Contact Dermatitis

To the Editor:

A 69-year-old woman presented to the allergy clinic for evaluation of a rash on the left breast. The patient had a history of breast cancer that was treated with a lumpectomy followed by external beam radiation therapy (total dose, 6000 cGy) to the lateral aspect of the left breast approximately 4 years prior. She developed acute breast dermatitis from the radiation, which was self-treated with over-the-counter hydrocortisone cream. The patient subsequently developed a blistering skin eruption over the area where she applied the cream. She did not recall the subtype of hydrocortisone she used (butyrate and acetate are available over-the-counter). She discontinued the hydrocortisone and was started on triamcinolone cream 0.1%, which was well tolerated, and the rash resolved.

The patient had a history of a similar reaction to hydrocortisone butyrate after blepharoplasty approximately 10 years prior to the current presentation, characterized by facial erythema, pruritus, and blistering. A patch test confirmed reactivity to hydrocortisone-17-butyrate and tixocortol pivalate. However, a skin-prick test for hydrocortisone acetate cream 1% was negative.

Subsequently, the patient developed acute-onset dyspepsia, gnawing epigastric pain, regurgitation, and bloating. A diagnosis of eosinophilic gastritis was established via biopsy, which found increased eosinophils in the lamina propria (>50 eosinophils per high-power field). Helicobacter pylori was not identified. She was started on the proton-pump inhibitor dexlansoprazole but symptoms did not improve. Her other medications included benazepril, alprazolam as needed, vitamin D, and magnesium. The patient subsequently was started on a trial of oral prednisone 40 mg/d. Three days after initiation, she developed an erythematous macular rash over the left breast.

The next day she presented to the allergy clinic. Physical examination of the left breast revealed a 20×10-cm, nipple-sparing patch of well-demarcated erythema without fluctuance or overlying lesions. The area of erythema overlapped with the prior radiation field based on radiation marker tattoos and the lumpectomy scar (Figure). There was no evidence to suggest inflammation of deeper tissue or the pectoral muscles. Vital signs were normal, and the remainder of the examination was unremarkable, including breast, lymph node, and complete skin examinations.

In contrast, triamcinolone is a class B steroid, which has a C16,17-cis-diol or -ketal. Other than budesonide, which can cross-react with D2 steroids, class B steroids do not cross-react with hydrocortisone or prednisone. Triamcinolone does not usually cross-react with D2 corticosteroids, which likely explains why our patient was later able to tolerate triamcinolone to treat eosinophilic gastrointestinal tract disease.

In summary, we present a case of radiation recall dermatitis triggered by prednisone. Radiation can prime an area for a future inflammatory response by upregulating proinflammatory cytokines or triggering stem cell mutation. In our case, clinical reactivity to hydrocortisone-17-butyrate and sensitization to tixocortol pivalate via patch testing could have increased the likelihood of a reaction with prednisone use due to cross-reactivity. This case instructs dermatologists, allergists, and oncologists to be aware of prednisone as a potential trigger of radiation recall dermatitis.

To the Editor:

A 69-year-old woman presented to the allergy clinic for evaluation of a rash on the left breast. The patient had a history of breast cancer that was treated with a lumpectomy followed by external beam radiation therapy (total dose, 6000 cGy) to the lateral aspect of the left breast approximately 4 years prior. She developed acute breast dermatitis from the radiation, which was self-treated with over-the-counter hydrocortisone cream. The patient subsequently developed a blistering skin eruption over the area where she applied the cream. She did not recall the subtype of hydrocortisone she used (butyrate and acetate are available over-the-counter). She discontinued the hydrocortisone and was started on triamcinolone cream 0.1%, which was well tolerated, and the rash resolved.

The patient had a history of a similar reaction to hydrocortisone butyrate after blepharoplasty approximately 10 years prior to the current presentation, characterized by facial erythema, pruritus, and blistering. A patch test confirmed reactivity to hydrocortisone-17-butyrate and tixocortol pivalate. However, a skin-prick test for hydrocortisone acetate cream 1% was negative.

Subsequently, the patient developed acute-onset dyspepsia, gnawing epigastric pain, regurgitation, and bloating. A diagnosis of eosinophilic gastritis was established via biopsy, which found increased eosinophils in the lamina propria (>50 eosinophils per high-power field). Helicobacter pylori was not identified. She was started on the proton-pump inhibitor dexlansoprazole but symptoms did not improve. Her other medications included benazepril, alprazolam as needed, vitamin D, and magnesium. The patient subsequently was started on a trial of oral prednisone 40 mg/d. Three days after initiation, she developed an erythematous macular rash over the left breast.

The next day she presented to the allergy clinic. Physical examination of the left breast revealed a 20×10-cm, nipple-sparing patch of well-demarcated erythema without fluctuance or overlying lesions. The area of erythema overlapped with the prior radiation field based on radiation marker tattoos and the lumpectomy scar (Figure). There was no evidence to suggest inflammation of deeper tissue or the pectoral muscles. Vital signs were normal, and the remainder of the examination was unremarkable, including breast, lymph node, and complete skin examinations.

In contrast, triamcinolone is a class B steroid, which has a C16,17-cis-diol or -ketal. Other than budesonide, which can cross-react with D2 steroids, class B steroids do not cross-react with hydrocortisone or prednisone. Triamcinolone does not usually cross-react with D2 corticosteroids, which likely explains why our patient was later able to tolerate triamcinolone to treat eosinophilic gastrointestinal tract disease.

In summary, we present a case of radiation recall dermatitis triggered by prednisone. Radiation can prime an area for a future inflammatory response by upregulating proinflammatory cytokines or triggering stem cell mutation. In our case, clinical reactivity to hydrocortisone-17-butyrate and sensitization to tixocortol pivalate via patch testing could have increased the likelihood of a reaction with prednisone use due to cross-reactivity. This case instructs dermatologists, allergists, and oncologists to be aware of prednisone as a potential trigger of radiation recall dermatitis.

To the Editor:

A 69-year-old woman presented to the allergy clinic for evaluation of a rash on the left breast. The patient had a history of breast cancer that was treated with a lumpectomy followed by external beam radiation therapy (total dose, 6000 cGy) to the lateral aspect of the left breast approximately 4 years prior. She developed acute breast dermatitis from the radiation, which was self-treated with over-the-counter hydrocortisone cream. The patient subsequently developed a blistering skin eruption over the area where she applied the cream. She did not recall the subtype of hydrocortisone she used (butyrate and acetate are available over-the-counter). She discontinued the hydrocortisone and was started on triamcinolone cream 0.1%, which was well tolerated, and the rash resolved.

The patient had a history of a similar reaction to hydrocortisone butyrate after blepharoplasty approximately 10 years prior to the current presentation, characterized by facial erythema, pruritus, and blistering. A patch test confirmed reactivity to hydrocortisone-17-butyrate and tixocortol pivalate. However, a skin-prick test for hydrocortisone acetate cream 1% was negative.

Subsequently, the patient developed acute-onset dyspepsia, gnawing epigastric pain, regurgitation, and bloating. A diagnosis of eosinophilic gastritis was established via biopsy, which found increased eosinophils in the lamina propria (>50 eosinophils per high-power field). Helicobacter pylori was not identified. She was started on the proton-pump inhibitor dexlansoprazole but symptoms did not improve. Her other medications included benazepril, alprazolam as needed, vitamin D, and magnesium. The patient subsequently was started on a trial of oral prednisone 40 mg/d. Three days after initiation, she developed an erythematous macular rash over the left breast.

The next day she presented to the allergy clinic. Physical examination of the left breast revealed a 20×10-cm, nipple-sparing patch of well-demarcated erythema without fluctuance or overlying lesions. The area of erythema overlapped with the prior radiation field based on radiation marker tattoos and the lumpectomy scar (Figure). There was no evidence to suggest inflammation of deeper tissue or the pectoral muscles. Vital signs were normal, and the remainder of the examination was unremarkable, including breast, lymph node, and complete skin examinations.

In contrast, triamcinolone is a class B steroid, which has a C16,17-cis-diol or -ketal. Other than budesonide, which can cross-react with D2 steroids, class B steroids do not cross-react with hydrocortisone or prednisone. Triamcinolone does not usually cross-react with D2 corticosteroids, which likely explains why our patient was later able to tolerate triamcinolone to treat eosinophilic gastrointestinal tract disease.

In summary, we present a case of radiation recall dermatitis triggered by prednisone. Radiation can prime an area for a future inflammatory response by upregulating proinflammatory cytokines or triggering stem cell mutation. In our case, clinical reactivity to hydrocortisone-17-butyrate and sensitization to tixocortol pivalate via patch testing could have increased the likelihood of a reaction with prednisone use due to cross-reactivity. This case instructs dermatologists, allergists, and oncologists to be aware of prednisone as a potential trigger of radiation recall dermatitis.

Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Each year, the American Contact Dermatitis Society names an Allergen of the Year with the purpose of promoting greater awareness of a key allergen and its impact on patients. Often, the Allergen of the Year is an emerging allergen that may represent an underrecognized or novel cause of allergic contact dermatitis (ACD).In 2020, the American Contact Dermatitis Society chose isobornyl acrylate as the Allergen of the Year.¹ Not only has isobornyl acrylate been implicated in an epidemic of contact allergy to diabetic devices, but it also illustrates the challenges of investigating contact allergy to medical devices in general.

What Is Isobornyl Acrylate?

Isobornyl acrylate, also known as the isobornyl ester of acrylic acid, is a chemical used in glues, adhesives, coatings, sealants, inks, and paints. Similar to other acrylates, such as those involved in gel nail treatments, it is photopolymerizable; that is, when exposed to UV light, it can transform from a liquid monomer into a hard polymer, contributing to its utility as an adhesive. Prior to its recent implication in diabetic device contact allergy, isobornyl acrylate was not thought to be a common skin sensitizer. In a 2013 Dutch study of patients with acrylate allergy, only 1 of 14 patients with a contact allergy to other acrylates had a positive patch test reaction to isobornyl acrylate, which led the authors to conclude that adding it to their acrylate patch test series was not indicated.²

Isobornyl Acrylate in Diabetic Devices

Devices such as glucose monitoring systems and insulin pumps are used by millions of patients with diabetes worldwide. Not only are continuous glucose monitoring devices more convenient than self-monitoring of blood glucose, but they also are associated with a reduction in hemoglobin A_1c levels and lower risk for hypoglycemia.³ However, these devices have been increasingly recognized as a source of irritant contact dermatitis and ACD.

Early cases of contact allergy to isobornyl acrylate in diabetic devices were reported in 1995 when 2 Belgian patients using insulin pumps developed ACD.⁴ The patients had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum and other allergens including acrylates. In addition, patch testing with plastic scrapings from their insulin pumps also was positive, and it was determined that the glue affixing the needle to the plastic had diffused into the plastic. The patients were switched to insulin pumps produced by heat staking instead of glue, and their symptoms resolved. In retrospect, this case series may seem prescient, as it was written 2 decades before isobornyl acrylate became recognized as a widespread cause of ACD in users of diabetic devices. Admittedly, other acrylate components of the glue also were positive on patch testing in these patients, so it was not until much later that the focus turned more exclusively to isobornyl acrylate.⁴

Similar to the insulin pumps in the 1995 Belgian series, diffusion of glue to other parts of modern glucose sensors also appears to cause isobornyl acrylate contact allergy. This theory was supported by a 2017 study from Belgian and Swedish investigators in which gas chromatography–mass spectrometry was used to identify concentrations of isobornyl acrylate in various components of a popular continuous glucose monitoring sensor.⁵ The concentration of isobornyl acrylate was approximately 100-fold higher at the site where the top and bottom plastic components of the sensor were joined as compared to the adhesive patch in contact with the patient’s skin. Therefore, the adhesive patch itself was not the source of the isobornyl acrylate exposure; rather, the isobornyl acrylate diffused into the adhesive patch from the glue used to join the components of the sensor together.⁵ One ramification is that patients with diabetic device contact allergy can have a false-negative patch test result if the adhesive patch is tested by itself, whereas they may react to patch testing with the whole sensor or an acetonic extract thereof.

Frequency of Sensitization to Isobornyl Acrylate

It is difficult to estimate the frequency of sensitization to isobornyl acrylate among users of diabetic devices, in part because those with mild allergy may not seek medical treatment. Nevertheless, there are studies that demonstrate a high prevalence of sensitization among users with suspected allergy. In a 2019 Finnish study of 6567 patients using an isobornyl acrylate–containing glucose sensor, 63 were patch tested for suspected ACD.⁶ Of these 63 patients, 51 (81%) had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum. These findings were consistent with the original 2017 study from Belgium and Sweden, in which 10 of 11 (91%) patients who used an isobornyl acrylate–containing glucose sensor and had suspected contact allergy had positive patch test reactions to isobornyl acrylate 0.1% in petrolatum compared to no positive reactions in the 14 control patients.⁵ Given that there are more than 1.5 million users of this isobornyl acrylate–containing glucose sensor across 46 countries,⁷ it requires no stretch of the imagination to understand why investigators refer to isobornyl acrylate allergy as an epidemic, even if only a small percentage of users are sensitized to the device.

The Journey to Discover Isobornyl Acrylate as a Culprit Allergen

Similar to the discoveries of radiography and penicillin, the discovery of isobornyl acrylate as a culprit allergen in a modern glucose sensor was purely accidental. In 2016, a 9-year-old boy with diabetes presented to a Belgian dermatology department with ACD to a glucose sensor.¹ A patch test nurse serendipitously applied isobornyl acrylate—0.01%, 0.05%, and 0.1% in petrolatum—which was not intended to be applied as part of the typical acrylate series. The only positive patch test reactions in this patient were to isobornyl acrylate at all 3 concentrations. This lucky error inspired isobornyl acrylate to be tested at multiple other dermatology departments in Europe in patients with ACD to their glucose sensors, leading to its discovery as a culprit allergen.¹

One challenge facing investigators was obtaining information and materials from the diabetic device industry. Medical device manufacturers are not required to disclose chemicals present in a device on its label.⁸ Therefore, for patients or investigators to determine whether a potential allergen is present in a given device, they must request that information from the manufacturer, which can be a time-consuming and frustrating effort. Luckily, investigators collaborated with one another, and Belgian investigators suggested that Swedish investigators performing chemical analyses on a glucose monitoring device should focus on isobornyl acrylate, which enabled its detection in an extract from the device.⁵

Testing for Isobornyl Acrylate Allergy in Your Clinic

Patients with suspected ACD to a diabetic device—insulin pump or glucose sensor—should be patch tested with isobornyl acrylate, in addition to other previously reported allergens. The vehicle typically is petrolatum, and the commonly tested concentration is 0.1%. Testing with lower concentrations such as 0.01% can result in false-negative reactions,⁹ and testing at higher concentrations such as 0.3% can result in irritant skin reactions.² Isobornyl acrylate 0.1% in petrolatum currently is available from one commercial allergen supplier (Chemotechnique Diagnostics). A positive patch test reaction to isobornyl acrylate 0.1% in petrolatum is shown in the Figure.

Management of Diabetic Device ACD

For patients with diabetic device ACD, there are several strategies that can reduce direct contact between the device and the patient’s skin. Methods that have been tried with varying success to allow patients to continue using their glucose sensors include barrier sprays (eg, Cavilon [3M], Silesse Skin Barrier [ConvaTec]); barrier pads (eg, Compeed [HRA Pharma], Surround skin protectors [Eakin], DuoDERM dressings [ConvaTec], Tegaderm dressings [3M]); and topical corticosteroids, calcineurin inhibitors, and phosphodiesterase 4 inhibitors. Nevertheless, a 2019 Finnish study showed that only 14 of 63 (22%) patients with ACD to their isobornyl acrylate–containing glucose sensor were able to continue using the device, with all 14 requiring use of a barrier agent. Despite using the barrier agent, 13 (93%) of these patients had residual dermatitis.⁶ There also is concern that use of barrier methods might hamper the proper functioning of glucose sensors and related devices.

Patients with known isobornyl acrylate contact allergy also may switch to a different diabetic device. A 2019 German study showed that in 5 patients with isobornyl acrylate ACD, none had reactions to the one particular system that has been shown by gas chromatography–mass spectrometry to not contain isobornyl acrylate.¹⁰ However, as a word of caution, the same device also has been associated with ACD^11,12 but has been resolved by using heat staking during the production process.¹³ As manufacturers update device components, identification of other isobornyl acrylate–free devices may require a degree of trial and error, as neither isobornyl acrylate nor any other potential allergen is listed on device labels.

Final Interpretation

Isobornyl acrylate is not a common sensitizer in general patch test populations but is a recently identified major culprit in ACD to diabetic devices. Patch testing with isobornyl acrylate 0.1% in petrolatum is not necessary in standard screening panels but should be considered in patients with suspected ACD to glucose sensors or insulin pumps. If a patient with ACD wants to continue to experience the convenience provided by a diabetic device, options include using topical steroids or barrier agents and/or changing the brand of the diabetic device, though none of these methods are foolproof. Hopefully, the identification of isobornyl acrylate as a culprit allergen will help to improve the lives of patients who use diabetic devices worldwide.

Handwashing with antimicrobial soaps or alcohol-based sanitizers is an effective measure in preventing microbial disease transmission. In the context of coronavirus disease 2019 (COVID-19) prevention, the World Health Organization and Centers for Disease Control and Prevention have recommended handwashing with soap and water after coughing/sneezing, visiting a public place, touching surfaces outside the home, and taking care of a sick person(s), as well as before and after eating. When soap and water are not available, alcohol-based sanitizers may be used.^1,2

Irritant contact dermatitis (ICD) is most commonly associated with wet work and is frequently seen in health care workers in relation to hand hygiene, with survey-based studies reporting 25% to 55% of nurses affected.^3-5 In a prospective study (N=102), health care workers who washed their hands more than 10 times per day were55% more likely to develop hand dermatitis.⁶ Frequent ICD of the hands has been reported in Chinese health care workers in association with COVID-19.⁷ Handwashing and/or glove wearing may be newly prioritized by workers who handle frequently touched goods and surfaces, such as flight attendants (Figure). Patients with obsessive-compulsive disorder may be another vulnerable population.⁸

Propensity for ICD is a limiting factor in hand hygiene adherence.¹⁷ In a double-blind randomized trial (N=54), scheduled use of an oil-containing lotion was shown to increase compliance with hand hygiene protocols in health care workers by preventing cracks, scaling, and pain.¹⁸ Using sanitizers containing humectants (eg, aloe vera gel) or moisturizers with petrolatum, liquid paraffin, glycerin, or mineral oil have all been shown to decrease the incidence of ICD in frequent handwashers.^19,20 Thorough hand drying also is important in preventing dermatitis. Drying with disposable paper towels is preferred over automated air dryers to prevent aerosolization of microbes.²¹ Because latex has been implicated in development of ICD, use of latex-free gloves is recommended.²²

Alcohol-based sanitizer is not only an effective virucidal agent but also is less likely to cause ICD, therefore promoting hand hygiene adherence. Handwashing with soap still is necessary when hands are visibly dirty but should be performed less frequently if feasible. Hand hygiene and emollient usage education is important for physicians and patients alike, particularly during the COVID-19 crisis.

Handwashing with antimicrobial soaps or alcohol-based sanitizers is an effective measure in preventing microbial disease transmission. In the context of coronavirus disease 2019 (COVID-19) prevention, the World Health Organization and Centers for Disease Control and Prevention have recommended handwashing with soap and water after coughing/sneezing, visiting a public place, touching surfaces outside the home, and taking care of a sick person(s), as well as before and after eating. When soap and water are not available, alcohol-based sanitizers may be used.^1,2

Irritant contact dermatitis (ICD) is most commonly associated with wet work and is frequently seen in health care workers in relation to hand hygiene, with survey-based studies reporting 25% to 55% of nurses affected.^3-5 In a prospective study (N=102), health care workers who washed their hands more than 10 times per day were55% more likely to develop hand dermatitis.⁶ Frequent ICD of the hands has been reported in Chinese health care workers in association with COVID-19.⁷ Handwashing and/or glove wearing may be newly prioritized by workers who handle frequently touched goods and surfaces, such as flight attendants (Figure). Patients with obsessive-compulsive disorder may be another vulnerable population.⁸

Propensity for ICD is a limiting factor in hand hygiene adherence.¹⁷ In a double-blind randomized trial (N=54), scheduled use of an oil-containing lotion was shown to increase compliance with hand hygiene protocols in health care workers by preventing cracks, scaling, and pain.¹⁸ Using sanitizers containing humectants (eg, aloe vera gel) or moisturizers with petrolatum, liquid paraffin, glycerin, or mineral oil have all been shown to decrease the incidence of ICD in frequent handwashers.^19,20 Thorough hand drying also is important in preventing dermatitis. Drying with disposable paper towels is preferred over automated air dryers to prevent aerosolization of microbes.²¹ Because latex has been implicated in development of ICD, use of latex-free gloves is recommended.²²

Alcohol-based sanitizer is not only an effective virucidal agent but also is less likely to cause ICD, therefore promoting hand hygiene adherence. Handwashing with soap still is necessary when hands are visibly dirty but should be performed less frequently if feasible. Hand hygiene and emollient usage education is important for physicians and patients alike, particularly during the COVID-19 crisis.

Handwashing with antimicrobial soaps or alcohol-based sanitizers is an effective measure in preventing microbial disease transmission. In the context of coronavirus disease 2019 (COVID-19) prevention, the World Health Organization and Centers for Disease Control and Prevention have recommended handwashing with soap and water after coughing/sneezing, visiting a public place, touching surfaces outside the home, and taking care of a sick person(s), as well as before and after eating. When soap and water are not available, alcohol-based sanitizers may be used.^1,2

Irritant contact dermatitis (ICD) is most commonly associated with wet work and is frequently seen in health care workers in relation to hand hygiene, with survey-based studies reporting 25% to 55% of nurses affected.^3-5 In a prospective study (N=102), health care workers who washed their hands more than 10 times per day were55% more likely to develop hand dermatitis.⁶ Frequent ICD of the hands has been reported in Chinese health care workers in association with COVID-19.⁷ Handwashing and/or glove wearing may be newly prioritized by workers who handle frequently touched goods and surfaces, such as flight attendants (Figure). Patients with obsessive-compulsive disorder may be another vulnerable population.⁸

Propensity for ICD is a limiting factor in hand hygiene adherence.¹⁷ In a double-blind randomized trial (N=54), scheduled use of an oil-containing lotion was shown to increase compliance with hand hygiene protocols in health care workers by preventing cracks, scaling, and pain.¹⁸ Using sanitizers containing humectants (eg, aloe vera gel) or moisturizers with petrolatum, liquid paraffin, glycerin, or mineral oil have all been shown to decrease the incidence of ICD in frequent handwashers.^19,20 Thorough hand drying also is important in preventing dermatitis. Drying with disposable paper towels is preferred over automated air dryers to prevent aerosolization of microbes.²¹ Because latex has been implicated in development of ICD, use of latex-free gloves is recommended.²²

Alcohol-based sanitizer is not only an effective virucidal agent but also is less likely to cause ICD, therefore promoting hand hygiene adherence. Handwashing with soap still is necessary when hands are visibly dirty but should be performed less frequently if feasible. Hand hygiene and emollient usage education is important for physicians and patients alike, particularly during the COVID-19 crisis.

In a survey of products labeled as hypoallergenic for children, about half of shampoos and almost 44% of soaps contained cocamidopropyl betaine (CAPB), a suspected sensitizer for hypersensitivity reactions in people with atopic dermatitis (AD) and allergic contact dermatitis, according to a research letter in the Journal of the American Academy of Dermatology.

Pirotehnik/iStock/Getty Images

In the letter, the authors, Reid W. Collis, of Washington University in St. Louis, and David M. Sheinbein, MD, of the division of dermatology at the university, referred to a previous study showing an association between contact sensitivity with CAPB and people with a history of AD. This was supported by the results of their own recent study in pediatric patients, they wrote, which found that reactions to CAPB were “exclusively” in patients with AD.

In the survey, they looked at children’s shampoo and soap products available on online databases of six of the biggest retailers, and analyzed the top 20 best-selling products for each retailer in 2018. Of the unique products, CAPB was found to be an ingredient in 52% (39 of 75) of the shampoos and 44% (29 of 66) of the soap products. But each of these products “contained the term ‘hypoallergenic; on the product itself or in the product’s description,” they noted.

“CAPB is a prevalent sensitizer in pediatric patients and should be avoided in patients with AD,” the investigators wrote. That said, it’s not included among the 35 prevalent allergens in the T.R.U.E. test, and they recommended that pediatricians and dermatologists “be aware of common products containing CAPB when counseling patients about their product choices,” considering that CAPB sensitivity is more likely in patients with AD.

The study had no funding source, and the authors had no disclosures.

[email protected]

SOURCE: Cho SI et al. J Am Acad Dermatol. 2020 May. doi: 10.1016/j.jaad.2019.12.036.

In a survey of products labeled as hypoallergenic for children, about half of shampoos and almost 44% of soaps contained cocamidopropyl betaine (CAPB), a suspected sensitizer for hypersensitivity reactions in people with atopic dermatitis (AD) and allergic contact dermatitis, according to a research letter in the Journal of the American Academy of Dermatology.

Pirotehnik/iStock/Getty Images

In the letter, the authors, Reid W. Collis, of Washington University in St. Louis, and David M. Sheinbein, MD, of the division of dermatology at the university, referred to a previous study showing an association between contact sensitivity with CAPB and people with a history of AD. This was supported by the results of their own recent study in pediatric patients, they wrote, which found that reactions to CAPB were “exclusively” in patients with AD.

In the survey, they looked at children’s shampoo and soap products available on online databases of six of the biggest retailers, and analyzed the top 20 best-selling products for each retailer in 2018. Of the unique products, CAPB was found to be an ingredient in 52% (39 of 75) of the shampoos and 44% (29 of 66) of the soap products. But each of these products “contained the term ‘hypoallergenic; on the product itself or in the product’s description,” they noted.

“CAPB is a prevalent sensitizer in pediatric patients and should be avoided in patients with AD,” the investigators wrote. That said, it’s not included among the 35 prevalent allergens in the T.R.U.E. test, and they recommended that pediatricians and dermatologists “be aware of common products containing CAPB when counseling patients about their product choices,” considering that CAPB sensitivity is more likely in patients with AD.

The study had no funding source, and the authors had no disclosures.

[email protected]

SOURCE: Cho SI et al. J Am Acad Dermatol. 2020 May. doi: 10.1016/j.jaad.2019.12.036.

In a survey of products labeled as hypoallergenic for children, about half of shampoos and almost 44% of soaps contained cocamidopropyl betaine (CAPB), a suspected sensitizer for hypersensitivity reactions in people with atopic dermatitis (AD) and allergic contact dermatitis, according to a research letter in the Journal of the American Academy of Dermatology.

Pirotehnik/iStock/Getty Images

In the letter, the authors, Reid W. Collis, of Washington University in St. Louis, and David M. Sheinbein, MD, of the division of dermatology at the university, referred to a previous study showing an association between contact sensitivity with CAPB and people with a history of AD. This was supported by the results of their own recent study in pediatric patients, they wrote, which found that reactions to CAPB were “exclusively” in patients with AD.

In the survey, they looked at children’s shampoo and soap products available on online databases of six of the biggest retailers, and analyzed the top 20 best-selling products for each retailer in 2018. Of the unique products, CAPB was found to be an ingredient in 52% (39 of 75) of the shampoos and 44% (29 of 66) of the soap products. But each of these products “contained the term ‘hypoallergenic; on the product itself or in the product’s description,” they noted.

“CAPB is a prevalent sensitizer in pediatric patients and should be avoided in patients with AD,” the investigators wrote. That said, it’s not included among the 35 prevalent allergens in the T.R.U.E. test, and they recommended that pediatricians and dermatologists “be aware of common products containing CAPB when counseling patients about their product choices,” considering that CAPB sensitivity is more likely in patients with AD.

The study had no funding source, and the authors had no disclosures.

[email protected]

SOURCE: Cho SI et al. J Am Acad Dermatol. 2020 May. doi: 10.1016/j.jaad.2019.12.036.

The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.¹ Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.¹ This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.^2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.²  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.¹  

The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.¹ Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.¹ This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.^2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.²  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.¹  

The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.¹ Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.¹ This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.^2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.²  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.¹  

To the Editor:

Phytophotodermatitis is common in dermatology during the summer months, especially in individuals who spend time outdoors; however, identification of the offending plant can be challenging. We report a case of phytophotodermatitis in which the causative plant, common rue, was not identified until it was revealed that the patient was a butterfly enthusiast.

A 60-year-old woman presented to the outpatient dermatology clinic in late summer for a routine skin examination. An eruption was noted over the right thigh and knee that had first appeared approximately 2 weeks prior. The rash started as pruritic blisters but gradually progressed to erythema and then eventually to brown markings, which were observed at the current presentation. Physical examination revealed hyperpigmented, brown, streaky, linear patches and plaques over the right thigh, knee, and lower leg (Figure). When asked about her hobbies, the patient reported an affinity for butterflies and noted that she attracts them with specific species of plants in her garden. She recalled recently planting the herb of grace, or common rue, to attract the giant swallowtail butterfly (Papilio cresphontes). Upon further inquiry, she remembered working in the garden on her knees and digging up roots near the common rue plant while wearing shorts approximately 2 weeks prior to the current presentation. Given the streaky linear pattern of the eruption along with recent sun exposure and exposure to the common rue plant, a diagnosis of phytophotodermatitis was made. No further treatment was sought, as the eruption was not bothersome to her. She was intrigued that the common rue plant had caused the dermatitis and planned on taking proper precautions when working near the plant in the future.

This case illustrates a unique perspective of phytophotodermatitis, as butterfly enthusiasm is not commonly reported in association with the common rue plant with respect to phytophotodermatitis. This case underscores the importance of inquiring about patients’ professions and hobbies, both in dermatology and other specialties.

To the Editor:

Phytophotodermatitis is common in dermatology during the summer months, especially in individuals who spend time outdoors; however, identification of the offending plant can be challenging. We report a case of phytophotodermatitis in which the causative plant, common rue, was not identified until it was revealed that the patient was a butterfly enthusiast.

A 60-year-old woman presented to the outpatient dermatology clinic in late summer for a routine skin examination. An eruption was noted over the right thigh and knee that had first appeared approximately 2 weeks prior. The rash started as pruritic blisters but gradually progressed to erythema and then eventually to brown markings, which were observed at the current presentation. Physical examination revealed hyperpigmented, brown, streaky, linear patches and plaques over the right thigh, knee, and lower leg (Figure). When asked about her hobbies, the patient reported an affinity for butterflies and noted that she attracts them with specific species of plants in her garden. She recalled recently planting the herb of grace, or common rue, to attract the giant swallowtail butterfly (Papilio cresphontes). Upon further inquiry, she remembered working in the garden on her knees and digging up roots near the common rue plant while wearing shorts approximately 2 weeks prior to the current presentation. Given the streaky linear pattern of the eruption along with recent sun exposure and exposure to the common rue plant, a diagnosis of phytophotodermatitis was made. No further treatment was sought, as the eruption was not bothersome to her. She was intrigued that the common rue plant had caused the dermatitis and planned on taking proper precautions when working near the plant in the future.

This case illustrates a unique perspective of phytophotodermatitis, as butterfly enthusiasm is not commonly reported in association with the common rue plant with respect to phytophotodermatitis. This case underscores the importance of inquiring about patients’ professions and hobbies, both in dermatology and other specialties.

To the Editor:

Phytophotodermatitis is common in dermatology during the summer months, especially in individuals who spend time outdoors; however, identification of the offending plant can be challenging. We report a case of phytophotodermatitis in which the causative plant, common rue, was not identified until it was revealed that the patient was a butterfly enthusiast.

A 60-year-old woman presented to the outpatient dermatology clinic in late summer for a routine skin examination. An eruption was noted over the right thigh and knee that had first appeared approximately 2 weeks prior. The rash started as pruritic blisters but gradually progressed to erythema and then eventually to brown markings, which were observed at the current presentation. Physical examination revealed hyperpigmented, brown, streaky, linear patches and plaques over the right thigh, knee, and lower leg (Figure). When asked about her hobbies, the patient reported an affinity for butterflies and noted that she attracts them with specific species of plants in her garden. She recalled recently planting the herb of grace, or common rue, to attract the giant swallowtail butterfly (Papilio cresphontes). Upon further inquiry, she remembered working in the garden on her knees and digging up roots near the common rue plant while wearing shorts approximately 2 weeks prior to the current presentation. Given the streaky linear pattern of the eruption along with recent sun exposure and exposure to the common rue plant, a diagnosis of phytophotodermatitis was made. No further treatment was sought, as the eruption was not bothersome to her. She was intrigued that the common rue plant had caused the dermatitis and planned on taking proper precautions when working near the plant in the future.

This case illustrates a unique perspective of phytophotodermatitis, as butterfly enthusiasm is not commonly reported in association with the common rue plant with respect to phytophotodermatitis. This case underscores the importance of inquiring about patients’ professions and hobbies, both in dermatology and other specialties.

What is an essential oil?

An essential oil (EO) is defined by the International Organization for Standardization as a ‘‘product obtained from a natural raw material of plant origin, by steam distillation, by mechanical processes from the epicarp of citrus fruits, or by dry distillation, after separation of the aqueous phase—if any—by physical processes.’’¹ Steam distillation is the primary method used for the production of commercial EOs,² and believe it or not, most EOs contain 100 to 250 individual chemical components.³

The term essential oil often is incorrectly used for a variety of products obtained from plant material by methods other than distillation or cold-pressing, such as extraction. Products that are obtained via the extraction method include absolutes found in fine fragrances; hydrolates such as rose water; concretes such as jasmine or violet leaves; and vegetable oils including olive oil, coconut oil, and sesame oil.² These products are not true EOs.

Where do EOs come from?

Essential oils are produced in many countries around the world.⁴ Individual oils may be obtained from species of different plants, from different parts of the same plant, or from various cultivars (plants selectively bred to obtain desirable levels of chemical constituents such as monoterpenes or sesquiterpenes and biochemical properties such as antibacterial or antioxidant activities).^3,5 It is estimated that EOs can be obtained from approximately 30,000 plant species, but only 150 EOs are produced commercially.^2,6

Why are people using EOs? What is their claim to fame?

Essential oils are employed by the flavor, food (eg, soft drinks, milk, candies, chocolate, meats, sausages, alcoholic beverages, spices, herbs, tea, preservatives, animal foods), fragrance, cosmetic, tobacco, and pharmaceutical industries. They also are used in household products (eg, detergents, fabric softeners, air fresheners, candles, incense) and for medicinal purposes (eg, folk and traditional medicine, phytotherapy, balneotherapy, aromatherapy).² The oils usually are applied to the skin but also can be administered orally, inhaled, diffused through the air, or used by other means.⁴ One 2019 survey of Minnesota State Fair attendees (N=282) found the most common reasons for using EOs were a desire for alternative treatments (53.4%), the opinion that EOs are safer than traditional therapies (47.6%), and/or failure of standard medical treatments (10.7%). The survey results also indicated that 46.7% of EO users utilized EOs to treat medical conditions or symptoms.⁷ Of note, review of the website of an international company that produces EOs confirmed that EOs are marketed not only for adults but also for children to help them concentrate,⁸ sleep,⁹ improve the appearance of their skin,¹⁰ soothe upset stomachs,¹¹ and decrease sniffles due to colds.¹²

Why are people selling EOs to family and friends? They must be making major bucks!

In general, the cost of EOs depends on the complexity of cultivated plant species; the mode of harvesting, which is sometimes done by hand; and the yield of oil. Prices range from $4.50 to an incredible $150,000 per kilogram.² On average, one bottle containing 5 to 15 mL of an EO or oil blend can cost anywhere from $7 to $251.¹³ In the United States, the consumer EO market is partially composed of multilevel/network marketing companies in which direct consumer sales occur via a hierarchy of individual distributors. Goodier et al⁷ found that 36.4% of participants who obtained EOs from family and friends purchased them through multilevel/network marketing companies. In 2018, individual distributors of an international EO-producing company made on average anywhere from $4 to as much as $1.54 million annually by selling the company’s EO products and enrolling additional members/individual distributors to purchase or sell the company’s EO products.¹⁴

Sometimes EOs are described as natural and pure, but are they really?

Just because a product is labeled as “pure” or “natural” does not ensure that it is a good-quality EO. Organically produced (ie, grown without the use of herbicides or pesticides) plant material can include up to 30% of extraneous herbs and weeds, which can change the composition of the oil.²

Lesser-quality EOs are the result of adulteration, contamination, inadequate oil production, or aging.² Adulteration (eg, cutting, stretching, bouquetting) occurs when foreign substances are introduced into pure EOs for the benefit of a higher profit; to ensure a sufficient supply of oils; or to meet demands for cheaper oils by “stretching” a more expensive, pure oil by combining with a cheaper, less pure oil. Inadequate oil production leading to lower-quality oils can occur when a biomass is incorrectly distilled, either from too much steam or temperatures that are too high or due to lack of adequate cooling units. Aging occurs when the oils are not stored properly, resulting in a change in the chemical composition due to esterification, reduction, and oxidization of chemicals, which leads to the formation of peroxides and hydroperoxides that can be contact allergens.¹⁵

Can patients develop contact allergies to EOs?

The short answer is yes! Contact allergy to almost 80 EOs has been reported,¹⁵ including tea tree oil,^16,17 ylang-ylang oil,^17,18 lavender oil, peppermint oil,¹⁸ jasmine absolute,¹⁷ geranium oil, rose oil,¹⁸ turpentine oil,^19,20 and sandalwood oil.¹⁸ The recent increased prevalence of allergic reactions to EOs likely is due to increased consumer use as well as increased detection from availability of commercial patch-test preparations.

Essential oils have many common ingredients. De Groot and Schmidt³ documented that 14 of 23 chemicals present in more than 80% of EOs have been reported to cause contact allergy. Interestingly, allergic patients often react to more than one EO, which may be explained by the many shared chemical components in EOs.

Essential oils are “natural” so they must be safe?

In general, most safety profiles are good, but rare toxic reactions from EOs have been observed.⁴ A recent Australian study reviewed EO exposure calls to the New South Wales Poisons Information Centre.²¹ The majority of EO poisonings were accidental or the result of therapeutic error such as mistaking EOs for liquid pharmaceuticals. Additionally, this study found that from July 2014 to June 2018, there was a 5% increase in the number of calls per year. More than half of EO poisoning calls involved children, with toddlers being the most frequent cases, suggesting the need for child-resistant top closures. The most frequently involved EOs in poisonings were eucalyptus (46.4% [n=2049]), tea tree (17% [n=749]), lavender (6.1% [n=271]), clove (4.1% [n=179]), and peppermint (3.5% [n=154]).²¹ Essential oils do not come without potential pitfalls.

What is the clinical presentation and workup?

The workup of EO allergic contact dermatitis begins with obtaining a history to evaluate for use of EO diffusers, perfumes, hygiene products, cosmetics, massage oils, toothpastes, and/or pharmaceutical products. Exploration of potential exposures through occupation, environment, and hobbies also is indicated. Clinical presentation is dependent on the mechanism of exposure. Contact allergy may result from direct application of an allergen to the skin or mucous membranes, contact with a contaminated environmental item (eg, lavender oil on a pillow), contact with EOs used by partners or coworkers (consort dermatitis), airborne exposure (EO diffusers), or systemic exposure (flavorings). Airborne dermatitis from EO diffusers may involve the exposed areas of the face, neck, forearms, arms, behind the earlobes, bilateral eyelids, nasolabial folds, and under the chin. History and clinical presentation can raise suspicion for allergic contact dermatitis, and patch testing is necessary to confirm the diagnosis.

How do we patch test for EO contact allergy?

There are many EOs commercially available for patch testing, and they typically are tested at 2% to 5% concentrations in petrolatum.¹⁵ A North American and European study of 62,354 patch-tested patients found that 7.4% of EO-positive individuals did not react to fragrance allergens in a standard screening series including fragrance mix I, fragrance mix II, and balsam of Peru, highlighting the importance of patch testing with specific EOs.²² Currently, only 3 EOs—tea tree oil, peppermint oil, and ylang-ylang oil—are included in the 2019-2020 North American Contact Dermatitis Group screening series, making supplemental testing for other EOs important if contact allergy is suspected; however, testing the patient’s own products is imperative, as there is strong variability in the composition of EOs. Additionally, aged oils may have been exposed to light, oxygen, or varying temperatures, which could result in the formation of additional allergenic chemicals not present in commercially available preparations.¹⁵ In addition to commercially available allergens, we test patient-provided EOs either as is in semi-open fashion (ie, EOs are applied to patient’s back with a cotton swab, allowed to dry, covered with adhesive tape, and read at the same interval as other patch tests²³) or occasionally dilute them to 1% or 10% (in olive oil or mineral oil).

How should I manage a positive patch-test reaction to EOs?

Patients should avoid relevant EO allergens in their products and environment, which can be easily achieved with the use of the American Contact Dermatitis Society’s Contact Allergen Management Program or similar databases.

Final Interpretation

We are ubiquitously exposed to EOs every day—through the products we use at home, at work, and in our environment. Essential oils make their place in the world by providing sweet-smelling aromas in addition to their alleged therapeutic properties; however, beware, EOs may be the culprit of your next patient’s allergic contact dermatitis.

What is an essential oil?

An essential oil (EO) is defined by the International Organization for Standardization as a ‘‘product obtained from a natural raw material of plant origin, by steam distillation, by mechanical processes from the epicarp of citrus fruits, or by dry distillation, after separation of the aqueous phase—if any—by physical processes.’’¹ Steam distillation is the primary method used for the production of commercial EOs,² and believe it or not, most EOs contain 100 to 250 individual chemical components.³

The term essential oil often is incorrectly used for a variety of products obtained from plant material by methods other than distillation or cold-pressing, such as extraction. Products that are obtained via the extraction method include absolutes found in fine fragrances; hydrolates such as rose water; concretes such as jasmine or violet leaves; and vegetable oils including olive oil, coconut oil, and sesame oil.² These products are not true EOs.

Where do EOs come from?

Essential oils are produced in many countries around the world.⁴ Individual oils may be obtained from species of different plants, from different parts of the same plant, or from various cultivars (plants selectively bred to obtain desirable levels of chemical constituents such as monoterpenes or sesquiterpenes and biochemical properties such as antibacterial or antioxidant activities).^3,5 It is estimated that EOs can be obtained from approximately 30,000 plant species, but only 150 EOs are produced commercially.^2,6

Why are people using EOs? What is their claim to fame?

Essential oils are employed by the flavor, food (eg, soft drinks, milk, candies, chocolate, meats, sausages, alcoholic beverages, spices, herbs, tea, preservatives, animal foods), fragrance, cosmetic, tobacco, and pharmaceutical industries. They also are used in household products (eg, detergents, fabric softeners, air fresheners, candles, incense) and for medicinal purposes (eg, folk and traditional medicine, phytotherapy, balneotherapy, aromatherapy).² The oils usually are applied to the skin but also can be administered orally, inhaled, diffused through the air, or used by other means.⁴ One 2019 survey of Minnesota State Fair attendees (N=282) found the most common reasons for using EOs were a desire for alternative treatments (53.4%), the opinion that EOs are safer than traditional therapies (47.6%), and/or failure of standard medical treatments (10.7%). The survey results also indicated that 46.7% of EO users utilized EOs to treat medical conditions or symptoms.⁷ Of note, review of the website of an international company that produces EOs confirmed that EOs are marketed not only for adults but also for children to help them concentrate,⁸ sleep,⁹ improve the appearance of their skin,¹⁰ soothe upset stomachs,¹¹ and decrease sniffles due to colds.¹²

Why are people selling EOs to family and friends? They must be making major bucks!

In general, the cost of EOs depends on the complexity of cultivated plant species; the mode of harvesting, which is sometimes done by hand; and the yield of oil. Prices range from $4.50 to an incredible $150,000 per kilogram.² On average, one bottle containing 5 to 15 mL of an EO or oil blend can cost anywhere from $7 to $251.¹³ In the United States, the consumer EO market is partially composed of multilevel/network marketing companies in which direct consumer sales occur via a hierarchy of individual distributors. Goodier et al⁷ found that 36.4% of participants who obtained EOs from family and friends purchased them through multilevel/network marketing companies. In 2018, individual distributors of an international EO-producing company made on average anywhere from $4 to as much as $1.54 million annually by selling the company’s EO products and enrolling additional members/individual distributors to purchase or sell the company’s EO products.¹⁴

Sometimes EOs are described as natural and pure, but are they really?

Just because a product is labeled as “pure” or “natural” does not ensure that it is a good-quality EO. Organically produced (ie, grown without the use of herbicides or pesticides) plant material can include up to 30% of extraneous herbs and weeds, which can change the composition of the oil.²

Lesser-quality EOs are the result of adulteration, contamination, inadequate oil production, or aging.² Adulteration (eg, cutting, stretching, bouquetting) occurs when foreign substances are introduced into pure EOs for the benefit of a higher profit; to ensure a sufficient supply of oils; or to meet demands for cheaper oils by “stretching” a more expensive, pure oil by combining with a cheaper, less pure oil. Inadequate oil production leading to lower-quality oils can occur when a biomass is incorrectly distilled, either from too much steam or temperatures that are too high or due to lack of adequate cooling units. Aging occurs when the oils are not stored properly, resulting in a change in the chemical composition due to esterification, reduction, and oxidization of chemicals, which leads to the formation of peroxides and hydroperoxides that can be contact allergens.¹⁵

Can patients develop contact allergies to EOs?

The short answer is yes! Contact allergy to almost 80 EOs has been reported,¹⁵ including tea tree oil,^16,17 ylang-ylang oil,^17,18 lavender oil, peppermint oil,¹⁸ jasmine absolute,¹⁷ geranium oil, rose oil,¹⁸ turpentine oil,^19,20 and sandalwood oil.¹⁸ The recent increased prevalence of allergic reactions to EOs likely is due to increased consumer use as well as increased detection from availability of commercial patch-test preparations.

Essential oils have many common ingredients. De Groot and Schmidt³ documented that 14 of 23 chemicals present in more than 80% of EOs have been reported to cause contact allergy. Interestingly, allergic patients often react to more than one EO, which may be explained by the many shared chemical components in EOs.

Essential oils are “natural” so they must be safe?

In general, most safety profiles are good, but rare toxic reactions from EOs have been observed.⁴ A recent Australian study reviewed EO exposure calls to the New South Wales Poisons Information Centre.²¹ The majority of EO poisonings were accidental or the result of therapeutic error such as mistaking EOs for liquid pharmaceuticals. Additionally, this study found that from July 2014 to June 2018, there was a 5% increase in the number of calls per year. More than half of EO poisoning calls involved children, with toddlers being the most frequent cases, suggesting the need for child-resistant top closures. The most frequently involved EOs in poisonings were eucalyptus (46.4% [n=2049]), tea tree (17% [n=749]), lavender (6.1% [n=271]), clove (4.1% [n=179]), and peppermint (3.5% [n=154]).²¹ Essential oils do not come without potential pitfalls.

What is the clinical presentation and workup?

The workup of EO allergic contact dermatitis begins with obtaining a history to evaluate for use of EO diffusers, perfumes, hygiene products, cosmetics, massage oils, toothpastes, and/or pharmaceutical products. Exploration of potential exposures through occupation, environment, and hobbies also is indicated. Clinical presentation is dependent on the mechanism of exposure. Contact allergy may result from direct application of an allergen to the skin or mucous membranes, contact with a contaminated environmental item (eg, lavender oil on a pillow), contact with EOs used by partners or coworkers (consort dermatitis), airborne exposure (EO diffusers), or systemic exposure (flavorings). Airborne dermatitis from EO diffusers may involve the exposed areas of the face, neck, forearms, arms, behind the earlobes, bilateral eyelids, nasolabial folds, and under the chin. History and clinical presentation can raise suspicion for allergic contact dermatitis, and patch testing is necessary to confirm the diagnosis.

How do we patch test for EO contact allergy?

There are many EOs commercially available for patch testing, and they typically are tested at 2% to 5% concentrations in petrolatum.¹⁵ A North American and European study of 62,354 patch-tested patients found that 7.4% of EO-positive individuals did not react to fragrance allergens in a standard screening series including fragrance mix I, fragrance mix II, and balsam of Peru, highlighting the importance of patch testing with specific EOs.²² Currently, only 3 EOs—tea tree oil, peppermint oil, and ylang-ylang oil—are included in the 2019-2020 North American Contact Dermatitis Group screening series, making supplemental testing for other EOs important if contact allergy is suspected; however, testing the patient’s own products is imperative, as there is strong variability in the composition of EOs. Additionally, aged oils may have been exposed to light, oxygen, or varying temperatures, which could result in the formation of additional allergenic chemicals not present in commercially available preparations.¹⁵ In addition to commercially available allergens, we test patient-provided EOs either as is in semi-open fashion (ie, EOs are applied to patient’s back with a cotton swab, allowed to dry, covered with adhesive tape, and read at the same interval as other patch tests²³) or occasionally dilute them to 1% or 10% (in olive oil or mineral oil).

How should I manage a positive patch-test reaction to EOs?

Patients should avoid relevant EO allergens in their products and environment, which can be easily achieved with the use of the American Contact Dermatitis Society’s Contact Allergen Management Program or similar databases.

Final Interpretation

We are ubiquitously exposed to EOs every day—through the products we use at home, at work, and in our environment. Essential oils make their place in the world by providing sweet-smelling aromas in addition to their alleged therapeutic properties; however, beware, EOs may be the culprit of your next patient’s allergic contact dermatitis.

What is an essential oil?

An essential oil (EO) is defined by the International Organization for Standardization as a ‘‘product obtained from a natural raw material of plant origin, by steam distillation, by mechanical processes from the epicarp of citrus fruits, or by dry distillation, after separation of the aqueous phase—if any—by physical processes.’’¹ Steam distillation is the primary method used for the production of commercial EOs,² and believe it or not, most EOs contain 100 to 250 individual chemical components.³

The term essential oil often is incorrectly used for a variety of products obtained from plant material by methods other than distillation or cold-pressing, such as extraction. Products that are obtained via the extraction method include absolutes found in fine fragrances; hydrolates such as rose water; concretes such as jasmine or violet leaves; and vegetable oils including olive oil, coconut oil, and sesame oil.² These products are not true EOs.

Where do EOs come from?

Essential oils are produced in many countries around the world.⁴ Individual oils may be obtained from species of different plants, from different parts of the same plant, or from various cultivars (plants selectively bred to obtain desirable levels of chemical constituents such as monoterpenes or sesquiterpenes and biochemical properties such as antibacterial or antioxidant activities).^3,5 It is estimated that EOs can be obtained from approximately 30,000 plant species, but only 150 EOs are produced commercially.^2,6

Why are people using EOs? What is their claim to fame?

Essential oils are employed by the flavor, food (eg, soft drinks, milk, candies, chocolate, meats, sausages, alcoholic beverages, spices, herbs, tea, preservatives, animal foods), fragrance, cosmetic, tobacco, and pharmaceutical industries. They also are used in household products (eg, detergents, fabric softeners, air fresheners, candles, incense) and for medicinal purposes (eg, folk and traditional medicine, phytotherapy, balneotherapy, aromatherapy).² The oils usually are applied to the skin but also can be administered orally, inhaled, diffused through the air, or used by other means.⁴ One 2019 survey of Minnesota State Fair attendees (N=282) found the most common reasons for using EOs were a desire for alternative treatments (53.4%), the opinion that EOs are safer than traditional therapies (47.6%), and/or failure of standard medical treatments (10.7%). The survey results also indicated that 46.7% of EO users utilized EOs to treat medical conditions or symptoms.⁷ Of note, review of the website of an international company that produces EOs confirmed that EOs are marketed not only for adults but also for children to help them concentrate,⁸ sleep,⁹ improve the appearance of their skin,¹⁰ soothe upset stomachs,¹¹ and decrease sniffles due to colds.¹²

Why are people selling EOs to family and friends? They must be making major bucks!

In general, the cost of EOs depends on the complexity of cultivated plant species; the mode of harvesting, which is sometimes done by hand; and the yield of oil. Prices range from $4.50 to an incredible $150,000 per kilogram.² On average, one bottle containing 5 to 15 mL of an EO or oil blend can cost anywhere from $7 to $251.¹³ In the United States, the consumer EO market is partially composed of multilevel/network marketing companies in which direct consumer sales occur via a hierarchy of individual distributors. Goodier et al⁷ found that 36.4% of participants who obtained EOs from family and friends purchased them through multilevel/network marketing companies. In 2018, individual distributors of an international EO-producing company made on average anywhere from $4 to as much as $1.54 million annually by selling the company’s EO products and enrolling additional members/individual distributors to purchase or sell the company’s EO products.¹⁴

Sometimes EOs are described as natural and pure, but are they really?

Just because a product is labeled as “pure” or “natural” does not ensure that it is a good-quality EO. Organically produced (ie, grown without the use of herbicides or pesticides) plant material can include up to 30% of extraneous herbs and weeds, which can change the composition of the oil.²

Lesser-quality EOs are the result of adulteration, contamination, inadequate oil production, or aging.² Adulteration (eg, cutting, stretching, bouquetting) occurs when foreign substances are introduced into pure EOs for the benefit of a higher profit; to ensure a sufficient supply of oils; or to meet demands for cheaper oils by “stretching” a more expensive, pure oil by combining with a cheaper, less pure oil. Inadequate oil production leading to lower-quality oils can occur when a biomass is incorrectly distilled, either from too much steam or temperatures that are too high or due to lack of adequate cooling units. Aging occurs when the oils are not stored properly, resulting in a change in the chemical composition due to esterification, reduction, and oxidization of chemicals, which leads to the formation of peroxides and hydroperoxides that can be contact allergens.¹⁵

Can patients develop contact allergies to EOs?

The short answer is yes! Contact allergy to almost 80 EOs has been reported,¹⁵ including tea tree oil,^16,17 ylang-ylang oil,^17,18 lavender oil, peppermint oil,¹⁸ jasmine absolute,¹⁷ geranium oil, rose oil,¹⁸ turpentine oil,^19,20 and sandalwood oil.¹⁸ The recent increased prevalence of allergic reactions to EOs likely is due to increased consumer use as well as increased detection from availability of commercial patch-test preparations.

Essential oils have many common ingredients. De Groot and Schmidt³ documented that 14 of 23 chemicals present in more than 80% of EOs have been reported to cause contact allergy. Interestingly, allergic patients often react to more than one EO, which may be explained by the many shared chemical components in EOs.

Essential oils are “natural” so they must be safe?

In general, most safety profiles are good, but rare toxic reactions from EOs have been observed.⁴ A recent Australian study reviewed EO exposure calls to the New South Wales Poisons Information Centre.²¹ The majority of EO poisonings were accidental or the result of therapeutic error such as mistaking EOs for liquid pharmaceuticals. Additionally, this study found that from July 2014 to June 2018, there was a 5% increase in the number of calls per year. More than half of EO poisoning calls involved children, with toddlers being the most frequent cases, suggesting the need for child-resistant top closures. The most frequently involved EOs in poisonings were eucalyptus (46.4% [n=2049]), tea tree (17% [n=749]), lavender (6.1% [n=271]), clove (4.1% [n=179]), and peppermint (3.5% [n=154]).²¹ Essential oils do not come without potential pitfalls.

What is the clinical presentation and workup?

The workup of EO allergic contact dermatitis begins with obtaining a history to evaluate for use of EO diffusers, perfumes, hygiene products, cosmetics, massage oils, toothpastes, and/or pharmaceutical products. Exploration of potential exposures through occupation, environment, and hobbies also is indicated. Clinical presentation is dependent on the mechanism of exposure. Contact allergy may result from direct application of an allergen to the skin or mucous membranes, contact with a contaminated environmental item (eg, lavender oil on a pillow), contact with EOs used by partners or coworkers (consort dermatitis), airborne exposure (EO diffusers), or systemic exposure (flavorings). Airborne dermatitis from EO diffusers may involve the exposed areas of the face, neck, forearms, arms, behind the earlobes, bilateral eyelids, nasolabial folds, and under the chin. History and clinical presentation can raise suspicion for allergic contact dermatitis, and patch testing is necessary to confirm the diagnosis.

How do we patch test for EO contact allergy?

There are many EOs commercially available for patch testing, and they typically are tested at 2% to 5% concentrations in petrolatum.¹⁵ A North American and European study of 62,354 patch-tested patients found that 7.4% of EO-positive individuals did not react to fragrance allergens in a standard screening series including fragrance mix I, fragrance mix II, and balsam of Peru, highlighting the importance of patch testing with specific EOs.²² Currently, only 3 EOs—tea tree oil, peppermint oil, and ylang-ylang oil—are included in the 2019-2020 North American Contact Dermatitis Group screening series, making supplemental testing for other EOs important if contact allergy is suspected; however, testing the patient’s own products is imperative, as there is strong variability in the composition of EOs. Additionally, aged oils may have been exposed to light, oxygen, or varying temperatures, which could result in the formation of additional allergenic chemicals not present in commercially available preparations.¹⁵ In addition to commercially available allergens, we test patient-provided EOs either as is in semi-open fashion (ie, EOs are applied to patient’s back with a cotton swab, allowed to dry, covered with adhesive tape, and read at the same interval as other patch tests²³) or occasionally dilute them to 1% or 10% (in olive oil or mineral oil).

How should I manage a positive patch-test reaction to EOs?

Patients should avoid relevant EO allergens in their products and environment, which can be easily achieved with the use of the American Contact Dermatitis Society’s Contact Allergen Management Program or similar databases.

Final Interpretation

We are ubiquitously exposed to EOs every day—through the products we use at home, at work, and in our environment. Essential oils make their place in the world by providing sweet-smelling aromas in addition to their alleged therapeutic properties; however, beware, EOs may be the culprit of your next patient’s allergic contact dermatitis.

To the Editor:

In 1998, 2-octyl-cyanoacrylate (2-CA) tissue adhesive gained US Food and Drug Administration approval for topical application to easily hold closed approximated skin edges from surgical excisions and simple trauma-induced lacerations.¹ It has since been employed for a number of off-label indications, including sutureless circumcision,² skin graft fixation,³ pericatheter leakage,⁴ and intracorporeal use to control air leaks during lung resection.⁵ Animal investigations additionally have attempted to elucidate potential future uses of 2-CA for procedures such as inguinal hernia repair,⁶ bowel anastomosis,⁷ incisional hernia repair with mesh,⁸ and microvascular anastomosis.⁹ Compared to sutures, 2-CA offers ease and rapidity of application, a water-resistant barrier, and equivalent cosmetic results, as well as eliminates the need for suture removal.¹⁰ As 2-CA is used with increasing frequency across a variety of settings, there arises a greater need to be mindful of the potential complications of its use, such as irritant contact dermatitis (ICD), allergic contact dermatitis (ACD), and cutaneous id reaction.

A 14-year-old adolescent boy with no notable medical history and no known allergies underwent a minimally invasive Nuss procedure¹¹ (performed by P.L.G.) for the repair of severe pectus excavatum. Two 4-cm incisions were made—one in each lateral chest wall at the approximately eighth intercostal space—to facilitate the introduction of the Nuss bar. The surgical wounds were closed with 2 layers of running polyglactin 910 suture before 2-CA was applied topically to the incision sites. The surgery was well tolerated, and the patient’s wounds healed without incident. When the patient was evaluated for Nuss bar removal 3 years later, incision sites were noted to be well healed, and he exhibited no other skin lesions. The original incision sites (bilateral chest walls) were utilized to facilitate surgical Nuss bar removal. The wounds were closed in 4 layers and 2-CA was again applied topically to the incision sites. There were no intraoperative complications; no devices, drains, or tissue implants were left in the patient at the conclusion of the procedure.

One week later, via text message and digital photographs, the patient reported intense pruritus at the bilateral chest wall incision sites, which were now surrounded by symmetric 1-cm erythematous plaques and associated sparse erythematous satellite papules (Figure 1). The patient denied any fevers, pain, swelling, or purulent discharge from the wounds. He was started on hydrocortisone cream 1% twice daily as well as oral diphenhydramine 25 mg at bedtime with initial good effect.

Allergic contact dermatitis is a type IV hypersensitivity reaction that appears after initial sensitization to an allergen followed by re-exposure. Our patient presented with symmetric erythematous plaques at the surgical incision sites 1 week after 2-CA had been applied. During this interval, sensitization to the inciting allergen occurred. The allergen is taken up by antigen-presenting cells, which then migrate to lymph nodes where they encounter naïve T lymphocytes that subsequently undergo clonal expansion to produce a cohort of T cells that are capable of recognizing the allergen. If subsequent exposure to the specific allergen takes place, an elicitation phase occurs in which primed T cells are incited to release mediators of inflammation that engender the manifestations of ACD within 24 to 72 hours.^18,20 Sensitization may be promoted by skin barrier impairments such as dermatitis or a frank wound.^12,20 In most cases, the patient is unaware that sensitization has occurred, though a primary ACD within 5 to 15 days after initial exposure to the inciting allergen rarely may be observed.¹⁸ Although our patient had 2-CA applied to his surgical wounds at 14 years of age, it was unlikely that sensitization took place at that time, as it was 1 week rather than 1 to 3 days before he experienced the cutaneous eruption associated with his second 2-CA exposure at 17 years of age.

Cyanoacrylate tissue adhesive also may cause ICD resulting from histotoxic degradation products such as formaldehyde and cyanoacetate that are capable of compromising cutaneous barrier function. Keratinocytes that have had their membranes disturbed release proinflammatory cytokines, which recruit cells of the innate immune system as well as T lymphocytes to the site of insult to facilitate the inflammatory response. The manifestations of ICD include erythema, edema, and local necrosis that can compromise wound healing.²⁰ The speed at which a given cyanoacrylate adhesive degrades is proportional to the length of its carbon side chain. Those with shorter side chains—ethyl and methyl cyanoacrylate—degrade more rapidly into formaldehyde and cyanoacetate; 2-CA possesses a longer side chain and therefore degrades more slowly, which should, in theory, lessen its potential to cause ICD.²⁰ Because it may take 7 to 14 days before 2-CA will spontaneously peel from the application site, however, its potential to evoke ICD nevertheless exists.

Treatment of ICD entails removing the irritant while concurrently working to restore the skin’s barrier with emollients. Although topical corticosteroids often are reflexively prescribed to treat rashes, some believe that their use should be avoided in cases of ICD, as their inhibitory effects on epidermal lipid synthesis may further impair the skin’s barrier.²¹ For cases of ACD, with or without an accompanying id reaction, topical corticosteroids are the mainstay of therapy. It is customary to start with a higher-potency topical steroid such as clobetasol and taper to lower-potency steroids as the patient’s condition improves. Steroid ointments are petroleum based and are capable of causing 2-CA to separate from the skin.¹⁰ As a result, they should be used with care when being applied to an area where 2-CA is maintaining dermal closure. Systemic corticosteroids may be warranted in cases with involvement of more than 20% of the body surface area and should start to provide relief within 12 to 24 hours.²² Oral antihistamines and cold water compresses can be added to help address pruritus and discomfort in both ACD and ICD.

Instances of contact dermatitis caused by 2-CA are rare, and progression to an id reaction is rarer still. Physicians should be aware of the possibility of encountering a patient that manifests one or both of these complications whenever 2-CA is employed for skin closure. Physicians who employ 2-CA for skin closure should first ask patients about prior cutaneous reactions to cyanoacrylates including 2-CA and other commonly encountered acrylate-containing products including adhesive wound dressings, dental cements and prostheses, superglue, artificial nails, and adhesives for wigs and false eyelashes. Still, many patients who exhibit acrylate-induced contact dermatitis, with or without an associated id reaction, will not attest to a history of adverse reactions; they simply may not recognize acrylate as the inciting agent. Practitioners across a range of specialties outside of dermatology—surgeons, emergency physicians, and primary care providers—should be prepared to both recognize contact dermatitis and id reaction arising from the use of 2-CA and implement a basic treatment plan that will bring the patient relief without compromising wound closure.

To the Editor:

In 1998, 2-octyl-cyanoacrylate (2-CA) tissue adhesive gained US Food and Drug Administration approval for topical application to easily hold closed approximated skin edges from surgical excisions and simple trauma-induced lacerations.¹ It has since been employed for a number of off-label indications, including sutureless circumcision,² skin graft fixation,³ pericatheter leakage,⁴ and intracorporeal use to control air leaks during lung resection.⁵ Animal investigations additionally have attempted to elucidate potential future uses of 2-CA for procedures such as inguinal hernia repair,⁶ bowel anastomosis,⁷ incisional hernia repair with mesh,⁸ and microvascular anastomosis.⁹ Compared to sutures, 2-CA offers ease and rapidity of application, a water-resistant barrier, and equivalent cosmetic results, as well as eliminates the need for suture removal.¹⁰ As 2-CA is used with increasing frequency across a variety of settings, there arises a greater need to be mindful of the potential complications of its use, such as irritant contact dermatitis (ICD), allergic contact dermatitis (ACD), and cutaneous id reaction.

A 14-year-old adolescent boy with no notable medical history and no known allergies underwent a minimally invasive Nuss procedure¹¹ (performed by P.L.G.) for the repair of severe pectus excavatum. Two 4-cm incisions were made—one in each lateral chest wall at the approximately eighth intercostal space—to facilitate the introduction of the Nuss bar. The surgical wounds were closed with 2 layers of running polyglactin 910 suture before 2-CA was applied topically to the incision sites. The surgery was well tolerated, and the patient’s wounds healed without incident. When the patient was evaluated for Nuss bar removal 3 years later, incision sites were noted to be well healed, and he exhibited no other skin lesions. The original incision sites (bilateral chest walls) were utilized to facilitate surgical Nuss bar removal. The wounds were closed in 4 layers and 2-CA was again applied topically to the incision sites. There were no intraoperative complications; no devices, drains, or tissue implants were left in the patient at the conclusion of the procedure.

One week later, via text message and digital photographs, the patient reported intense pruritus at the bilateral chest wall incision sites, which were now surrounded by symmetric 1-cm erythematous plaques and associated sparse erythematous satellite papules (Figure 1). The patient denied any fevers, pain, swelling, or purulent discharge from the wounds. He was started on hydrocortisone cream 1% twice daily as well as oral diphenhydramine 25 mg at bedtime with initial good effect.

Allergic contact dermatitis is a type IV hypersensitivity reaction that appears after initial sensitization to an allergen followed by re-exposure. Our patient presented with symmetric erythematous plaques at the surgical incision sites 1 week after 2-CA had been applied. During this interval, sensitization to the inciting allergen occurred. The allergen is taken up by antigen-presenting cells, which then migrate to lymph nodes where they encounter naïve T lymphocytes that subsequently undergo clonal expansion to produce a cohort of T cells that are capable of recognizing the allergen. If subsequent exposure to the specific allergen takes place, an elicitation phase occurs in which primed T cells are incited to release mediators of inflammation that engender the manifestations of ACD within 24 to 72 hours.^18,20 Sensitization may be promoted by skin barrier impairments such as dermatitis or a frank wound.^12,20 In most cases, the patient is unaware that sensitization has occurred, though a primary ACD within 5 to 15 days after initial exposure to the inciting allergen rarely may be observed.¹⁸ Although our patient had 2-CA applied to his surgical wounds at 14 years of age, it was unlikely that sensitization took place at that time, as it was 1 week rather than 1 to 3 days before he experienced the cutaneous eruption associated with his second 2-CA exposure at 17 years of age.

Cyanoacrylate tissue adhesive also may cause ICD resulting from histotoxic degradation products such as formaldehyde and cyanoacetate that are capable of compromising cutaneous barrier function. Keratinocytes that have had their membranes disturbed release proinflammatory cytokines, which recruit cells of the innate immune system as well as T lymphocytes to the site of insult to facilitate the inflammatory response. The manifestations of ICD include erythema, edema, and local necrosis that can compromise wound healing.²⁰ The speed at which a given cyanoacrylate adhesive degrades is proportional to the length of its carbon side chain. Those with shorter side chains—ethyl and methyl cyanoacrylate—degrade more rapidly into formaldehyde and cyanoacetate; 2-CA possesses a longer side chain and therefore degrades more slowly, which should, in theory, lessen its potential to cause ICD.²⁰ Because it may take 7 to 14 days before 2-CA will spontaneously peel from the application site, however, its potential to evoke ICD nevertheless exists.

Treatment of ICD entails removing the irritant while concurrently working to restore the skin’s barrier with emollients. Although topical corticosteroids often are reflexively prescribed to treat rashes, some believe that their use should be avoided in cases of ICD, as their inhibitory effects on epidermal lipid synthesis may further impair the skin’s barrier.²¹ For cases of ACD, with or without an accompanying id reaction, topical corticosteroids are the mainstay of therapy. It is customary to start with a higher-potency topical steroid such as clobetasol and taper to lower-potency steroids as the patient’s condition improves. Steroid ointments are petroleum based and are capable of causing 2-CA to separate from the skin.¹⁰ As a result, they should be used with care when being applied to an area where 2-CA is maintaining dermal closure. Systemic corticosteroids may be warranted in cases with involvement of more than 20% of the body surface area and should start to provide relief within 12 to 24 hours.²² Oral antihistamines and cold water compresses can be added to help address pruritus and discomfort in both ACD and ICD.

Instances of contact dermatitis caused by 2-CA are rare, and progression to an id reaction is rarer still. Physicians should be aware of the possibility of encountering a patient that manifests one or both of these complications whenever 2-CA is employed for skin closure. Physicians who employ 2-CA for skin closure should first ask patients about prior cutaneous reactions to cyanoacrylates including 2-CA and other commonly encountered acrylate-containing products including adhesive wound dressings, dental cements and prostheses, superglue, artificial nails, and adhesives for wigs and false eyelashes. Still, many patients who exhibit acrylate-induced contact dermatitis, with or without an associated id reaction, will not attest to a history of adverse reactions; they simply may not recognize acrylate as the inciting agent. Practitioners across a range of specialties outside of dermatology—surgeons, emergency physicians, and primary care providers—should be prepared to both recognize contact dermatitis and id reaction arising from the use of 2-CA and implement a basic treatment plan that will bring the patient relief without compromising wound closure.

To the Editor:

In 1998, 2-octyl-cyanoacrylate (2-CA) tissue adhesive gained US Food and Drug Administration approval for topical application to easily hold closed approximated skin edges from surgical excisions and simple trauma-induced lacerations.¹ It has since been employed for a number of off-label indications, including sutureless circumcision,² skin graft fixation,³ pericatheter leakage,⁴ and intracorporeal use to control air leaks during lung resection.⁵ Animal investigations additionally have attempted to elucidate potential future uses of 2-CA for procedures such as inguinal hernia repair,⁶ bowel anastomosis,⁷ incisional hernia repair with mesh,⁸ and microvascular anastomosis.⁹ Compared to sutures, 2-CA offers ease and rapidity of application, a water-resistant barrier, and equivalent cosmetic results, as well as eliminates the need for suture removal.¹⁰ As 2-CA is used with increasing frequency across a variety of settings, there arises a greater need to be mindful of the potential complications of its use, such as irritant contact dermatitis (ICD), allergic contact dermatitis (ACD), and cutaneous id reaction.

A 14-year-old adolescent boy with no notable medical history and no known allergies underwent a minimally invasive Nuss procedure¹¹ (performed by P.L.G.) for the repair of severe pectus excavatum. Two 4-cm incisions were made—one in each lateral chest wall at the approximately eighth intercostal space—to facilitate the introduction of the Nuss bar. The surgical wounds were closed with 2 layers of running polyglactin 910 suture before 2-CA was applied topically to the incision sites. The surgery was well tolerated, and the patient’s wounds healed without incident. When the patient was evaluated for Nuss bar removal 3 years later, incision sites were noted to be well healed, and he exhibited no other skin lesions. The original incision sites (bilateral chest walls) were utilized to facilitate surgical Nuss bar removal. The wounds were closed in 4 layers and 2-CA was again applied topically to the incision sites. There were no intraoperative complications; no devices, drains, or tissue implants were left in the patient at the conclusion of the procedure.

One week later, via text message and digital photographs, the patient reported intense pruritus at the bilateral chest wall incision sites, which were now surrounded by symmetric 1-cm erythematous plaques and associated sparse erythematous satellite papules (Figure 1). The patient denied any fevers, pain, swelling, or purulent discharge from the wounds. He was started on hydrocortisone cream 1% twice daily as well as oral diphenhydramine 25 mg at bedtime with initial good effect.

Allergic contact dermatitis is a type IV hypersensitivity reaction that appears after initial sensitization to an allergen followed by re-exposure. Our patient presented with symmetric erythematous plaques at the surgical incision sites 1 week after 2-CA had been applied. During this interval, sensitization to the inciting allergen occurred. The allergen is taken up by antigen-presenting cells, which then migrate to lymph nodes where they encounter naïve T lymphocytes that subsequently undergo clonal expansion to produce a cohort of T cells that are capable of recognizing the allergen. If subsequent exposure to the specific allergen takes place, an elicitation phase occurs in which primed T cells are incited to release mediators of inflammation that engender the manifestations of ACD within 24 to 72 hours.^18,20 Sensitization may be promoted by skin barrier impairments such as dermatitis or a frank wound.^12,20 In most cases, the patient is unaware that sensitization has occurred, though a primary ACD within 5 to 15 days after initial exposure to the inciting allergen rarely may be observed.¹⁸ Although our patient had 2-CA applied to his surgical wounds at 14 years of age, it was unlikely that sensitization took place at that time, as it was 1 week rather than 1 to 3 days before he experienced the cutaneous eruption associated with his second 2-CA exposure at 17 years of age.

Cyanoacrylate tissue adhesive also may cause ICD resulting from histotoxic degradation products such as formaldehyde and cyanoacetate that are capable of compromising cutaneous barrier function. Keratinocytes that have had their membranes disturbed release proinflammatory cytokines, which recruit cells of the innate immune system as well as T lymphocytes to the site of insult to facilitate the inflammatory response. The manifestations of ICD include erythema, edema, and local necrosis that can compromise wound healing.²⁰ The speed at which a given cyanoacrylate adhesive degrades is proportional to the length of its carbon side chain. Those with shorter side chains—ethyl and methyl cyanoacrylate—degrade more rapidly into formaldehyde and cyanoacetate; 2-CA possesses a longer side chain and therefore degrades more slowly, which should, in theory, lessen its potential to cause ICD.²⁰ Because it may take 7 to 14 days before 2-CA will spontaneously peel from the application site, however, its potential to evoke ICD nevertheless exists.

Treatment of ICD entails removing the irritant while concurrently working to restore the skin’s barrier with emollients. Although topical corticosteroids often are reflexively prescribed to treat rashes, some believe that their use should be avoided in cases of ICD, as their inhibitory effects on epidermal lipid synthesis may further impair the skin’s barrier.²¹ For cases of ACD, with or without an accompanying id reaction, topical corticosteroids are the mainstay of therapy. It is customary to start with a higher-potency topical steroid such as clobetasol and taper to lower-potency steroids as the patient’s condition improves. Steroid ointments are petroleum based and are capable of causing 2-CA to separate from the skin.¹⁰ As a result, they should be used with care when being applied to an area where 2-CA is maintaining dermal closure. Systemic corticosteroids may be warranted in cases with involvement of more than 20% of the body surface area and should start to provide relief within 12 to 24 hours.²² Oral antihistamines and cold water compresses can be added to help address pruritus and discomfort in both ACD and ICD.

Instances of contact dermatitis caused by 2-CA are rare, and progression to an id reaction is rarer still. Physicians should be aware of the possibility of encountering a patient that manifests one or both of these complications whenever 2-CA is employed for skin closure. Physicians who employ 2-CA for skin closure should first ask patients about prior cutaneous reactions to cyanoacrylates including 2-CA and other commonly encountered acrylate-containing products including adhesive wound dressings, dental cements and prostheses, superglue, artificial nails, and adhesives for wigs and false eyelashes. Still, many patients who exhibit acrylate-induced contact dermatitis, with or without an associated id reaction, will not attest to a history of adverse reactions; they simply may not recognize acrylate as the inciting agent. Practitioners across a range of specialties outside of dermatology—surgeons, emergency physicians, and primary care providers—should be prepared to both recognize contact dermatitis and id reaction arising from the use of 2-CA and implement a basic treatment plan that will bring the patient relief without compromising wound closure.

A variety of toys and other play products can cause contact dermatitis in children because of the nature of their ingredients, according to the results of a review of 25 published articles.

Motortion/Getty Images

“In recent years the products have become a reflection of the compounds used frequently in manufacturing, including metals and plastic compounds,” wrote Justine Fenner, MD, and coauthors, from the departments of dermatology and pediatrics at the Icahn School of Medicine at Mount Sinai, New York,

In a study published in Contact Dermatitis, the researchers identified 25 articles describing dermatitis, rash, or eczema associated with a range of toy and play product terms including Nintendo, PlayStation, putty, glue, doll, game, car, bicycle, slime, iPad, and iPhone.

Overall, nickel was the most common allergen. Cases of nickel dermatitis were associated with laptops, videogame controllers, iPads, and cell phones. Cell phones were the most common electronics associated with contact dermatitis, which was observed on the cheek, periauricular area, and hand, as well as the breast in one case of a patient who kept her phone in her bra.

Other sources of metal allergens were identified in toy cars and costume jewelry, the researchers noted.

In addition, temporary tattoos have been associated with contact dermatitis in children, as have homemade “slime” products, which often contain not only borax or other household detergents, but also glue, shaving cream, or coloring.

However, identification of true allergic contact dermatitis from toys “requires both identification of the chemical contents of toys, which are proprietary in nature, and then epicutaneous allergy testing of these ingredients,” the researchers said.

The study findings were limited by several factors including the consideration only of English-language articles and of cases in children, which thus eliminates other potential cases, the researchers noted. However, the results suggest that dermatologists consider toys as a source of contact dermatitis in children, especially if the time to diagnosis is months to years, they said. “Additionally, it may be useful, as it was in several of the above cases, to have the patient bring in his or her favorite toys for the dermatologist to examine and help further understand the etiology of patient’s rash,” they noted. Moreover, “there is an unmet need for corporations to reveal the chemical ingredients of their toys when allergic contact dermatitis is suspected in order to properly evaluate the patient,” they added.

“Contact dermatitis has been underreported in children and constitutes an ongoing concern,” senior author Nanette Silverberg, MD, chief of pediatric dermatology for the Mount Sinai Health System, said in an interview.

“In particular, toy-related allergy is concerning due to the rise in allergen inclusion in common play items,” she commented. The current analysis identified many case reports of allergens that pediatric dermatologists are frequently seeing in their offices, notably metals such as nickel, she pointed out. “The allergen that always stands out ahead of others is nickel,” Dr. Silverberg said. “Nickel allergy affects about 25% of Americans, often starting in early childhood,” she said. “In the European Union, legislation has been passed to reduce nickel release from metals, which has resulted in less sensitization to nickel. We lack such legislation in the United States,” she added. 

Other trending allergens include methylchloroisothiazolinone/methylisothiazolinone, which may be components of glue or other ingredients in some “slime” products, Dr. Silverberg said.

She advised clinicians to consider patch testing when addressing localized or persistent dermatitis in children. “Furthermore, consider toys as potential relevant allergens that should be modified in order to achieve skin improvement,” she said.

“Greater reporting of pediatric allergic contact dermatitis is needed,” Dr. Silverberg emphasized. “Additionally, surveillance and monitoring for trends in allergen exposures in toys and personal care items is required to analyze this ongoing concern of childhood,” she said.

The study received no outside funding. The researchers had no financial conflicts to disclose.

SOURCE: Fenner J et al. Contact Dermatitis. 2020 Feb 22. doi: 10.1111/cod.13500.

A variety of toys and other play products can cause contact dermatitis in children because of the nature of their ingredients, according to the results of a review of 25 published articles.

Motortion/Getty Images

“In recent years the products have become a reflection of the compounds used frequently in manufacturing, including metals and plastic compounds,” wrote Justine Fenner, MD, and coauthors, from the departments of dermatology and pediatrics at the Icahn School of Medicine at Mount Sinai, New York,

In a study published in Contact Dermatitis, the researchers identified 25 articles describing dermatitis, rash, or eczema associated with a range of toy and play product terms including Nintendo, PlayStation, putty, glue, doll, game, car, bicycle, slime, iPad, and iPhone.

Overall, nickel was the most common allergen. Cases of nickel dermatitis were associated with laptops, videogame controllers, iPads, and cell phones. Cell phones were the most common electronics associated with contact dermatitis, which was observed on the cheek, periauricular area, and hand, as well as the breast in one case of a patient who kept her phone in her bra.

Other sources of metal allergens were identified in toy cars and costume jewelry, the researchers noted.

In addition, temporary tattoos have been associated with contact dermatitis in children, as have homemade “slime” products, which often contain not only borax or other household detergents, but also glue, shaving cream, or coloring.

However, identification of true allergic contact dermatitis from toys “requires both identification of the chemical contents of toys, which are proprietary in nature, and then epicutaneous allergy testing of these ingredients,” the researchers said.

The study findings were limited by several factors including the consideration only of English-language articles and of cases in children, which thus eliminates other potential cases, the researchers noted. However, the results suggest that dermatologists consider toys as a source of contact dermatitis in children, especially if the time to diagnosis is months to years, they said. “Additionally, it may be useful, as it was in several of the above cases, to have the patient bring in his or her favorite toys for the dermatologist to examine and help further understand the etiology of patient’s rash,” they noted. Moreover, “there is an unmet need for corporations to reveal the chemical ingredients of their toys when allergic contact dermatitis is suspected in order to properly evaluate the patient,” they added.

“Contact dermatitis has been underreported in children and constitutes an ongoing concern,” senior author Nanette Silverberg, MD, chief of pediatric dermatology for the Mount Sinai Health System, said in an interview.

“In particular, toy-related allergy is concerning due to the rise in allergen inclusion in common play items,” she commented. The current analysis identified many case reports of allergens that pediatric dermatologists are frequently seeing in their offices, notably metals such as nickel, she pointed out. “The allergen that always stands out ahead of others is nickel,” Dr. Silverberg said. “Nickel allergy affects about 25% of Americans, often starting in early childhood,” she said. “In the European Union, legislation has been passed to reduce nickel release from metals, which has resulted in less sensitization to nickel. We lack such legislation in the United States,” she added. 

Other trending allergens include methylchloroisothiazolinone/methylisothiazolinone, which may be components of glue or other ingredients in some “slime” products, Dr. Silverberg said.

She advised clinicians to consider patch testing when addressing localized or persistent dermatitis in children. “Furthermore, consider toys as potential relevant allergens that should be modified in order to achieve skin improvement,” she said.

“Greater reporting of pediatric allergic contact dermatitis is needed,” Dr. Silverberg emphasized. “Additionally, surveillance and monitoring for trends in allergen exposures in toys and personal care items is required to analyze this ongoing concern of childhood,” she said.

The study received no outside funding. The researchers had no financial conflicts to disclose.

SOURCE: Fenner J et al. Contact Dermatitis. 2020 Feb 22. doi: 10.1111/cod.13500.

A variety of toys and other play products can cause contact dermatitis in children because of the nature of their ingredients, according to the results of a review of 25 published articles.

Motortion/Getty Images

“In recent years the products have become a reflection of the compounds used frequently in manufacturing, including metals and plastic compounds,” wrote Justine Fenner, MD, and coauthors, from the departments of dermatology and pediatrics at the Icahn School of Medicine at Mount Sinai, New York,

In a study published in Contact Dermatitis, the researchers identified 25 articles describing dermatitis, rash, or eczema associated with a range of toy and play product terms including Nintendo, PlayStation, putty, glue, doll, game, car, bicycle, slime, iPad, and iPhone.

Overall, nickel was the most common allergen. Cases of nickel dermatitis were associated with laptops, videogame controllers, iPads, and cell phones. Cell phones were the most common electronics associated with contact dermatitis, which was observed on the cheek, periauricular area, and hand, as well as the breast in one case of a patient who kept her phone in her bra.

Other sources of metal allergens were identified in toy cars and costume jewelry, the researchers noted.

In addition, temporary tattoos have been associated with contact dermatitis in children, as have homemade “slime” products, which often contain not only borax or other household detergents, but also glue, shaving cream, or coloring.

However, identification of true allergic contact dermatitis from toys “requires both identification of the chemical contents of toys, which are proprietary in nature, and then epicutaneous allergy testing of these ingredients,” the researchers said.

The study findings were limited by several factors including the consideration only of English-language articles and of cases in children, which thus eliminates other potential cases, the researchers noted. However, the results suggest that dermatologists consider toys as a source of contact dermatitis in children, especially if the time to diagnosis is months to years, they said. “Additionally, it may be useful, as it was in several of the above cases, to have the patient bring in his or her favorite toys for the dermatologist to examine and help further understand the etiology of patient’s rash,” they noted. Moreover, “there is an unmet need for corporations to reveal the chemical ingredients of their toys when allergic contact dermatitis is suspected in order to properly evaluate the patient,” they added.

“Contact dermatitis has been underreported in children and constitutes an ongoing concern,” senior author Nanette Silverberg, MD, chief of pediatric dermatology for the Mount Sinai Health System, said in an interview.

“In particular, toy-related allergy is concerning due to the rise in allergen inclusion in common play items,” she commented. The current analysis identified many case reports of allergens that pediatric dermatologists are frequently seeing in their offices, notably metals such as nickel, she pointed out. “The allergen that always stands out ahead of others is nickel,” Dr. Silverberg said. “Nickel allergy affects about 25% of Americans, often starting in early childhood,” she said. “In the European Union, legislation has been passed to reduce nickel release from metals, which has resulted in less sensitization to nickel. We lack such legislation in the United States,” she added. 

Other trending allergens include methylchloroisothiazolinone/methylisothiazolinone, which may be components of glue or other ingredients in some “slime” products, Dr. Silverberg said.

She advised clinicians to consider patch testing when addressing localized or persistent dermatitis in children. “Furthermore, consider toys as potential relevant allergens that should be modified in order to achieve skin improvement,” she said.

“Greater reporting of pediatric allergic contact dermatitis is needed,” Dr. Silverberg emphasized. “Additionally, surveillance and monitoring for trends in allergen exposures in toys and personal care items is required to analyze this ongoing concern of childhood,” she said.

The study received no outside funding. The researchers had no financial conflicts to disclose.

SOURCE: Fenner J et al. Contact Dermatitis. 2020 Feb 22. doi: 10.1111/cod.13500.

ORLANDO – Do you have pediatric patients with atopic dermatitis (AD) flares despite complying with treatment, or those who have a new rash in an unusual area? Consider patch testing to assess whether they have allergic contact dermatitis.

Jeff Craven/MDedge News

“Of the patients who are sent to me by local pediatric dermatologists, 50% of them are positive” for allergens, said Jonathan H. Zippin, MD, PhD, director of the contact, occupational, and photodermatitis service at Cornell University, New York.

Speaking at the ODAC Dermatology, Aesthetic, and Surgical Conference, Dr. Zippin noted the prevalence of allergen sensitization is between 13% and 25% among children who are asymptomatic, while the prevalence of sensitization to at least one allergen among children with suspected allergic contact dermatitis (ACD) is between 25% and 96%. In 2014, a study from the National American Contact Dermatitis Group (NACDG) showed that of 883 children who were patch tested, 56.7% had at least one relevant positive patch test (RPPT) result.

“The take-home message here is that pediatric contact dermatitis is common, much more common than a lot of people realize,” Dr. Zippin said.

He described three common scenarios to keep in mind: a worsening rash, a new rash, and failure of a rash to improve after the patient avoids all of his or her positive allergens.

When a rash worsens, patch testing is likely to offer answers. In an analysis of 1,142 patients with suspected ACD aged 18 years or younger (mean age, 10.5 years; 64% female) in the Pediatric Contact Dermatitis Registry study database, 65% had at least one positive patch test, and 48% had at least 1 RPPT (Dermatitis 2016; 27[5] 293-302).

But not all patch testing is the same: The study also found that 24% of the RPPT cases would have been missed if assessed with the T.R.U.E. TEST compared with extended patch testing. If a T.R.U.E. TEST fails to explain generalized atopic dermatitis, the patient should be sent for more comprehensive testing where available, Dr. Zippin advised.

Pediatric patients also have unique allergens clinicians should consider. In the same study, children had a number of allergens similar to those of adults as reported in previous studies, such as nickel, cobalt, and neomycin. However, propylene glycol and cocamidopropyl betaine were allergens identified as unique to the pediatric population.

Another study looking at the same group of patients found that compared with children who did not have AD, children with AD had 7.4 times higher odds of having an RPPT to cocamidopropyl betaine, 7.6 times higher odds of having an RPPT to parthenolide, 5.3 times higher odds of having an RPPT to tixocortol pivalate, 4.2 times higher odds of having an RPPT to wool alcohols, and 4 times higher odds of having an RPPT to lanolin (JAMA Dermatology 2017;153[8]:765-70).

All of these are components of topical medicaments used to treat AD, “either components of emollients that we recommend, or components of steroids that we recommend,” Dr. Zippin pointed out.

One of these allergens could be the culprit when a child develops a new rash but there are no new apparent changes in products, exposures, and activities. Lanolin, also called wool grease, is used in many skin care products, for example. Dr. Zippin described the case of a 6-year-old girl with a history of AD, who presented with a new rash on her scalp and behind her ears, not explained by any obvious changes to products, exposures, or activities. Subsequent patch testing determined that the rash was caused by baby shampoo, which contained cocamidopropyl betaine, which is used in hypoallergenic products. The rash resolved after a different shampoo was used.

“Sometimes, we really have to be thinking when the rash is getting worse, is there something they’re being exposed to that might be an allergen?” Dr. Zippin said.

In patients who have avoided all their positive allergens but a rash has not improved, clinicians should consider systemic contact dermatitis (SCD). Patients can develop SCD through different types of exposures, including transepidermal, transmucosal, oral, intravenous, subcutaneous, intramuscular, inhalation, and implantation routes.

SCD also has a variety of presentations, including pompholyx/dyshidrosis/vesicular dermatitis, maculopapular eruption, chronic pruritus, exfoliative erythroderma/toxiderma, chronic urticaria, erythema multiforme and vasculitis, hyperkeratotic papules of the elbows, acute generalized exanthematous pustulosis, and pruritus ani, according to Dr. Zippin.

SCD should be considered when a patient has a positive patch test to an allergen that is known to cause SCD, and does not clear after avoiding cutaneous exposure to the allergen, Dr. Zippin advised.

Patients will most often develop SCD from plants and herbs, Dr. Zippin noted. Chrysanthemums and chamomile tea are common culprits for compositae allergy and can trigger SCD; other causes are Anacardiaceae, Balsam of Peru, and propolis. Metals (nickel, cobalt, gold, and chromium), medications (aminoglycosides, corticosteroids, and ethylenediamine), and other sources (formaldehyde, propylene glycol in frozen foods, gallates, and methylisothiazolinone) can cause SCD as well.

Methylisothiazolinone in particular is a very common sensitizer, Dr. Zippin said. “If you have a patient who is positive to this, it’s almost always the cause of their problem.”

Balsam of Peru is in a number of different foods, and patients who need to follow a diet free of Balsam of Peru should avoid a long list of foods including citrus; bakery goods; Danish pastry; candy; gum; spices such as cinnamon, cloves, vanilla, curry, allspice, anise, and ginger; spicy condiments such as ketchup, chili sauce, barbecue sauce; chili, pizza, and foods with red sauces; tomatoes; pickles; alcohol (wine, beer, gin, vermouth); tea (perfumed or flavored); tobacco; chocolate and ice cream; and soft drinks (cola or spiced soft drinks).

Patients starting a nickel-free diet should avoid soy, peanuts and other nuts, legumes, chocolate, cocoa, oats, fish, and whole wheat flours. Any elimination diet should last for 3 months but should at least be tried for 3-4 weeks, with gradual reintroduction of foods suspected as triggers once per week. Any type I allergies that are discovered or suspected can be referred to an allergist for allergen challenge and desensitization therapy.

For more information, Dr. Zippin recommended the American Contact Dermatitis Society website for more information.

Dr. Zippin reported that he is the founder and holds stock options at CEP Biotech; is on the medical advisory board and receives stock options from YouV Labs., is a paid consultant and performs industry-sponsored research for Pfizer, receives stock options from Regeneron, and is on the medical advisory board for Hoth Therapeutics Inc. He is on the board of directors for the American Contact Dermatitis Society.

ORLANDO – Do you have pediatric patients with atopic dermatitis (AD) flares despite complying with treatment, or those who have a new rash in an unusual area? Consider patch testing to assess whether they have allergic contact dermatitis.

Jeff Craven/MDedge News

“Of the patients who are sent to me by local pediatric dermatologists, 50% of them are positive” for allergens, said Jonathan H. Zippin, MD, PhD, director of the contact, occupational, and photodermatitis service at Cornell University, New York.

Speaking at the ODAC Dermatology, Aesthetic, and Surgical Conference, Dr. Zippin noted the prevalence of allergen sensitization is between 13% and 25% among children who are asymptomatic, while the prevalence of sensitization to at least one allergen among children with suspected allergic contact dermatitis (ACD) is between 25% and 96%. In 2014, a study from the National American Contact Dermatitis Group (NACDG) showed that of 883 children who were patch tested, 56.7% had at least one relevant positive patch test (RPPT) result.

“The take-home message here is that pediatric contact dermatitis is common, much more common than a lot of people realize,” Dr. Zippin said.

He described three common scenarios to keep in mind: a worsening rash, a new rash, and failure of a rash to improve after the patient avoids all of his or her positive allergens.

When a rash worsens, patch testing is likely to offer answers. In an analysis of 1,142 patients with suspected ACD aged 18 years or younger (mean age, 10.5 years; 64% female) in the Pediatric Contact Dermatitis Registry study database, 65% had at least one positive patch test, and 48% had at least 1 RPPT (Dermatitis 2016; 27[5] 293-302).

But not all patch testing is the same: The study also found that 24% of the RPPT cases would have been missed if assessed with the T.R.U.E. TEST compared with extended patch testing. If a T.R.U.E. TEST fails to explain generalized atopic dermatitis, the patient should be sent for more comprehensive testing where available, Dr. Zippin advised.

Pediatric patients also have unique allergens clinicians should consider. In the same study, children had a number of allergens similar to those of adults as reported in previous studies, such as nickel, cobalt, and neomycin. However, propylene glycol and cocamidopropyl betaine were allergens identified as unique to the pediatric population.

Another study looking at the same group of patients found that compared with children who did not have AD, children with AD had 7.4 times higher odds of having an RPPT to cocamidopropyl betaine, 7.6 times higher odds of having an RPPT to parthenolide, 5.3 times higher odds of having an RPPT to tixocortol pivalate, 4.2 times higher odds of having an RPPT to wool alcohols, and 4 times higher odds of having an RPPT to lanolin (JAMA Dermatology 2017;153[8]:765-70).

All of these are components of topical medicaments used to treat AD, “either components of emollients that we recommend, or components of steroids that we recommend,” Dr. Zippin pointed out.

One of these allergens could be the culprit when a child develops a new rash but there are no new apparent changes in products, exposures, and activities. Lanolin, also called wool grease, is used in many skin care products, for example. Dr. Zippin described the case of a 6-year-old girl with a history of AD, who presented with a new rash on her scalp and behind her ears, not explained by any obvious changes to products, exposures, or activities. Subsequent patch testing determined that the rash was caused by baby shampoo, which contained cocamidopropyl betaine, which is used in hypoallergenic products. The rash resolved after a different shampoo was used.

“Sometimes, we really have to be thinking when the rash is getting worse, is there something they’re being exposed to that might be an allergen?” Dr. Zippin said.

In patients who have avoided all their positive allergens but a rash has not improved, clinicians should consider systemic contact dermatitis (SCD). Patients can develop SCD through different types of exposures, including transepidermal, transmucosal, oral, intravenous, subcutaneous, intramuscular, inhalation, and implantation routes.

SCD also has a variety of presentations, including pompholyx/dyshidrosis/vesicular dermatitis, maculopapular eruption, chronic pruritus, exfoliative erythroderma/toxiderma, chronic urticaria, erythema multiforme and vasculitis, hyperkeratotic papules of the elbows, acute generalized exanthematous pustulosis, and pruritus ani, according to Dr. Zippin.

SCD should be considered when a patient has a positive patch test to an allergen that is known to cause SCD, and does not clear after avoiding cutaneous exposure to the allergen, Dr. Zippin advised.

Patients will most often develop SCD from plants and herbs, Dr. Zippin noted. Chrysanthemums and chamomile tea are common culprits for compositae allergy and can trigger SCD; other causes are Anacardiaceae, Balsam of Peru, and propolis. Metals (nickel, cobalt, gold, and chromium), medications (aminoglycosides, corticosteroids, and ethylenediamine), and other sources (formaldehyde, propylene glycol in frozen foods, gallates, and methylisothiazolinone) can cause SCD as well.

Methylisothiazolinone in particular is a very common sensitizer, Dr. Zippin said. “If you have a patient who is positive to this, it’s almost always the cause of their problem.”

Balsam of Peru is in a number of different foods, and patients who need to follow a diet free of Balsam of Peru should avoid a long list of foods including citrus; bakery goods; Danish pastry; candy; gum; spices such as cinnamon, cloves, vanilla, curry, allspice, anise, and ginger; spicy condiments such as ketchup, chili sauce, barbecue sauce; chili, pizza, and foods with red sauces; tomatoes; pickles; alcohol (wine, beer, gin, vermouth); tea (perfumed or flavored); tobacco; chocolate and ice cream; and soft drinks (cola or spiced soft drinks).

Patients starting a nickel-free diet should avoid soy, peanuts and other nuts, legumes, chocolate, cocoa, oats, fish, and whole wheat flours. Any elimination diet should last for 3 months but should at least be tried for 3-4 weeks, with gradual reintroduction of foods suspected as triggers once per week. Any type I allergies that are discovered or suspected can be referred to an allergist for allergen challenge and desensitization therapy.

For more information, Dr. Zippin recommended the American Contact Dermatitis Society website for more information.

Dr. Zippin reported that he is the founder and holds stock options at CEP Biotech; is on the medical advisory board and receives stock options from YouV Labs., is a paid consultant and performs industry-sponsored research for Pfizer, receives stock options from Regeneron, and is on the medical advisory board for Hoth Therapeutics Inc. He is on the board of directors for the American Contact Dermatitis Society.

ORLANDO – Do you have pediatric patients with atopic dermatitis (AD) flares despite complying with treatment, or those who have a new rash in an unusual area? Consider patch testing to assess whether they have allergic contact dermatitis.

Jeff Craven/MDedge News

“Of the patients who are sent to me by local pediatric dermatologists, 50% of them are positive” for allergens, said Jonathan H. Zippin, MD, PhD, director of the contact, occupational, and photodermatitis service at Cornell University, New York.

Speaking at the ODAC Dermatology, Aesthetic, and Surgical Conference, Dr. Zippin noted the prevalence of allergen sensitization is between 13% and 25% among children who are asymptomatic, while the prevalence of sensitization to at least one allergen among children with suspected allergic contact dermatitis (ACD) is between 25% and 96%. In 2014, a study from the National American Contact Dermatitis Group (NACDG) showed that of 883 children who were patch tested, 56.7% had at least one relevant positive patch test (RPPT) result.

“The take-home message here is that pediatric contact dermatitis is common, much more common than a lot of people realize,” Dr. Zippin said.

He described three common scenarios to keep in mind: a worsening rash, a new rash, and failure of a rash to improve after the patient avoids all of his or her positive allergens.

When a rash worsens, patch testing is likely to offer answers. In an analysis of 1,142 patients with suspected ACD aged 18 years or younger (mean age, 10.5 years; 64% female) in the Pediatric Contact Dermatitis Registry study database, 65% had at least one positive patch test, and 48% had at least 1 RPPT (Dermatitis 2016; 27[5] 293-302).

But not all patch testing is the same: The study also found that 24% of the RPPT cases would have been missed if assessed with the T.R.U.E. TEST compared with extended patch testing. If a T.R.U.E. TEST fails to explain generalized atopic dermatitis, the patient should be sent for more comprehensive testing where available, Dr. Zippin advised.

Pediatric patients also have unique allergens clinicians should consider. In the same study, children had a number of allergens similar to those of adults as reported in previous studies, such as nickel, cobalt, and neomycin. However, propylene glycol and cocamidopropyl betaine were allergens identified as unique to the pediatric population.

Another study looking at the same group of patients found that compared with children who did not have AD, children with AD had 7.4 times higher odds of having an RPPT to cocamidopropyl betaine, 7.6 times higher odds of having an RPPT to parthenolide, 5.3 times higher odds of having an RPPT to tixocortol pivalate, 4.2 times higher odds of having an RPPT to wool alcohols, and 4 times higher odds of having an RPPT to lanolin (JAMA Dermatology 2017;153[8]:765-70).

All of these are components of topical medicaments used to treat AD, “either components of emollients that we recommend, or components of steroids that we recommend,” Dr. Zippin pointed out.

One of these allergens could be the culprit when a child develops a new rash but there are no new apparent changes in products, exposures, and activities. Lanolin, also called wool grease, is used in many skin care products, for example. Dr. Zippin described the case of a 6-year-old girl with a history of AD, who presented with a new rash on her scalp and behind her ears, not explained by any obvious changes to products, exposures, or activities. Subsequent patch testing determined that the rash was caused by baby shampoo, which contained cocamidopropyl betaine, which is used in hypoallergenic products. The rash resolved after a different shampoo was used.

“Sometimes, we really have to be thinking when the rash is getting worse, is there something they’re being exposed to that might be an allergen?” Dr. Zippin said.

In patients who have avoided all their positive allergens but a rash has not improved, clinicians should consider systemic contact dermatitis (SCD). Patients can develop SCD through different types of exposures, including transepidermal, transmucosal, oral, intravenous, subcutaneous, intramuscular, inhalation, and implantation routes.

SCD also has a variety of presentations, including pompholyx/dyshidrosis/vesicular dermatitis, maculopapular eruption, chronic pruritus, exfoliative erythroderma/toxiderma, chronic urticaria, erythema multiforme and vasculitis, hyperkeratotic papules of the elbows, acute generalized exanthematous pustulosis, and pruritus ani, according to Dr. Zippin.

SCD should be considered when a patient has a positive patch test to an allergen that is known to cause SCD, and does not clear after avoiding cutaneous exposure to the allergen, Dr. Zippin advised.

Patients will most often develop SCD from plants and herbs, Dr. Zippin noted. Chrysanthemums and chamomile tea are common culprits for compositae allergy and can trigger SCD; other causes are Anacardiaceae, Balsam of Peru, and propolis. Metals (nickel, cobalt, gold, and chromium), medications (aminoglycosides, corticosteroids, and ethylenediamine), and other sources (formaldehyde, propylene glycol in frozen foods, gallates, and methylisothiazolinone) can cause SCD as well.

Methylisothiazolinone in particular is a very common sensitizer, Dr. Zippin said. “If you have a patient who is positive to this, it’s almost always the cause of their problem.”

Balsam of Peru is in a number of different foods, and patients who need to follow a diet free of Balsam of Peru should avoid a long list of foods including citrus; bakery goods; Danish pastry; candy; gum; spices such as cinnamon, cloves, vanilla, curry, allspice, anise, and ginger; spicy condiments such as ketchup, chili sauce, barbecue sauce; chili, pizza, and foods with red sauces; tomatoes; pickles; alcohol (wine, beer, gin, vermouth); tea (perfumed or flavored); tobacco; chocolate and ice cream; and soft drinks (cola or spiced soft drinks).

Patients starting a nickel-free diet should avoid soy, peanuts and other nuts, legumes, chocolate, cocoa, oats, fish, and whole wheat flours. Any elimination diet should last for 3 months but should at least be tried for 3-4 weeks, with gradual reintroduction of foods suspected as triggers once per week. Any type I allergies that are discovered or suspected can be referred to an allergist for allergen challenge and desensitization therapy.

For more information, Dr. Zippin recommended the American Contact Dermatitis Society website for more information.

Dr. Zippin reported that he is the founder and holds stock options at CEP Biotech; is on the medical advisory board and receives stock options from YouV Labs., is a paid consultant and performs industry-sponsored research for Pfizer, receives stock options from Regeneron, and is on the medical advisory board for Hoth Therapeutics Inc. He is on the board of directors for the American Contact Dermatitis Society.