as both friend and foe. The flowers and fruit are beautiful, and the plant is well adapted to xeriscape gardens in areas under perpetual water restriction. The fruit and flesh are edible if handled properly, and prickly pear jam is delicious. While the spines are capable of inflicting local injury and migrating to internal sites, causing arthritis and other deep tissue injury, extracts of the fruit and stems have potential uses for their anti-inflammatory effects and ability to protect against toxic injury. Further studies are needed to evaluate the therapeutic potential of Opuntia and related species.

The genus of flowering plants commonly known as prickly pear cacti (Opuntia) or sabra are native to the Americas but are naturalized in many parts of the world, particularly southwest Asia and Sicily, Italy, where they are grown commercially and commonly are seen growing on rocky hillsides. (Figure 1). A prickly pear cactus has paddles that represent modified stems, and the spines are modified leaves (Figure 2). Its bright red or yellow flowers, dark-red fruit, low water requirement, and adaptability to poor-quality soil make it an attractive plant for landscaping and an important agricultural crop in many parts of the world, including the United States, Mexico, and Southern Europe. The prickly pear fruit is tasty but loaded with seeds and often is eaten fresh or used to make jam. The paddles are sometimes cut into strips, breaded or battered, and fried. The spines are easily embedded in skin and are an important cause of dermatitis.

Identifying Features

Opuntia species are found in both warm and temperate zones and grow well in arid climates. Like other cacti, they are distinguished by their water-hoarding stems and glochids (needlelike modified leaves). In prickly pears, the stems flatten to leaflike paddles that alternate in direction. Photosynthesis occurs in the stem tissues, while modified leaves (spines) are purely for defense against predators and unsuspecting humans. Opuntia species are easily identified by their broad flattened stems and dark-red fruits, both of which bear glochids (Figures 3-5).

Dermatologic Implications of Prickly Pear Injury

Prickly pear spines are very small, sharp, and difficult to see. They embed in the skin in great numbers when the plant or its fruit are handled by unsuspecting humans and have a tendency to burrow into soft tissue and underlying structures. It is very difficult to remove prickly pear spines with forceps, and attempts to do so often drive them deeper into the skin.¹ Better results are obtained by tape stripping or using water-activated cosmetic pore strips.

Cactus spine injuries may lead to mucoceles of the oral mucosa and sinuses, especially in individuals who attempt to bite into the fruit without first scorching the spines with a blow torch.² Inflammatory responses to the embedded spines are common and often result in prolonged erythematous inflammatory papules at sites of injury. Recalcitrant dermatitis and edema of underlying tissues typically occur near the point of entry of a prickly pear spine and extend to areas where the spine migrates.^3,4 Individuals who casually brush up against the plant may not be aware that they have been inoculated with the spines and may not relate the prior accidental contact with the onset of erythematous papules and edema that occurs days later. Biopsy may reveal the prickly pear spines or a granulomatous reaction pattern within the dermis. Linear patterns of necrosis surrounded by palisading histiocytes may be noted, representing the tract of the inoculation injury.

If identified in tissue, glochids are variably refractile and measure 40 to 70 µm in diameter. Glochids initiate a delayed-type hypersensitivity and foreign body response. A T-helper 1 cytokine signal is typical, and there may be a secondary influx of neutrophils, but tissue eosinophilia is uncommon. Systemic inflammation also has been reported, including eosinophilic cholangitis without biliary stricture⁵ and septic and aseptic arthritis near the site of leaf puncture and at distant sites.^6,7 Allergic contact dermatitis has been reported due to contact with the fruit of the plant and can be confirmed by patch testing.^8,9

Potential Medicinal Benefits

Prickly pear cacti have shown potential medicinal properties. While the spines may produce intense inflammation when embedded in the skin, extracts of the fruit and leaf juices have shown anti-inflammatory properties. Various vesicle and polysaccharide extracts of Opuntia cacti have been shown to reduce environmental and chemical stressors associated with open wounds.^10-12 Preclinical studies also have suggested that they could be helpful in speeding the wound-healing process when applied topically. Opuntia species also have shown promise in reducing hyperpigmentation after topical application.¹³ Preliminary data in animals also have suggested that oral administration of the fruit may slow kidney deterioration in patients with diabetes.¹⁴ Following tissue penetration by the spines, Opuntia extracts have demonstrated the ability to prevent calcium deposition in soft tissue.¹⁵ Similar preliminary data also have suggested that Opuntia extracts may reduce toxicity from cadmium, chromium, methotrexate, and acetaminophen.^16-19 Extracts from the peel of the red pitaya (Hylocereus polyrhizus), a closely related cactus, have been studied for their potential to prevent the advance of alcohol-associated liver disease, suggesting that studies evaluating the benefits of prickly pear cacti and related species may be worth pursuing.²⁰

Final Thoughts

Prickly pear cacti have the potential to act as both friend and foe. The flowers and fruit are beautiful, and the plant is well adapted to xeriscape gardens in areas under perpetual water restriction. The fruit and flesh are edible if handled properly, and prickly pear jam is delicious. While the spines are capable of inflicting local injury and migrating to internal sites, causing arthritis and other deep tissue injury, extracts of the fruit and stems have potential uses for their anti-inflammatory effects and ability to protect against toxic injury. Further studies are needed to evaluate the therapeutic potential of Opuntia and related species.

The genus of flowering plants commonly known as prickly pear cacti (Opuntia) or sabra are native to the Americas but are naturalized in many parts of the world, particularly southwest Asia and Sicily, Italy, where they are grown commercially and commonly are seen growing on rocky hillsides. (Figure 1). A prickly pear cactus has paddles that represent modified stems, and the spines are modified leaves (Figure 2). Its bright red or yellow flowers, dark-red fruit, low water requirement, and adaptability to poor-quality soil make it an attractive plant for landscaping and an important agricultural crop in many parts of the world, including the United States, Mexico, and Southern Europe. The prickly pear fruit is tasty but loaded with seeds and often is eaten fresh or used to make jam. The paddles are sometimes cut into strips, breaded or battered, and fried. The spines are easily embedded in skin and are an important cause of dermatitis.

Identifying Features

Opuntia species are found in both warm and temperate zones and grow well in arid climates. Like other cacti, they are distinguished by their water-hoarding stems and glochids (needlelike modified leaves). In prickly pears, the stems flatten to leaflike paddles that alternate in direction. Photosynthesis occurs in the stem tissues, while modified leaves (spines) are purely for defense against predators and unsuspecting humans. Opuntia species are easily identified by their broad flattened stems and dark-red fruits, both of which bear glochids (Figures 3-5).

Dermatologic Implications of Prickly Pear Injury

Prickly pear spines are very small, sharp, and difficult to see. They embed in the skin in great numbers when the plant or its fruit are handled by unsuspecting humans and have a tendency to burrow into soft tissue and underlying structures. It is very difficult to remove prickly pear spines with forceps, and attempts to do so often drive them deeper into the skin.¹ Better results are obtained by tape stripping or using water-activated cosmetic pore strips.

Cactus spine injuries may lead to mucoceles of the oral mucosa and sinuses, especially in individuals who attempt to bite into the fruit without first scorching the spines with a blow torch.² Inflammatory responses to the embedded spines are common and often result in prolonged erythematous inflammatory papules at sites of injury. Recalcitrant dermatitis and edema of underlying tissues typically occur near the point of entry of a prickly pear spine and extend to areas where the spine migrates.^3,4 Individuals who casually brush up against the plant may not be aware that they have been inoculated with the spines and may not relate the prior accidental contact with the onset of erythematous papules and edema that occurs days later. Biopsy may reveal the prickly pear spines or a granulomatous reaction pattern within the dermis. Linear patterns of necrosis surrounded by palisading histiocytes may be noted, representing the tract of the inoculation injury.

If identified in tissue, glochids are variably refractile and measure 40 to 70 µm in diameter. Glochids initiate a delayed-type hypersensitivity and foreign body response. A T-helper 1 cytokine signal is typical, and there may be a secondary influx of neutrophils, but tissue eosinophilia is uncommon. Systemic inflammation also has been reported, including eosinophilic cholangitis without biliary stricture⁵ and septic and aseptic arthritis near the site of leaf puncture and at distant sites.^6,7 Allergic contact dermatitis has been reported due to contact with the fruit of the plant and can be confirmed by patch testing.^8,9

Potential Medicinal Benefits

Prickly pear cacti have shown potential medicinal properties. While the spines may produce intense inflammation when embedded in the skin, extracts of the fruit and leaf juices have shown anti-inflammatory properties. Various vesicle and polysaccharide extracts of Opuntia cacti have been shown to reduce environmental and chemical stressors associated with open wounds.^10-12 Preclinical studies also have suggested that they could be helpful in speeding the wound-healing process when applied topically. Opuntia species also have shown promise in reducing hyperpigmentation after topical application.¹³ Preliminary data in animals also have suggested that oral administration of the fruit may slow kidney deterioration in patients with diabetes.¹⁴ Following tissue penetration by the spines, Opuntia extracts have demonstrated the ability to prevent calcium deposition in soft tissue.¹⁵ Similar preliminary data also have suggested that Opuntia extracts may reduce toxicity from cadmium, chromium, methotrexate, and acetaminophen.^16-19 Extracts from the peel of the red pitaya (Hylocereus polyrhizus), a closely related cactus, have been studied for their potential to prevent the advance of alcohol-associated liver disease, suggesting that studies evaluating the benefits of prickly pear cacti and related species may be worth pursuing.²⁰

Final Thoughts

Prickly pear cacti have the potential to act as both friend and foe. The flowers and fruit are beautiful, and the plant is well adapted to xeriscape gardens in areas under perpetual water restriction. The fruit and flesh are edible if handled properly, and prickly pear jam is delicious. While the spines are capable of inflicting local injury and migrating to internal sites, causing arthritis and other deep tissue injury, extracts of the fruit and stems have potential uses for their anti-inflammatory effects and ability to protect against toxic injury. Further studies are needed to evaluate the therapeutic potential of Opuntia and related species.

Dermatology trainees are no strangers to standardized examinations that assess basic science and medical knowledge, from the Medical College Admission Test and the National Board of Medical Examiners Subject Examinations to the United States Medical Licensing Examination series (I know, cue the collective flashbacks!). As a dermatology resident, you will complete a series of 6 examinations, culminating with the final APPLIED Exam, which assesses a trainee's ability to apply therapeutic knowledge and clinical reasoning in scenarios relevant to the practice of general dermatology.¹ This article features high-yield tips and study resources alongside test-day strategies to help you perform at your best.

The Path to Board Certification for Dermatology Trainees

After years of dedicated study in medical school, navigating the demanding match process, and completing your intern year, you have finally made it to dermatology! With the USMLE Step 3 out of the way, you are now officially able to trade in electrocardiograms for Kodachromes and dermoscopy. As a dermatology trainee, you will complete the American Board of Dermatology (ABD) Certification Pathway—a staged evaluation beginning with a BASIC Exam for first-year residents, which covers dermatology fundamentals and is proctored at your home institution.¹ This exam is solely for informational purposes, and ultimately no minimum score is required for certification purposes. Subsequently, second- and third-year residents sit for 4 CORE Exam modules assessing advanced knowledge of the major clinical areas of the specialty: medical dermatology, surgical dermatology, pediatric dermatology, and dermatopathology. These exams consist of 75 to 100 multiple-choice questions per each 2-hour module and are administered either online in a private setting, via a secure online proctoring system, or at an approved testing center. The APPLIED Exam is the final component of the pathway and prioritizes clinical acumen and judgement. This 8-hour, 200-question exam is offered exclusively in person at approved testing centers to residents who have passed all 4 compulsory CORE modules and completed residency training. There is a 20-minute break between sections 1 and 2, a 60-minute break between sections 2 and 3, and a 20-minute break between sections 3 and 4.¹ Following successful completion of the ABD Certification Pathway, dermatologists maintain board certification through quarterly CertLink questions, which you must complete at least 3 quarters of each year, and regular completion of focused practice improvement modules every 5 years. Additionally, one must maintain a full and unrestricted medical license in the United States or Canada and pay an annual fee of $150.

High-Yield Study Resources and Exam Preparation Strategies

Growing up, I was taught that proper preparation prevents poor performance. This principle holds particularly true when approaching the ABD Certification Pathway. Before diving into high-yield study resources and comprehensive exam preparation strategies, here are some big-picture essentials you need to know:

• Your residency program covers the fee for the BASIC Exam, but the CORE and APPLIED Exams are out-of-pocket expenses. As of 2026, you should plan to budget $2450 ($200 for 4 CORE module attempts and $2250 for the APPLIED Exam) for all 5 exams.²
• Testing center space is limited for each test date. While the ABD offers CORE Exams 3 times annually in 2-week windows (Winter [February], Summer [July], and Fall [October/November]), the APPLIED Exam is only given once per year. For the best chance of getting your preferred date, be sure to register as early as possible (especially if you live and train in a city with limited testing sites).
• After you have successfully passed your first CORE Exam module, you may take up to 3 in one sitting. When taking multiple modules consecutively on the same day, a 15-minute break is configured between each module.

Study Resources

When it comes to studying, there are more resources available than you will have time to explore; therefore, it is crucial to prioritize the ones that best match your learning style. Whether you retain information through visuals, audio, reading comprehension, practice questions, or spaced repetition, there are complimentary and paid high-yield tools designed to support how you learn and make the most of your valuable time outside of clinical responsibilities (Table). Furthermore, there are numerous discipline-specific textbooks and resources encompassing dermatopathology, dermoscopy, trichology, pediatric dermatology, surgical dermatology, cosmetic dermatology, and skin of color.^11-13 As a trainee, you also have access to the American Academy of Dermatology’s Learning Center (https://learning.aad.org/Catalogue/AAD-Learning-Center) featuring the Question of the Week series, Board Prep Plus question bank, Dialogues in Dermatology podcast, and continuing medical education articles. Additionally, board review sessions occur at many local, regional, and national dermatology conferences annually.

Exam Preparation Strategy

A comprehensive preparation strategy should begin during your first year of residency and appropriately intensify in the months leading up to the BASIC, CORE, and APPLIED Exams. Ultimately, active learning is ongoing, and your daily clinical work combined with program-sanctioned didactics, journal reading, and conference attendance comprise your framework. I often found it helpful to spend 30 to 60 minutes after clinic each evening reviewing high-yield or interesting cases from the day, as our patients are our greatest teachers. To reinforce key concepts, I used a combination of premade Anki decks¹⁴ and custom flashcards for topics that required rote memorization and spaced repetition. Podcasts such as Cutaneous Miscellaneous, The Grenz Zone, and Dermasphere became valuable learning tools that I incorporated into my commutes and long runs. I also enjoyed listening to the Derm In-Review audio study guide.¹⁹ Early in residency, I also created a digital notebook on OneNote (https://onenote.cloud.microsoft/en-us/)—organized by postgraduate year and subject—to consolidate notes and procedural pearls. As a fellow, I still use this note-taking system to organize notes from laser and energy-based device trainings and catalogue high-yield conference takeaways. Finally, task management applications can further help you achieve your study goals by organizing assignments, setting deadlines, and breaking larger objectives into manageable steps, making it easier to stay focused and on track.

Test Day Strategies

After sitting for many standardized examinations on the journey to dermatology residency, I am certain that you have cultivated your own reliable test day rituals and strategies; however, if you are looking for additional ones to add to your toolbox, here are a few that helped me stay calm, focused, and in the zone throughout my time in residency.

The Day Before the Test

• Secure your test-day snacks and preferred form of hydration. I am a fan of cheese sticks for protein and fruit for vitamins and antioxidants. Additionally, I always bring something salty and something sweet (usually chocolate or sour gummy snacks) just in case I happen to get a specific craving on test day.
• Make sure you have valid forms of identification in accordance with the test center policy.¹⁶
• Confirm your exam location and time. Testing center details can be found on the Pearson Vue portal,¹⁶ which is easily accessed via the “ABD Tools” tab on the official ABD website (https://www.abderm.org/). Additionally, the exam location, time, and directions to the test center are located in your Pearson Vue confirmation email.
• Trust that you are prepared. Try your best to avoid last-minute cramming and prioritize a good night’s sleep.

The Day of the Test

• Center yourself before the exam. I prefer to start my morning with a run to clear my mind; however, you can also consider other mindfulness exercises such as deep breathing or positive grounding affirmations.
• Arrive early and dress in layers. You never know if the testing location will run warm or cold.
• Pace yourself, trust your gut instincts, and do not be afraid to mark and move on if you get stuck on a particular question. Ultimately, make sure you answer every question, as you will not have points deducted for guessing.
• Make sure to plan something you are excited about for after the exam! That may mean celebrating with co-residents, spending time with loved ones, or just relaxing on the couch and finally catching up on that show you have been meaning to watch for weeks but have not had time for because you have been focused on studying (yes, we all have that one show).

Final Thoughts

While this article is not comprehensive of all ABD Certification Pathway preparation materials and resources, I hope that you will find it helpful along your residency journey. Starting dermatology residency can feel like drinking from a firehose: there is an overwhelming volume of new information, unfamiliar terminology, and a demanding workflow that varies considerably from that of intern year.¹⁷ As a resident, it is vital to prioritize your mental health and well-being, as the journey is a marathon rather than a sprint.¹⁸

Never forget that you have already come this far; trust in your journey and remember what is meant for you will not miss you. Juggling 6 exams during residency alongside clinical and personal responsibilities is no small feat. With a strong study plan and smart test-day strategies, I have no doubt you will become a board-certified dermatologist!

Dermatology trainees are no strangers to standardized examinations that assess basic science and medical knowledge, from the Medical College Admission Test and the National Board of Medical Examiners Subject Examinations to the United States Medical Licensing Examination series (I know, cue the collective flashbacks!). As a dermatology resident, you will complete a series of 6 examinations, culminating with the final APPLIED Exam, which assesses a trainee's ability to apply therapeutic knowledge and clinical reasoning in scenarios relevant to the practice of general dermatology.¹ This article features high-yield tips and study resources alongside test-day strategies to help you perform at your best.

The Path to Board Certification for Dermatology Trainees

After years of dedicated study in medical school, navigating the demanding match process, and completing your intern year, you have finally made it to dermatology! With the USMLE Step 3 out of the way, you are now officially able to trade in electrocardiograms for Kodachromes and dermoscopy. As a dermatology trainee, you will complete the American Board of Dermatology (ABD) Certification Pathway—a staged evaluation beginning with a BASIC Exam for first-year residents, which covers dermatology fundamentals and is proctored at your home institution.¹ This exam is solely for informational purposes, and ultimately no minimum score is required for certification purposes. Subsequently, second- and third-year residents sit for 4 CORE Exam modules assessing advanced knowledge of the major clinical areas of the specialty: medical dermatology, surgical dermatology, pediatric dermatology, and dermatopathology. These exams consist of 75 to 100 multiple-choice questions per each 2-hour module and are administered either online in a private setting, via a secure online proctoring system, or at an approved testing center. The APPLIED Exam is the final component of the pathway and prioritizes clinical acumen and judgement. This 8-hour, 200-question exam is offered exclusively in person at approved testing centers to residents who have passed all 4 compulsory CORE modules and completed residency training. There is a 20-minute break between sections 1 and 2, a 60-minute break between sections 2 and 3, and a 20-minute break between sections 3 and 4.¹ Following successful completion of the ABD Certification Pathway, dermatologists maintain board certification through quarterly CertLink questions, which you must complete at least 3 quarters of each year, and regular completion of focused practice improvement modules every 5 years. Additionally, one must maintain a full and unrestricted medical license in the United States or Canada and pay an annual fee of $150.

High-Yield Study Resources and Exam Preparation Strategies

Growing up, I was taught that proper preparation prevents poor performance. This principle holds particularly true when approaching the ABD Certification Pathway. Before diving into high-yield study resources and comprehensive exam preparation strategies, here are some big-picture essentials you need to know:

• Your residency program covers the fee for the BASIC Exam, but the CORE and APPLIED Exams are out-of-pocket expenses. As of 2026, you should plan to budget $2450 ($200 for 4 CORE module attempts and $2250 for the APPLIED Exam) for all 5 exams.²
• Testing center space is limited for each test date. While the ABD offers CORE Exams 3 times annually in 2-week windows (Winter [February], Summer [July], and Fall [October/November]), the APPLIED Exam is only given once per year. For the best chance of getting your preferred date, be sure to register as early as possible (especially if you live and train in a city with limited testing sites).
• After you have successfully passed your first CORE Exam module, you may take up to 3 in one sitting. When taking multiple modules consecutively on the same day, a 15-minute break is configured between each module.

Study Resources

When it comes to studying, there are more resources available than you will have time to explore; therefore, it is crucial to prioritize the ones that best match your learning style. Whether you retain information through visuals, audio, reading comprehension, practice questions, or spaced repetition, there are complimentary and paid high-yield tools designed to support how you learn and make the most of your valuable time outside of clinical responsibilities (Table). Furthermore, there are numerous discipline-specific textbooks and resources encompassing dermatopathology, dermoscopy, trichology, pediatric dermatology, surgical dermatology, cosmetic dermatology, and skin of color.^11-13 As a trainee, you also have access to the American Academy of Dermatology’s Learning Center (https://learning.aad.org/Catalogue/AAD-Learning-Center) featuring the Question of the Week series, Board Prep Plus question bank, Dialogues in Dermatology podcast, and continuing medical education articles. Additionally, board review sessions occur at many local, regional, and national dermatology conferences annually.

Exam Preparation Strategy

A comprehensive preparation strategy should begin during your first year of residency and appropriately intensify in the months leading up to the BASIC, CORE, and APPLIED Exams. Ultimately, active learning is ongoing, and your daily clinical work combined with program-sanctioned didactics, journal reading, and conference attendance comprise your framework. I often found it helpful to spend 30 to 60 minutes after clinic each evening reviewing high-yield or interesting cases from the day, as our patients are our greatest teachers. To reinforce key concepts, I used a combination of premade Anki decks¹⁴ and custom flashcards for topics that required rote memorization and spaced repetition. Podcasts such as Cutaneous Miscellaneous, The Grenz Zone, and Dermasphere became valuable learning tools that I incorporated into my commutes and long runs. I also enjoyed listening to the Derm In-Review audio study guide.¹⁹ Early in residency, I also created a digital notebook on OneNote (https://onenote.cloud.microsoft/en-us/)—organized by postgraduate year and subject—to consolidate notes and procedural pearls. As a fellow, I still use this note-taking system to organize notes from laser and energy-based device trainings and catalogue high-yield conference takeaways. Finally, task management applications can further help you achieve your study goals by organizing assignments, setting deadlines, and breaking larger objectives into manageable steps, making it easier to stay focused and on track.

Test Day Strategies

After sitting for many standardized examinations on the journey to dermatology residency, I am certain that you have cultivated your own reliable test day rituals and strategies; however, if you are looking for additional ones to add to your toolbox, here are a few that helped me stay calm, focused, and in the zone throughout my time in residency.

The Day Before the Test

• Secure your test-day snacks and preferred form of hydration. I am a fan of cheese sticks for protein and fruit for vitamins and antioxidants. Additionally, I always bring something salty and something sweet (usually chocolate or sour gummy snacks) just in case I happen to get a specific craving on test day.
• Make sure you have valid forms of identification in accordance with the test center policy.¹⁶
• Confirm your exam location and time. Testing center details can be found on the Pearson Vue portal,¹⁶ which is easily accessed via the “ABD Tools” tab on the official ABD website (https://www.abderm.org/). Additionally, the exam location, time, and directions to the test center are located in your Pearson Vue confirmation email.
• Trust that you are prepared. Try your best to avoid last-minute cramming and prioritize a good night’s sleep.

The Day of the Test

• Center yourself before the exam. I prefer to start my morning with a run to clear my mind; however, you can also consider other mindfulness exercises such as deep breathing or positive grounding affirmations.
• Arrive early and dress in layers. You never know if the testing location will run warm or cold.
• Pace yourself, trust your gut instincts, and do not be afraid to mark and move on if you get stuck on a particular question. Ultimately, make sure you answer every question, as you will not have points deducted for guessing.
• Make sure to plan something you are excited about for after the exam! That may mean celebrating with co-residents, spending time with loved ones, or just relaxing on the couch and finally catching up on that show you have been meaning to watch for weeks but have not had time for because you have been focused on studying (yes, we all have that one show).

Final Thoughts

While this article is not comprehensive of all ABD Certification Pathway preparation materials and resources, I hope that you will find it helpful along your residency journey. Starting dermatology residency can feel like drinking from a firehose: there is an overwhelming volume of new information, unfamiliar terminology, and a demanding workflow that varies considerably from that of intern year.¹⁷ As a resident, it is vital to prioritize your mental health and well-being, as the journey is a marathon rather than a sprint.¹⁸

Never forget that you have already come this far; trust in your journey and remember what is meant for you will not miss you. Juggling 6 exams during residency alongside clinical and personal responsibilities is no small feat. With a strong study plan and smart test-day strategies, I have no doubt you will become a board-certified dermatologist!

Dermatology trainees are no strangers to standardized examinations that assess basic science and medical knowledge, from the Medical College Admission Test and the National Board of Medical Examiners Subject Examinations to the United States Medical Licensing Examination series (I know, cue the collective flashbacks!). As a dermatology resident, you will complete a series of 6 examinations, culminating with the final APPLIED Exam, which assesses a trainee's ability to apply therapeutic knowledge and clinical reasoning in scenarios relevant to the practice of general dermatology.¹ This article features high-yield tips and study resources alongside test-day strategies to help you perform at your best.

The Path to Board Certification for Dermatology Trainees

After years of dedicated study in medical school, navigating the demanding match process, and completing your intern year, you have finally made it to dermatology! With the USMLE Step 3 out of the way, you are now officially able to trade in electrocardiograms for Kodachromes and dermoscopy. As a dermatology trainee, you will complete the American Board of Dermatology (ABD) Certification Pathway—a staged evaluation beginning with a BASIC Exam for first-year residents, which covers dermatology fundamentals and is proctored at your home institution.¹ This exam is solely for informational purposes, and ultimately no minimum score is required for certification purposes. Subsequently, second- and third-year residents sit for 4 CORE Exam modules assessing advanced knowledge of the major clinical areas of the specialty: medical dermatology, surgical dermatology, pediatric dermatology, and dermatopathology. These exams consist of 75 to 100 multiple-choice questions per each 2-hour module and are administered either online in a private setting, via a secure online proctoring system, or at an approved testing center. The APPLIED Exam is the final component of the pathway and prioritizes clinical acumen and judgement. This 8-hour, 200-question exam is offered exclusively in person at approved testing centers to residents who have passed all 4 compulsory CORE modules and completed residency training. There is a 20-minute break between sections 1 and 2, a 60-minute break between sections 2 and 3, and a 20-minute break between sections 3 and 4.¹ Following successful completion of the ABD Certification Pathway, dermatologists maintain board certification through quarterly CertLink questions, which you must complete at least 3 quarters of each year, and regular completion of focused practice improvement modules every 5 years. Additionally, one must maintain a full and unrestricted medical license in the United States or Canada and pay an annual fee of $150.

High-Yield Study Resources and Exam Preparation Strategies

Growing up, I was taught that proper preparation prevents poor performance. This principle holds particularly true when approaching the ABD Certification Pathway. Before diving into high-yield study resources and comprehensive exam preparation strategies, here are some big-picture essentials you need to know:

• Your residency program covers the fee for the BASIC Exam, but the CORE and APPLIED Exams are out-of-pocket expenses. As of 2026, you should plan to budget $2450 ($200 for 4 CORE module attempts and $2250 for the APPLIED Exam) for all 5 exams.²
• Testing center space is limited for each test date. While the ABD offers CORE Exams 3 times annually in 2-week windows (Winter [February], Summer [July], and Fall [October/November]), the APPLIED Exam is only given once per year. For the best chance of getting your preferred date, be sure to register as early as possible (especially if you live and train in a city with limited testing sites).
• After you have successfully passed your first CORE Exam module, you may take up to 3 in one sitting. When taking multiple modules consecutively on the same day, a 15-minute break is configured between each module.

Study Resources

When it comes to studying, there are more resources available than you will have time to explore; therefore, it is crucial to prioritize the ones that best match your learning style. Whether you retain information through visuals, audio, reading comprehension, practice questions, or spaced repetition, there are complimentary and paid high-yield tools designed to support how you learn and make the most of your valuable time outside of clinical responsibilities (Table). Furthermore, there are numerous discipline-specific textbooks and resources encompassing dermatopathology, dermoscopy, trichology, pediatric dermatology, surgical dermatology, cosmetic dermatology, and skin of color.^11-13 As a trainee, you also have access to the American Academy of Dermatology’s Learning Center (https://learning.aad.org/Catalogue/AAD-Learning-Center) featuring the Question of the Week series, Board Prep Plus question bank, Dialogues in Dermatology podcast, and continuing medical education articles. Additionally, board review sessions occur at many local, regional, and national dermatology conferences annually.

Exam Preparation Strategy

A comprehensive preparation strategy should begin during your first year of residency and appropriately intensify in the months leading up to the BASIC, CORE, and APPLIED Exams. Ultimately, active learning is ongoing, and your daily clinical work combined with program-sanctioned didactics, journal reading, and conference attendance comprise your framework. I often found it helpful to spend 30 to 60 minutes after clinic each evening reviewing high-yield or interesting cases from the day, as our patients are our greatest teachers. To reinforce key concepts, I used a combination of premade Anki decks¹⁴ and custom flashcards for topics that required rote memorization and spaced repetition. Podcasts such as Cutaneous Miscellaneous, The Grenz Zone, and Dermasphere became valuable learning tools that I incorporated into my commutes and long runs. I also enjoyed listening to the Derm In-Review audio study guide.¹⁹ Early in residency, I also created a digital notebook on OneNote (https://onenote.cloud.microsoft/en-us/)—organized by postgraduate year and subject—to consolidate notes and procedural pearls. As a fellow, I still use this note-taking system to organize notes from laser and energy-based device trainings and catalogue high-yield conference takeaways. Finally, task management applications can further help you achieve your study goals by organizing assignments, setting deadlines, and breaking larger objectives into manageable steps, making it easier to stay focused and on track.

Test Day Strategies

After sitting for many standardized examinations on the journey to dermatology residency, I am certain that you have cultivated your own reliable test day rituals and strategies; however, if you are looking for additional ones to add to your toolbox, here are a few that helped me stay calm, focused, and in the zone throughout my time in residency.

The Day Before the Test

• Secure your test-day snacks and preferred form of hydration. I am a fan of cheese sticks for protein and fruit for vitamins and antioxidants. Additionally, I always bring something salty and something sweet (usually chocolate or sour gummy snacks) just in case I happen to get a specific craving on test day.
• Make sure you have valid forms of identification in accordance with the test center policy.¹⁶
• Confirm your exam location and time. Testing center details can be found on the Pearson Vue portal,¹⁶ which is easily accessed via the “ABD Tools” tab on the official ABD website (https://www.abderm.org/). Additionally, the exam location, time, and directions to the test center are located in your Pearson Vue confirmation email.
• Trust that you are prepared. Try your best to avoid last-minute cramming and prioritize a good night’s sleep.

The Day of the Test

• Center yourself before the exam. I prefer to start my morning with a run to clear my mind; however, you can also consider other mindfulness exercises such as deep breathing or positive grounding affirmations.
• Arrive early and dress in layers. You never know if the testing location will run warm or cold.
• Pace yourself, trust your gut instincts, and do not be afraid to mark and move on if you get stuck on a particular question. Ultimately, make sure you answer every question, as you will not have points deducted for guessing.
• Make sure to plan something you are excited about for after the exam! That may mean celebrating with co-residents, spending time with loved ones, or just relaxing on the couch and finally catching up on that show you have been meaning to watch for weeks but have not had time for because you have been focused on studying (yes, we all have that one show).

Final Thoughts

While this article is not comprehensive of all ABD Certification Pathway preparation materials and resources, I hope that you will find it helpful along your residency journey. Starting dermatology residency can feel like drinking from a firehose: there is an overwhelming volume of new information, unfamiliar terminology, and a demanding workflow that varies considerably from that of intern year.¹⁷ As a resident, it is vital to prioritize your mental health and well-being, as the journey is a marathon rather than a sprint.¹⁸

Never forget that you have already come this far; trust in your journey and remember what is meant for you will not miss you. Juggling 6 exams during residency alongside clinical and personal responsibilities is no small feat. With a strong study plan and smart test-day strategies, I have no doubt you will become a board-certified dermatologist!

Acne keloidalis nuchae (AKN) classically presents as chronic inflammation of the hair follicles on the occipital scalp/nape of the neck manifesting as papules and pustules that may progress to keloidlike scarring.¹ Photographs depicting the typical clinical presentation of AKN are shown in the Figure. In the literature, AKN has been described as primarily occurring in postpubertal males of African descent.² Despite its similar name, AKN is not related to acne vulgaris.³ The underlying cause of AKN is hypothesized to be multifactorial, including inflammation, infection, and trauma.² Acne keloidalis nuchae is most common in males aged 14 to 50 years, which may indicate that increased androgens contribute to its development.³ In some cases, patients have reported developing AKN lesions after receiving a haircut or shaving, suggesting a potential role of trauma to the hair follicles and secondary infection.² Histopathology typically shows a perifollicular inflammatory infiltrate that obscures the hair follicles with associated proximal fibrosis.⁴ On physical examination, dermoscopy can be used to visualize perifollicular pustules and fibrosis, which appears white, in the early stages of AKN. Patients may present with tufted hairs in more advanced stages.⁵ Patients with AKN often describe the lesions as pruritic and painful.²

In this study, we evaluated the most common treatment regimens used over a 6-year period by patients in the Los Angeles County hospital system in California and their efficacy on AKN lesions. Our study includes one of the largest cohorts of patients reported to date and as such demonstrates the real-world effects that current treatment regimens for AKN have on patient outcomes nationwide.

Methods

We performed a retrospective cross-sectional analysis of patient medical records from the Los Angeles County hospital system i2b2 (i2b2 tranSMART Foundation) clinical data warehouse over a 6-year period (January 2017–January 2023). We used the International Statistical Classification of Diseases, Tenth Revision codes L73.0 (acne keloid) and L73.1 (pseudofolliculitis barbae) to conduct our search in order to identify as many patients with follicular disorders as possible to include in the study. Of the 478 total medical records we reviewed, 183 patients were included based on a diagnosis of AKN by a dermatologist.

We then collected data on patient demographics and treatments received, including whether patients had received monotherapy or combination therapy. Of the 183 patients we initially identified, 4 were excluded from the study because they had not received any treatment, and 78 were excluded because no treatment outcomes were documented. The 101 patients who were included had received either monotherapy or a combination of treatments. Treatment outcomes were categorized as either improvement in the number and appearance of papules and/or keloidlike plaques, maintenance of stable lesions (ie, well controlled), and/or resolution of lesions as documented by the treating physician. No patients had overall worsening of their disease.

Results

Of the 101 patients included in the study, 34 (33.7%) received a combination of topical, systemic, and procedural treatments; 34 (33.7%) received a combination of topical and procedural treatments; 17 (16.8%) were treated with topicals only; 13 (12.9%) were treated with a combination of topical and systemic treatments; and 3 (3.0%) were treated with monotherapy of either a topical, systemic, or procedural therapy. Systemic and/or procedural therapy combined with topicals was provided as a first-line treatment for 63 (62.4%) patients. Treatment escalation to systemic or procedural therapy for those who did not respond to topical treatment was observed in 23 (22.8%) patients. The average number of unique treatments received per patient was 3.67.

Clindamycin and clobetasol were the most prescribed topical treatments, doxycycline was the most prescribed systemic therapy, and intralesional (IL) triamcinolone was the most performed procedural therapy. The most common treatment regimens were topical clindamycin and clobetasol, topical clindamycin and clobetasol with IL triamcinolone, and topical clindamycin and clobetasol with both IL triamcinolone and doxycycline.

Improvement in AKN lesions was reported for the majority of patients with known treatment outcomes across all types of regimens. Ninety-eight percent (99/101) of patients had improvement in lesions, 55.5% (56/101) had well-controlled lesions, and 20.8% (21/101) achieved resolution of disease. The treatment outcomes are outlined in eTables 1 and 2.

Comment

Most clinicians opted for a multitherapy treatment regimen, and improvement was noted in most patients regardless of which regimen was chosen. As expected, patients who had mild or early disease generally received topical agents first, including most commonly a mid- to high-potency steroid, antibiotic, retinoid, and/or antifungal; specifically, clindamycin, clobetasol, and fluocinolone were the most common agents chosen. Patients with severe disease were more likely to receive systemic and/or procedural treatments, including oral antibiotics or IL steroid injections most commonly. Improvement was documented in the majority of patients using these treatment regimens, and some patients did achieve full resolution of disease.

Our data cannot be used to determine which treatment alone is most effective for patients with AKN, as the patients in our study had varying levels of disease activity and types of lesions, and most received combination therapy. What our data do show is that combination therapies often work well to control or improve disease, but also that current therapeutic options only rarely lead to full resolution of disease.

Limitations of our study included an inability to stratify disease, an inability to rigorously analyze specific treatment outcomes since most patients did not receive monotherapy. The strength of our study is its size, which allows us to show that many different treatment regimens currently are being employed by dermatologists to treat AKN, and most of these seem to be somewhat effective.

Conclusion

Acne keloidalis nuchae is difficult to treat due to a lack of understanding of which pathophysiologic mechanisms dominate in any given patient, a lack of good data on treatment outcomes, and the variability of ways that the disease manifests. Thus far, as shown by the patients described in this study, the most efficacious treatment regimens seem to be combination therapies that target the multifactorial causes of this disease. Physicians should continue to choose treatments based on disease severity and cutaneous manifestations, tailor their approach by accounting for patient preferences, and consider a multimodal approach to treatment.

Acne keloidalis nuchae (AKN) classically presents as chronic inflammation of the hair follicles on the occipital scalp/nape of the neck manifesting as papules and pustules that may progress to keloidlike scarring.¹ Photographs depicting the typical clinical presentation of AKN are shown in the Figure. In the literature, AKN has been described as primarily occurring in postpubertal males of African descent.² Despite its similar name, AKN is not related to acne vulgaris.³ The underlying cause of AKN is hypothesized to be multifactorial, including inflammation, infection, and trauma.² Acne keloidalis nuchae is most common in males aged 14 to 50 years, which may indicate that increased androgens contribute to its development.³ In some cases, patients have reported developing AKN lesions after receiving a haircut or shaving, suggesting a potential role of trauma to the hair follicles and secondary infection.² Histopathology typically shows a perifollicular inflammatory infiltrate that obscures the hair follicles with associated proximal fibrosis.⁴ On physical examination, dermoscopy can be used to visualize perifollicular pustules and fibrosis, which appears white, in the early stages of AKN. Patients may present with tufted hairs in more advanced stages.⁵ Patients with AKN often describe the lesions as pruritic and painful.²

In this study, we evaluated the most common treatment regimens used over a 6-year period by patients in the Los Angeles County hospital system in California and their efficacy on AKN lesions. Our study includes one of the largest cohorts of patients reported to date and as such demonstrates the real-world effects that current treatment regimens for AKN have on patient outcomes nationwide.

Methods

We performed a retrospective cross-sectional analysis of patient medical records from the Los Angeles County hospital system i2b2 (i2b2 tranSMART Foundation) clinical data warehouse over a 6-year period (January 2017–January 2023). We used the International Statistical Classification of Diseases, Tenth Revision codes L73.0 (acne keloid) and L73.1 (pseudofolliculitis barbae) to conduct our search in order to identify as many patients with follicular disorders as possible to include in the study. Of the 478 total medical records we reviewed, 183 patients were included based on a diagnosis of AKN by a dermatologist.

We then collected data on patient demographics and treatments received, including whether patients had received monotherapy or combination therapy. Of the 183 patients we initially identified, 4 were excluded from the study because they had not received any treatment, and 78 were excluded because no treatment outcomes were documented. The 101 patients who were included had received either monotherapy or a combination of treatments. Treatment outcomes were categorized as either improvement in the number and appearance of papules and/or keloidlike plaques, maintenance of stable lesions (ie, well controlled), and/or resolution of lesions as documented by the treating physician. No patients had overall worsening of their disease.

Results

Of the 101 patients included in the study, 34 (33.7%) received a combination of topical, systemic, and procedural treatments; 34 (33.7%) received a combination of topical and procedural treatments; 17 (16.8%) were treated with topicals only; 13 (12.9%) were treated with a combination of topical and systemic treatments; and 3 (3.0%) were treated with monotherapy of either a topical, systemic, or procedural therapy. Systemic and/or procedural therapy combined with topicals was provided as a first-line treatment for 63 (62.4%) patients. Treatment escalation to systemic or procedural therapy for those who did not respond to topical treatment was observed in 23 (22.8%) patients. The average number of unique treatments received per patient was 3.67.

Clindamycin and clobetasol were the most prescribed topical treatments, doxycycline was the most prescribed systemic therapy, and intralesional (IL) triamcinolone was the most performed procedural therapy. The most common treatment regimens were topical clindamycin and clobetasol, topical clindamycin and clobetasol with IL triamcinolone, and topical clindamycin and clobetasol with both IL triamcinolone and doxycycline.

Improvement in AKN lesions was reported for the majority of patients with known treatment outcomes across all types of regimens. Ninety-eight percent (99/101) of patients had improvement in lesions, 55.5% (56/101) had well-controlled lesions, and 20.8% (21/101) achieved resolution of disease. The treatment outcomes are outlined in eTables 1 and 2.

Comment

Most clinicians opted for a multitherapy treatment regimen, and improvement was noted in most patients regardless of which regimen was chosen. As expected, patients who had mild or early disease generally received topical agents first, including most commonly a mid- to high-potency steroid, antibiotic, retinoid, and/or antifungal; specifically, clindamycin, clobetasol, and fluocinolone were the most common agents chosen. Patients with severe disease were more likely to receive systemic and/or procedural treatments, including oral antibiotics or IL steroid injections most commonly. Improvement was documented in the majority of patients using these treatment regimens, and some patients did achieve full resolution of disease.

Our data cannot be used to determine which treatment alone is most effective for patients with AKN, as the patients in our study had varying levels of disease activity and types of lesions, and most received combination therapy. What our data do show is that combination therapies often work well to control or improve disease, but also that current therapeutic options only rarely lead to full resolution of disease.

Limitations of our study included an inability to stratify disease, an inability to rigorously analyze specific treatment outcomes since most patients did not receive monotherapy. The strength of our study is its size, which allows us to show that many different treatment regimens currently are being employed by dermatologists to treat AKN, and most of these seem to be somewhat effective.

Conclusion

Acne keloidalis nuchae is difficult to treat due to a lack of understanding of which pathophysiologic mechanisms dominate in any given patient, a lack of good data on treatment outcomes, and the variability of ways that the disease manifests. Thus far, as shown by the patients described in this study, the most efficacious treatment regimens seem to be combination therapies that target the multifactorial causes of this disease. Physicians should continue to choose treatments based on disease severity and cutaneous manifestations, tailor their approach by accounting for patient preferences, and consider a multimodal approach to treatment.

Acne keloidalis nuchae (AKN) classically presents as chronic inflammation of the hair follicles on the occipital scalp/nape of the neck manifesting as papules and pustules that may progress to keloidlike scarring.¹ Photographs depicting the typical clinical presentation of AKN are shown in the Figure. In the literature, AKN has been described as primarily occurring in postpubertal males of African descent.² Despite its similar name, AKN is not related to acne vulgaris.³ The underlying cause of AKN is hypothesized to be multifactorial, including inflammation, infection, and trauma.² Acne keloidalis nuchae is most common in males aged 14 to 50 years, which may indicate that increased androgens contribute to its development.³ In some cases, patients have reported developing AKN lesions after receiving a haircut or shaving, suggesting a potential role of trauma to the hair follicles and secondary infection.² Histopathology typically shows a perifollicular inflammatory infiltrate that obscures the hair follicles with associated proximal fibrosis.⁴ On physical examination, dermoscopy can be used to visualize perifollicular pustules and fibrosis, which appears white, in the early stages of AKN. Patients may present with tufted hairs in more advanced stages.⁵ Patients with AKN often describe the lesions as pruritic and painful.²

In this study, we evaluated the most common treatment regimens used over a 6-year period by patients in the Los Angeles County hospital system in California and their efficacy on AKN lesions. Our study includes one of the largest cohorts of patients reported to date and as such demonstrates the real-world effects that current treatment regimens for AKN have on patient outcomes nationwide.

Methods

We performed a retrospective cross-sectional analysis of patient medical records from the Los Angeles County hospital system i2b2 (i2b2 tranSMART Foundation) clinical data warehouse over a 6-year period (January 2017–January 2023). We used the International Statistical Classification of Diseases, Tenth Revision codes L73.0 (acne keloid) and L73.1 (pseudofolliculitis barbae) to conduct our search in order to identify as many patients with follicular disorders as possible to include in the study. Of the 478 total medical records we reviewed, 183 patients were included based on a diagnosis of AKN by a dermatologist.

We then collected data on patient demographics and treatments received, including whether patients had received monotherapy or combination therapy. Of the 183 patients we initially identified, 4 were excluded from the study because they had not received any treatment, and 78 were excluded because no treatment outcomes were documented. The 101 patients who were included had received either monotherapy or a combination of treatments. Treatment outcomes were categorized as either improvement in the number and appearance of papules and/or keloidlike plaques, maintenance of stable lesions (ie, well controlled), and/or resolution of lesions as documented by the treating physician. No patients had overall worsening of their disease.

Results

Of the 101 patients included in the study, 34 (33.7%) received a combination of topical, systemic, and procedural treatments; 34 (33.7%) received a combination of topical and procedural treatments; 17 (16.8%) were treated with topicals only; 13 (12.9%) were treated with a combination of topical and systemic treatments; and 3 (3.0%) were treated with monotherapy of either a topical, systemic, or procedural therapy. Systemic and/or procedural therapy combined with topicals was provided as a first-line treatment for 63 (62.4%) patients. Treatment escalation to systemic or procedural therapy for those who did not respond to topical treatment was observed in 23 (22.8%) patients. The average number of unique treatments received per patient was 3.67.

Clindamycin and clobetasol were the most prescribed topical treatments, doxycycline was the most prescribed systemic therapy, and intralesional (IL) triamcinolone was the most performed procedural therapy. The most common treatment regimens were topical clindamycin and clobetasol, topical clindamycin and clobetasol with IL triamcinolone, and topical clindamycin and clobetasol with both IL triamcinolone and doxycycline.

Improvement in AKN lesions was reported for the majority of patients with known treatment outcomes across all types of regimens. Ninety-eight percent (99/101) of patients had improvement in lesions, 55.5% (56/101) had well-controlled lesions, and 20.8% (21/101) achieved resolution of disease. The treatment outcomes are outlined in eTables 1 and 2.

Comment

Most clinicians opted for a multitherapy treatment regimen, and improvement was noted in most patients regardless of which regimen was chosen. As expected, patients who had mild or early disease generally received topical agents first, including most commonly a mid- to high-potency steroid, antibiotic, retinoid, and/or antifungal; specifically, clindamycin, clobetasol, and fluocinolone were the most common agents chosen. Patients with severe disease were more likely to receive systemic and/or procedural treatments, including oral antibiotics or IL steroid injections most commonly. Improvement was documented in the majority of patients using these treatment regimens, and some patients did achieve full resolution of disease.

Our data cannot be used to determine which treatment alone is most effective for patients with AKN, as the patients in our study had varying levels of disease activity and types of lesions, and most received combination therapy. What our data do show is that combination therapies often work well to control or improve disease, but also that current therapeutic options only rarely lead to full resolution of disease.

Limitations of our study included an inability to stratify disease, an inability to rigorously analyze specific treatment outcomes since most patients did not receive monotherapy. The strength of our study is its size, which allows us to show that many different treatment regimens currently are being employed by dermatologists to treat AKN, and most of these seem to be somewhat effective.

Conclusion

Acne keloidalis nuchae is difficult to treat due to a lack of understanding of which pathophysiologic mechanisms dominate in any given patient, a lack of good data on treatment outcomes, and the variability of ways that the disease manifests. Thus far, as shown by the patients described in this study, the most efficacious treatment regimens seem to be combination therapies that target the multifactorial causes of this disease. Physicians should continue to choose treatments based on disease severity and cutaneous manifestations, tailor their approach by accounting for patient preferences, and consider a multimodal approach to treatment.