Contact Dermatitis

The Diagnosis: Foreign Body Reaction With Sinus Tract  

A delayed foreign body reaction is a rare complication of retained temporary pacing wires following cardiovascular surgery. These epicardial pacing wires are important for the management of postoperative arrhythmia and normally are removed by external traction after normal rhythm has been re-established. However, it is not uncommon for these wires to be cut at the skin surface in the setting of difficult removal, as retained pacing wires generally are viewed as benign.¹ These reactions often take years after placement of the pacing wire to present themselves and most often resolve with either complete removal of the wire or resection of the distal end.²  

Our patient was referred to dermatology and underwent a shave biopsy. Results were consistent with chronic inflammatory granulation tissue. Bacterial tissue culture grew Staphylococcus epidermidis. Cultures for acid-fast bacilli and fungi were negative. The patient was referred to cardiothoracic surgery. Computed tomography identified a retained temporary pacing wire extending to the base of the lesion. The lesion was excised and the distal aspect of the pacing wire was removed, which resulted in resolution of the nodule.  

The differential diagnosis includes pyoderma gangrenosum, nodular basal cell carcinoma, Sister Mary Joseph nodule, and pyogenic granuloma. Pyoderma gangrenosum is a neutrophilic dermatosis that presents as a rapidly progressing, painful, necrotic ulcer. It is classically associated with inflammatory bowel disease and other systemic diseases but also can occur in isolation.³  

Nodular basal cell carcinomas often develop in chronically sun-exposed areas of the body. Morphologically, they present as pink, pearl appearing papules with rolled borders and overlying arborizing telangiectasia. Nodular basal cell carcinomas may present with recurrent bleeding but typically do not have continuous drainage.⁴  

Sister Mary Joseph nodule represents a periumbilical lymphatic metastasis from an underlying (usually intra-abdominal) malignancy. It typically presents as an umbilical or periumbilical nodule measuring 0.5 to 15 cm in diameter. The nodules often are painful and discharge a serous fluid. It is estimated that they are present in 1% to 3% of cases of abdominopelvic malignancy, but Sister Mary Joseph nodules also have been reported in several other types of solid organ tumors.⁵  

Pyogenic granuloma is a benign vascular lesion that classically develops rapidly over the course of a few weeks. It often presents as a single red, moist, friable papule with a collarette of scale and frequently is associated with pain, bleeding, and ulceration. Keratinized skin or mucosa can be affected, and pyogenic granuloma is most common in children and young adults.⁶  

The Diagnosis: Foreign Body Reaction With Sinus Tract  

A delayed foreign body reaction is a rare complication of retained temporary pacing wires following cardiovascular surgery. These epicardial pacing wires are important for the management of postoperative arrhythmia and normally are removed by external traction after normal rhythm has been re-established. However, it is not uncommon for these wires to be cut at the skin surface in the setting of difficult removal, as retained pacing wires generally are viewed as benign.¹ These reactions often take years after placement of the pacing wire to present themselves and most often resolve with either complete removal of the wire or resection of the distal end.²  

Our patient was referred to dermatology and underwent a shave biopsy. Results were consistent with chronic inflammatory granulation tissue. Bacterial tissue culture grew Staphylococcus epidermidis. Cultures for acid-fast bacilli and fungi were negative. The patient was referred to cardiothoracic surgery. Computed tomography identified a retained temporary pacing wire extending to the base of the lesion. The lesion was excised and the distal aspect of the pacing wire was removed, which resulted in resolution of the nodule.  

The differential diagnosis includes pyoderma gangrenosum, nodular basal cell carcinoma, Sister Mary Joseph nodule, and pyogenic granuloma. Pyoderma gangrenosum is a neutrophilic dermatosis that presents as a rapidly progressing, painful, necrotic ulcer. It is classically associated with inflammatory bowel disease and other systemic diseases but also can occur in isolation.³  

Nodular basal cell carcinomas often develop in chronically sun-exposed areas of the body. Morphologically, they present as pink, pearl appearing papules with rolled borders and overlying arborizing telangiectasia. Nodular basal cell carcinomas may present with recurrent bleeding but typically do not have continuous drainage.⁴  

Sister Mary Joseph nodule represents a periumbilical lymphatic metastasis from an underlying (usually intra-abdominal) malignancy. It typically presents as an umbilical or periumbilical nodule measuring 0.5 to 15 cm in diameter. The nodules often are painful and discharge a serous fluid. It is estimated that they are present in 1% to 3% of cases of abdominopelvic malignancy, but Sister Mary Joseph nodules also have been reported in several other types of solid organ tumors.⁵  

Pyogenic granuloma is a benign vascular lesion that classically develops rapidly over the course of a few weeks. It often presents as a single red, moist, friable papule with a collarette of scale and frequently is associated with pain, bleeding, and ulceration. Keratinized skin or mucosa can be affected, and pyogenic granuloma is most common in children and young adults.⁶  

The Diagnosis: Foreign Body Reaction With Sinus Tract  

A delayed foreign body reaction is a rare complication of retained temporary pacing wires following cardiovascular surgery. These epicardial pacing wires are important for the management of postoperative arrhythmia and normally are removed by external traction after normal rhythm has been re-established. However, it is not uncommon for these wires to be cut at the skin surface in the setting of difficult removal, as retained pacing wires generally are viewed as benign.¹ These reactions often take years after placement of the pacing wire to present themselves and most often resolve with either complete removal of the wire or resection of the distal end.²  

Our patient was referred to dermatology and underwent a shave biopsy. Results were consistent with chronic inflammatory granulation tissue. Bacterial tissue culture grew Staphylococcus epidermidis. Cultures for acid-fast bacilli and fungi were negative. The patient was referred to cardiothoracic surgery. Computed tomography identified a retained temporary pacing wire extending to the base of the lesion. The lesion was excised and the distal aspect of the pacing wire was removed, which resulted in resolution of the nodule.  

The differential diagnosis includes pyoderma gangrenosum, nodular basal cell carcinoma, Sister Mary Joseph nodule, and pyogenic granuloma. Pyoderma gangrenosum is a neutrophilic dermatosis that presents as a rapidly progressing, painful, necrotic ulcer. It is classically associated with inflammatory bowel disease and other systemic diseases but also can occur in isolation.³  

Nodular basal cell carcinomas often develop in chronically sun-exposed areas of the body. Morphologically, they present as pink, pearl appearing papules with rolled borders and overlying arborizing telangiectasia. Nodular basal cell carcinomas may present with recurrent bleeding but typically do not have continuous drainage.⁴  

Sister Mary Joseph nodule represents a periumbilical lymphatic metastasis from an underlying (usually intra-abdominal) malignancy. It typically presents as an umbilical or periumbilical nodule measuring 0.5 to 15 cm in diameter. The nodules often are painful and discharge a serous fluid. It is estimated that they are present in 1% to 3% of cases of abdominopelvic malignancy, but Sister Mary Joseph nodules also have been reported in several other types of solid organ tumors.⁵  

Pyogenic granuloma is a benign vascular lesion that classically develops rapidly over the course of a few weeks. It often presents as a single red, moist, friable papule with a collarette of scale and frequently is associated with pain, bleeding, and ulceration. Keratinized skin or mucosa can be affected, and pyogenic granuloma is most common in children and young adults.⁶  

Practice Gap

The Centers for Disease Control and Prevention recommends handwashing with soap and water or using alcohol-based hand sanitizers to prevent transmission of coronavirus disease 2019. Five steps are delineated for effective handwashing: wetting, lathering, scrubbing, rinsing, and drying. Although alcohol-based sanitizers may be perceived as more damaging to the skin, they are less likely to cause dermatitis than handwashing with soap and water.¹ Instructions are precise for handwashing, while there are no recommendations for effective use of alcohol-based hand sanitizers. A common inquiry regarding alcohol-based hand sanitizers is the volume needed for efficacy without causing skin irritation.

The Technique

Approximately 1 mL of alcohol-based hand sanitizer is recommended by some manufacturers. However, abundant evidence refutes this recommendation, including a study that tested the microbial efficacy of alcohol-based sanitizers by volume. A volume of 2 mL was necessary to achieve the 2.0 log reduction of contaminants as required by the US Food and Drug Administration for antimicrobial efficacy.² The precise measurement of hand sanitizer using a calibrated syringe before each use is impractical. Thus, we recommend using a screw-top toothpaste cap to assist in approximating the necessary volume (Figure). The cap holds approximately 1 mL of liquid as measured using a syringe; therefore, 2 caps filled with sanitizer should be used.

Practice Implications

The general public may be underutilizing hand sanitizer due to fear of excessive skin irritation or supply shortages, which will reduce efficacy. Patients and physicians can use this simple visual approximation to ensure adequate use of hand sanitizer volume.

Practice Gap

The Centers for Disease Control and Prevention recommends handwashing with soap and water or using alcohol-based hand sanitizers to prevent transmission of coronavirus disease 2019. Five steps are delineated for effective handwashing: wetting, lathering, scrubbing, rinsing, and drying. Although alcohol-based sanitizers may be perceived as more damaging to the skin, they are less likely to cause dermatitis than handwashing with soap and water.¹ Instructions are precise for handwashing, while there are no recommendations for effective use of alcohol-based hand sanitizers. A common inquiry regarding alcohol-based hand sanitizers is the volume needed for efficacy without causing skin irritation.

The Technique

Approximately 1 mL of alcohol-based hand sanitizer is recommended by some manufacturers. However, abundant evidence refutes this recommendation, including a study that tested the microbial efficacy of alcohol-based sanitizers by volume. A volume of 2 mL was necessary to achieve the 2.0 log reduction of contaminants as required by the US Food and Drug Administration for antimicrobial efficacy.² The precise measurement of hand sanitizer using a calibrated syringe before each use is impractical. Thus, we recommend using a screw-top toothpaste cap to assist in approximating the necessary volume (Figure). The cap holds approximately 1 mL of liquid as measured using a syringe; therefore, 2 caps filled with sanitizer should be used.

Practice Implications

The general public may be underutilizing hand sanitizer due to fear of excessive skin irritation or supply shortages, which will reduce efficacy. Patients and physicians can use this simple visual approximation to ensure adequate use of hand sanitizer volume.

Practice Gap

The Centers for Disease Control and Prevention recommends handwashing with soap and water or using alcohol-based hand sanitizers to prevent transmission of coronavirus disease 2019. Five steps are delineated for effective handwashing: wetting, lathering, scrubbing, rinsing, and drying. Although alcohol-based sanitizers may be perceived as more damaging to the skin, they are less likely to cause dermatitis than handwashing with soap and water.¹ Instructions are precise for handwashing, while there are no recommendations for effective use of alcohol-based hand sanitizers. A common inquiry regarding alcohol-based hand sanitizers is the volume needed for efficacy without causing skin irritation.

The Technique

Approximately 1 mL of alcohol-based hand sanitizer is recommended by some manufacturers. However, abundant evidence refutes this recommendation, including a study that tested the microbial efficacy of alcohol-based sanitizers by volume. A volume of 2 mL was necessary to achieve the 2.0 log reduction of contaminants as required by the US Food and Drug Administration for antimicrobial efficacy.² The precise measurement of hand sanitizer using a calibrated syringe before each use is impractical. Thus, we recommend using a screw-top toothpaste cap to assist in approximating the necessary volume (Figure). The cap holds approximately 1 mL of liquid as measured using a syringe; therefore, 2 caps filled with sanitizer should be used.

Practice Implications

The general public may be underutilizing hand sanitizer due to fear of excessive skin irritation or supply shortages, which will reduce efficacy. Patients and physicians can use this simple visual approximation to ensure adequate use of hand sanitizer volume.

Hypersensitivity to implantable devices, albeit rare, is a growing problem. Cutaneous and noncutaneous reactions can occur secondary to metals and metal alloys, according to a report on biological responses to metal implants released by the Food and Drug Administration in September 2019. Large controlled studies are lacking, and the FDA has initiated extensive postmarketing reviews of certain metal implants in response to safety concerns. Further research is needed on the composition of these implants, the diverse spectrum of metals used, the physical environment in which they are implanted, and the immune response associated with implants.

Local and systemic type IV hypersensitivity reactions can result from exposure to metal ions, which are thought to act as haptens and bind to proteins. The hapten-protein complex acts as the antigen for the T cell. Additionally, both acute and chronic inflammatory responses secondary to wound healing and foreign body reactions can occur. Neutrophils and macrophages elicit a tissue response, which can cause aseptic infection, loosening of joints, and tissue damage. Furthermore, corrosion of metal implants can lead to release of metal ions, which can have genotoxic and carcinogenic effects.

Clinical and subclinical effects of implantable devices depend on the device itself, the composition of the device, the tissue type, and an individual’s immune characteristics. Metal debris released from implants can activate innate and adaptive immune responses through a variety of different mechanisms, depending on the implant type and in what tissues the implant is placed. In the case of orthopedic implants, the most common implants, osteoclasts can sense metal and induce proinflammatory cytokines, which can result in corrosion and uptake of metal particles. Metal devices used in the central nervous system, such as intracerebral electrodes, can cause inflammatory responses leading to tissue encapsulation of electrodes. Corrosion of electrodes and release of metal ions can also impede ion channels in the CNS, blocking critical neuron-signaling pathways. Inflammatory reactions surrounding cardiac and vascular implants containing metal activate coagulation cascades, resulting in endothelial injury and activation of thrombi.

Despite the commonly used term “metal allergy” that delineates a type IV hypersensitivity reaction, reports in the literature supports the existence of both innate and adaptive immune responses to metal implanted in tissues. The recommended terminology is “adverse reactions to metal debris.” The clinical presentation may not be straightforward or easily attributed to the implant. Diagnostic tools are limited and may not detect a causal relationship.

Clinical symptoms can range from local rashes and pruritus to cardiac damage, depression, vertigo, and neurologic symptoms; autoimmune/autoinflammatory reactions including chronic fatigue and autoimmune-like systemic symptoms, such as joint pain, headaches, and hair loss, have also been reported in association with implants containing metal. In addition to pruritus, dermatologic manifestations can include erythema, edema, papules, vesicles, as well as systemic hypersensitivity reactions. Typically, cutaneous reactions usually present within 2 days to 24 months of implantation and may be considered surgical-site infections. Although these reactions can be treated with topical or oral corticosteroids, removal of the device is frequently needed for complete clearance.

In clinical practice, it has been frustrating that potential adverse reactions to metal implants are often overlooked because they are thought to be so rare. There are case series documenting metal implant hypersensitivity, but the actual prevalence of hypersensitivity or autoinflammatory reactions is not known. Testing methods are often inaccurate; therefore, identification of at-risk individuals and management of symptomatic patients with implants is important.

The 2016 American Contact Dermatitis Society guidelines do not recommend preimplantation patch testing unless there is a suspected metal allergy. However, patch testing cannot identify the extent of corrosion, autoinflammatory reactions, and foreign body reactions that can occur.

We must keep an open mind in patients who have implanted devices and have unusual or otherwise undefined symptoms. Often, the symptoms do not directly correspond to the site of implantation and the only way to discern whether the implant is the cause and to treat symptoms is removal of the implanted device.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.

 

References

Food and Drug Administration. Biological Responses to Metal Implants. 2019 Sep. https://www.fda.gov/media/131150/download.

Atwater AR, Reeder M. Cutis. 2020 Feb;105(2):68-70.

Schalock PC et al. Dermatitis. Sep-Oct 2016;27(5):241-7.

Hypersensitivity to implantable devices, albeit rare, is a growing problem. Cutaneous and noncutaneous reactions can occur secondary to metals and metal alloys, according to a report on biological responses to metal implants released by the Food and Drug Administration in September 2019. Large controlled studies are lacking, and the FDA has initiated extensive postmarketing reviews of certain metal implants in response to safety concerns. Further research is needed on the composition of these implants, the diverse spectrum of metals used, the physical environment in which they are implanted, and the immune response associated with implants.

Local and systemic type IV hypersensitivity reactions can result from exposure to metal ions, which are thought to act as haptens and bind to proteins. The hapten-protein complex acts as the antigen for the T cell. Additionally, both acute and chronic inflammatory responses secondary to wound healing and foreign body reactions can occur. Neutrophils and macrophages elicit a tissue response, which can cause aseptic infection, loosening of joints, and tissue damage. Furthermore, corrosion of metal implants can lead to release of metal ions, which can have genotoxic and carcinogenic effects.

Clinical and subclinical effects of implantable devices depend on the device itself, the composition of the device, the tissue type, and an individual’s immune characteristics. Metal debris released from implants can activate innate and adaptive immune responses through a variety of different mechanisms, depending on the implant type and in what tissues the implant is placed. In the case of orthopedic implants, the most common implants, osteoclasts can sense metal and induce proinflammatory cytokines, which can result in corrosion and uptake of metal particles. Metal devices used in the central nervous system, such as intracerebral electrodes, can cause inflammatory responses leading to tissue encapsulation of electrodes. Corrosion of electrodes and release of metal ions can also impede ion channels in the CNS, blocking critical neuron-signaling pathways. Inflammatory reactions surrounding cardiac and vascular implants containing metal activate coagulation cascades, resulting in endothelial injury and activation of thrombi.

Despite the commonly used term “metal allergy” that delineates a type IV hypersensitivity reaction, reports in the literature supports the existence of both innate and adaptive immune responses to metal implanted in tissues. The recommended terminology is “adverse reactions to metal debris.” The clinical presentation may not be straightforward or easily attributed to the implant. Diagnostic tools are limited and may not detect a causal relationship.

Clinical symptoms can range from local rashes and pruritus to cardiac damage, depression, vertigo, and neurologic symptoms; autoimmune/autoinflammatory reactions including chronic fatigue and autoimmune-like systemic symptoms, such as joint pain, headaches, and hair loss, have also been reported in association with implants containing metal. In addition to pruritus, dermatologic manifestations can include erythema, edema, papules, vesicles, as well as systemic hypersensitivity reactions. Typically, cutaneous reactions usually present within 2 days to 24 months of implantation and may be considered surgical-site infections. Although these reactions can be treated with topical or oral corticosteroids, removal of the device is frequently needed for complete clearance.

In clinical practice, it has been frustrating that potential adverse reactions to metal implants are often overlooked because they are thought to be so rare. There are case series documenting metal implant hypersensitivity, but the actual prevalence of hypersensitivity or autoinflammatory reactions is not known. Testing methods are often inaccurate; therefore, identification of at-risk individuals and management of symptomatic patients with implants is important.

The 2016 American Contact Dermatitis Society guidelines do not recommend preimplantation patch testing unless there is a suspected metal allergy. However, patch testing cannot identify the extent of corrosion, autoinflammatory reactions, and foreign body reactions that can occur.

We must keep an open mind in patients who have implanted devices and have unusual or otherwise undefined symptoms. Often, the symptoms do not directly correspond to the site of implantation and the only way to discern whether the implant is the cause and to treat symptoms is removal of the implanted device.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.

 

References

Food and Drug Administration. Biological Responses to Metal Implants. 2019 Sep. https://www.fda.gov/media/131150/download.

Atwater AR, Reeder M. Cutis. 2020 Feb;105(2):68-70.

Schalock PC et al. Dermatitis. Sep-Oct 2016;27(5):241-7.

Hypersensitivity to implantable devices, albeit rare, is a growing problem. Cutaneous and noncutaneous reactions can occur secondary to metals and metal alloys, according to a report on biological responses to metal implants released by the Food and Drug Administration in September 2019. Large controlled studies are lacking, and the FDA has initiated extensive postmarketing reviews of certain metal implants in response to safety concerns. Further research is needed on the composition of these implants, the diverse spectrum of metals used, the physical environment in which they are implanted, and the immune response associated with implants.

Local and systemic type IV hypersensitivity reactions can result from exposure to metal ions, which are thought to act as haptens and bind to proteins. The hapten-protein complex acts as the antigen for the T cell. Additionally, both acute and chronic inflammatory responses secondary to wound healing and foreign body reactions can occur. Neutrophils and macrophages elicit a tissue response, which can cause aseptic infection, loosening of joints, and tissue damage. Furthermore, corrosion of metal implants can lead to release of metal ions, which can have genotoxic and carcinogenic effects.

Clinical and subclinical effects of implantable devices depend on the device itself, the composition of the device, the tissue type, and an individual’s immune characteristics. Metal debris released from implants can activate innate and adaptive immune responses through a variety of different mechanisms, depending on the implant type and in what tissues the implant is placed. In the case of orthopedic implants, the most common implants, osteoclasts can sense metal and induce proinflammatory cytokines, which can result in corrosion and uptake of metal particles. Metal devices used in the central nervous system, such as intracerebral electrodes, can cause inflammatory responses leading to tissue encapsulation of electrodes. Corrosion of electrodes and release of metal ions can also impede ion channels in the CNS, blocking critical neuron-signaling pathways. Inflammatory reactions surrounding cardiac and vascular implants containing metal activate coagulation cascades, resulting in endothelial injury and activation of thrombi.

Despite the commonly used term “metal allergy” that delineates a type IV hypersensitivity reaction, reports in the literature supports the existence of both innate and adaptive immune responses to metal implanted in tissues. The recommended terminology is “adverse reactions to metal debris.” The clinical presentation may not be straightforward or easily attributed to the implant. Diagnostic tools are limited and may not detect a causal relationship.

Clinical symptoms can range from local rashes and pruritus to cardiac damage, depression, vertigo, and neurologic symptoms; autoimmune/autoinflammatory reactions including chronic fatigue and autoimmune-like systemic symptoms, such as joint pain, headaches, and hair loss, have also been reported in association with implants containing metal. In addition to pruritus, dermatologic manifestations can include erythema, edema, papules, vesicles, as well as systemic hypersensitivity reactions. Typically, cutaneous reactions usually present within 2 days to 24 months of implantation and may be considered surgical-site infections. Although these reactions can be treated with topical or oral corticosteroids, removal of the device is frequently needed for complete clearance.

In clinical practice, it has been frustrating that potential adverse reactions to metal implants are often overlooked because they are thought to be so rare. There are case series documenting metal implant hypersensitivity, but the actual prevalence of hypersensitivity or autoinflammatory reactions is not known. Testing methods are often inaccurate; therefore, identification of at-risk individuals and management of symptomatic patients with implants is important.

The 2016 American Contact Dermatitis Society guidelines do not recommend preimplantation patch testing unless there is a suspected metal allergy. However, patch testing cannot identify the extent of corrosion, autoinflammatory reactions, and foreign body reactions that can occur.

We must keep an open mind in patients who have implanted devices and have unusual or otherwise undefined symptoms. Often, the symptoms do not directly correspond to the site of implantation and the only way to discern whether the implant is the cause and to treat symptoms is removal of the implanted device.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.

 

References

Food and Drug Administration. Biological Responses to Metal Implants. 2019 Sep. https://www.fda.gov/media/131150/download.

Atwater AR, Reeder M. Cutis. 2020 Feb;105(2):68-70.

Schalock PC et al. Dermatitis. Sep-Oct 2016;27(5):241-7.

Sometimes regrettable yet increasingly common, tattoos are an ancient art form used in modern times as a mark of artistic and cultural expression. Allergic contact dermatitis (ACD) to tattoo ink is rare, but the popularity of tattoos makes ACD an increasingly recognized occurrence. In a retrospective study of 38,543 patch-tested patients, only 29 (0.08%) had tattoo-related ACD, with the majority of patients being female and young adults. The most common contact allergy was to paraphenylenediamine (PPD), which occurred in 22 (76%) patients.¹ In this article, we will walk you through the rainbow of tattoo ACD, covering hypersensitivity reactions to both temporary and permanent tattoo inks.

Temporary Tattoo Inks

Henna is the most common temporary tattoo ink. Derived from the plant Lawsonia inermis, henna is an orange dye that has been used in many parts of the world, particularly in Islamic and Hindu cultures, to dye skin, hair, and fabrics. Application of henna tattoos is common for weddings and other celebrations, and brides may wear elaborate henna patterns. To create these tattoos, henna powder is mixed with water and sometimes essential oils and is then applied to the skin for several hours. After application, the henna pigment lawsone (2-hydroxy-1,4-naphthoquinone) interacts with keratin and leaves a red-orange stain on the skin²; longer application time leads to a deeper color. Most traditional cutaneous henna designs fade in 2 to 6 weeks, but some last longer. Red henna generally is considered safe with low incidence of contact allergy. What is referred to as black henna usually is red henna mixed with PPD, a black dye, which is added to deepen the color. Paraphenylenediamine is highly sensitizing; patients can become sensitized to the PPD in the tattoo itself.² One study confirmed the presence of PPD in black henna tattoos, with chemical analysis of common preparations revealing concentrations ranging from less than 1% to 30%.² Patients who undergo patch testing for tattoo reactions often are strongly positive to PPD and have concomitant reactions to azo dyes, black rubber, and anesthetics. Other aromatic amines including aminophenols have been identified in black henna tattoo ink, and these chemicals also may contribute to ACD.³ Less common sources of contact allergy from temporary black henna tattoos include resorcinol,⁴ para-tertiary butylphenol formaldehyde resin,⁵ and fragrance.⁶

Clinically, ACD to PPD in temporary tattoos presents 1 to 3 days after application if the patient is already sensitized or 4 to 14 days if the patient is sensitized by the tattoo ink.² Most patients notice erythema, edema, vesicles, papules, and/or bullae, but other less common reactions including generalized dermatitis, systemic symptoms, urticaria, and pustules have been described.² Postinflammatory hypopigmentation or hyperpigmentation also can occur.

Because of the sensitizing nature of black henna tattoos, consumers are turning to natural temporary tattoos. Jagua temporary tattoos, with pigment derived from the sap of fruit from the Genipa americana tree, have been associated with ACD.⁷ This black dye is applied and washed off in a similar fashion to henna tattoos. Importantly, a recent analysis of jagua dye identified no PPD. In one case, a patient who developed ACD to a jagua tattoo was patch tested to components of the dye and had a positive reaction to genipin, a component of the fruit extract.⁷ Thus, jagua tattoos often are marketed as safe but are an emerging source of contact dermatitis to temporary tattoos.

Permanent Tattoo Inks

Permanent tattoos are created by injecting small amounts of ink into the dermis. As the name suggests, these tattoos are permanent. Tattoos are common; nearly one-third of Americans have at least 1 tattoo.¹ Historically, tattoos were created using black pigment composed of amorphous carbon or black iron oxides.^8,9 Metallic pigments (eg, mercury, chromium, cobalt, cadmium) were once used to add color to tattoos, but these metals are now only rarely used; in fact, a 2019 study of tattoo ink components identified 44 distinct pigments in 1416 permanent inks, with an average of 3 pigments per ink.⁸ Of the 44 pigments, 10 had metallic components including iron, barium, zinc, copper, molybdenum, and titanium. The remaining 34 pigments contained carbon, azo, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), or quinophthalone (yellow) dyes. The authors noted that nearly one-quarter of the tattoo pigments identified in their study had been reported as contact allergens.⁸

Typically, reactions to permanent tattoo inks manifest as an eczematous dermatitis occurring weeks to years after tattoo application.^9,10 The dermatitis usually is locally confined to the tattoo and may be limited to particular colors; occasionally, a new tattoo reaction may trigger concurrent inflammation in older tattoos. Many tattoo reactions occur as a response to red pigment but also have occurred with other tattoo ink components.⁹ Many researchers have speculated as to whether the reaction is related to the ink component itself or from the photochemical breakdown of the ink by exposure to UV radiation and/or laser therapy.⁹

Red Pigment
Red ink is the most common color reported to cause tattoo hypersensitivity reactions. Historically, red tattoo pigments include mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal,¹¹ but today’s tattoo inks primarily are composed of other pigments, such as quinacridone and azo dyes.¹² Several cases of red tattoo ink hypersensitivity reactions exist in the literature, many without completion of patch tests or without positive patch tests to relevant red pigments.^11-15

Black Pigment
In general, reactions to permanent black tattoo ink are rare; however, a few case reports exist. Black pigment can be created with India ink (carbon), logwood (chrome), iron oxide, and titanium.^16,17 Shellac can be used as a binding agent in tattoo ink; there is at least one report of a reaction to black tattoo ink with a positive patch test to shellac and the original black ink.¹⁸

Azo Pigments
Azo pigments frequently are used in modern tattoos due to their vibrant colors. One case of hypersensitivity to azo pigment involved an eczematous ulcerated plaque overlying yellow, red, and green ink in a recently applied tattoo. Patch testing with the inks originally used in the tattoo was negative. The authors noted that the 3 problematic ink colors all contained pigment yellow 65—an azo pigment—and attributed the reaction to this dye.²² In another azo reaction, a patient had erythema and pruritus overlying a tattoo applied 1 month prior. Patch testing was positive for aminoazobenzene, an azo pigment that was present in the orange ink of the tattoo.²³

Management of Tattoo Hypersensitivity Reactions

Hypersensitivity reactions to temporary tattoos are just that—temporary. Topical steroids and time generally will allow these reactions to resolve. In the setting of vigorous reactions, patients may develop postinflammatory hypopigmentation or hyperpigmentation that may last for months. Unfortunately, bullous tattoo reactions can lead to scarring and keloid formation, requiring more aggressive therapy.

Management of reactions to permanent tattoos is more challenging. High-potency topical steroids under occlusion or intralesional corticosteroid injections may aid in treating pruritus or discomfort. For severe reactions, oral corticosteroids may be required. Patients also may consider laser tattoo removal; however, providers should be aware that there have been rare reports of systemic urticarial reactions from this procedure.^24,25 Obviously limited by location and size, excision also may be offered.

Patch Testing for Tattoo Ink Contact Allergy

When patients present for evaluation and management of tattoo ACD, it is important to also consider other causes, including granulomatous tattoo reaction, pseudolymphoma, and lichenoid tattoo reaction. A biopsy can be helpful if the diagnosis is in question.

Patch testing for contact allergy to temporary tattoo inks should include PPD, fragrance, aminophenols, resorcinol, para-tertiary butylphenol formaldehyde, and essential oils. Jagua currently is not available for commercial purchase but also should be considered if the patient has the original product or in research settings. If the individual tattoo ingredients can be identified, they also should be tested. In this scenario, recall reactions may occur; testing with the tattoo paste should be avoided if the prior reaction was severe. Importantly, patients with a PPD allergy should be counseled to avoid hair dyes that contain PPD. Many patients who are sensitized to PPD have strong reactions on patch testing and are at risk for severe reactions if PPD or PPD-related compounds are encountered in hair dye.

Patch testing for ACD to permanent tattoos is complex. In most cases, patch testing is of limited utility because many of the chemicals that have been reported to cause ACD are not commercially available. Additionally, a 2014 study of 90 patients with chronic tattoo reactions found that the majority had negative patch testing to the European baseline series (66%), disperse dyes (87%), and tattoo inks (87%–92%). The investigators theorized that the allergens causing tattoo reactions are formed by haptenization of “parent” chemicals in the dermis, meaning application of chemicals present in the original tattoo ink may not identify the relevant allergen.²⁶ If patch testing is performed, it is most ideal if individual pigment ingredients can be identified. Allergens to be considered for testing include azo dyes, aromatic amines, iron oxide, barium, zinc, copper, molybdenum, titanium, gold sodium thiosulfate, nickel sulfate, carbon, shellac, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), quinophthalone (yellow) dyes, mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal, many of which are not commercially available for purchase.

Final Interpretation

As tattoos become increasingly trendy, tattoo ACD should be recognized by the astute dermatologist. The most common allergen associated with tattoo ACD is PPD, but other potential allergens include azo dyes and newer pigments. Unlike tattoos of the past, today’s inks are unlikely to contain toxic metals. Diagnosing ACD caused by permanent tattoo inks requires a high degree of suspicion, as patch testing may be of limited utility.

Sometimes regrettable yet increasingly common, tattoos are an ancient art form used in modern times as a mark of artistic and cultural expression. Allergic contact dermatitis (ACD) to tattoo ink is rare, but the popularity of tattoos makes ACD an increasingly recognized occurrence. In a retrospective study of 38,543 patch-tested patients, only 29 (0.08%) had tattoo-related ACD, with the majority of patients being female and young adults. The most common contact allergy was to paraphenylenediamine (PPD), which occurred in 22 (76%) patients.¹ In this article, we will walk you through the rainbow of tattoo ACD, covering hypersensitivity reactions to both temporary and permanent tattoo inks.

Temporary Tattoo Inks

Henna is the most common temporary tattoo ink. Derived from the plant Lawsonia inermis, henna is an orange dye that has been used in many parts of the world, particularly in Islamic and Hindu cultures, to dye skin, hair, and fabrics. Application of henna tattoos is common for weddings and other celebrations, and brides may wear elaborate henna patterns. To create these tattoos, henna powder is mixed with water and sometimes essential oils and is then applied to the skin for several hours. After application, the henna pigment lawsone (2-hydroxy-1,4-naphthoquinone) interacts with keratin and leaves a red-orange stain on the skin²; longer application time leads to a deeper color. Most traditional cutaneous henna designs fade in 2 to 6 weeks, but some last longer. Red henna generally is considered safe with low incidence of contact allergy. What is referred to as black henna usually is red henna mixed with PPD, a black dye, which is added to deepen the color. Paraphenylenediamine is highly sensitizing; patients can become sensitized to the PPD in the tattoo itself.² One study confirmed the presence of PPD in black henna tattoos, with chemical analysis of common preparations revealing concentrations ranging from less than 1% to 30%.² Patients who undergo patch testing for tattoo reactions often are strongly positive to PPD and have concomitant reactions to azo dyes, black rubber, and anesthetics. Other aromatic amines including aminophenols have been identified in black henna tattoo ink, and these chemicals also may contribute to ACD.³ Less common sources of contact allergy from temporary black henna tattoos include resorcinol,⁴ para-tertiary butylphenol formaldehyde resin,⁵ and fragrance.⁶

Clinically, ACD to PPD in temporary tattoos presents 1 to 3 days after application if the patient is already sensitized or 4 to 14 days if the patient is sensitized by the tattoo ink.² Most patients notice erythema, edema, vesicles, papules, and/or bullae, but other less common reactions including generalized dermatitis, systemic symptoms, urticaria, and pustules have been described.² Postinflammatory hypopigmentation or hyperpigmentation also can occur.

Because of the sensitizing nature of black henna tattoos, consumers are turning to natural temporary tattoos. Jagua temporary tattoos, with pigment derived from the sap of fruit from the Genipa americana tree, have been associated with ACD.⁷ This black dye is applied and washed off in a similar fashion to henna tattoos. Importantly, a recent analysis of jagua dye identified no PPD. In one case, a patient who developed ACD to a jagua tattoo was patch tested to components of the dye and had a positive reaction to genipin, a component of the fruit extract.⁷ Thus, jagua tattoos often are marketed as safe but are an emerging source of contact dermatitis to temporary tattoos.

Permanent Tattoo Inks

Permanent tattoos are created by injecting small amounts of ink into the dermis. As the name suggests, these tattoos are permanent. Tattoos are common; nearly one-third of Americans have at least 1 tattoo.¹ Historically, tattoos were created using black pigment composed of amorphous carbon or black iron oxides.^8,9 Metallic pigments (eg, mercury, chromium, cobalt, cadmium) were once used to add color to tattoos, but these metals are now only rarely used; in fact, a 2019 study of tattoo ink components identified 44 distinct pigments in 1416 permanent inks, with an average of 3 pigments per ink.⁸ Of the 44 pigments, 10 had metallic components including iron, barium, zinc, copper, molybdenum, and titanium. The remaining 34 pigments contained carbon, azo, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), or quinophthalone (yellow) dyes. The authors noted that nearly one-quarter of the tattoo pigments identified in their study had been reported as contact allergens.⁸

Typically, reactions to permanent tattoo inks manifest as an eczematous dermatitis occurring weeks to years after tattoo application.^9,10 The dermatitis usually is locally confined to the tattoo and may be limited to particular colors; occasionally, a new tattoo reaction may trigger concurrent inflammation in older tattoos. Many tattoo reactions occur as a response to red pigment but also have occurred with other tattoo ink components.⁹ Many researchers have speculated as to whether the reaction is related to the ink component itself or from the photochemical breakdown of the ink by exposure to UV radiation and/or laser therapy.⁹

Red Pigment
Red ink is the most common color reported to cause tattoo hypersensitivity reactions. Historically, red tattoo pigments include mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal,¹¹ but today’s tattoo inks primarily are composed of other pigments, such as quinacridone and azo dyes.¹² Several cases of red tattoo ink hypersensitivity reactions exist in the literature, many without completion of patch tests or without positive patch tests to relevant red pigments.^11-15

Black Pigment
In general, reactions to permanent black tattoo ink are rare; however, a few case reports exist. Black pigment can be created with India ink (carbon), logwood (chrome), iron oxide, and titanium.^16,17 Shellac can be used as a binding agent in tattoo ink; there is at least one report of a reaction to black tattoo ink with a positive patch test to shellac and the original black ink.¹⁸

Azo Pigments
Azo pigments frequently are used in modern tattoos due to their vibrant colors. One case of hypersensitivity to azo pigment involved an eczematous ulcerated plaque overlying yellow, red, and green ink in a recently applied tattoo. Patch testing with the inks originally used in the tattoo was negative. The authors noted that the 3 problematic ink colors all contained pigment yellow 65—an azo pigment—and attributed the reaction to this dye.²² In another azo reaction, a patient had erythema and pruritus overlying a tattoo applied 1 month prior. Patch testing was positive for aminoazobenzene, an azo pigment that was present in the orange ink of the tattoo.²³

Management of Tattoo Hypersensitivity Reactions

Hypersensitivity reactions to temporary tattoos are just that—temporary. Topical steroids and time generally will allow these reactions to resolve. In the setting of vigorous reactions, patients may develop postinflammatory hypopigmentation or hyperpigmentation that may last for months. Unfortunately, bullous tattoo reactions can lead to scarring and keloid formation, requiring more aggressive therapy.

Management of reactions to permanent tattoos is more challenging. High-potency topical steroids under occlusion or intralesional corticosteroid injections may aid in treating pruritus or discomfort. For severe reactions, oral corticosteroids may be required. Patients also may consider laser tattoo removal; however, providers should be aware that there have been rare reports of systemic urticarial reactions from this procedure.^24,25 Obviously limited by location and size, excision also may be offered.

Patch Testing for Tattoo Ink Contact Allergy

When patients present for evaluation and management of tattoo ACD, it is important to also consider other causes, including granulomatous tattoo reaction, pseudolymphoma, and lichenoid tattoo reaction. A biopsy can be helpful if the diagnosis is in question.

Patch testing for contact allergy to temporary tattoo inks should include PPD, fragrance, aminophenols, resorcinol, para-tertiary butylphenol formaldehyde, and essential oils. Jagua currently is not available for commercial purchase but also should be considered if the patient has the original product or in research settings. If the individual tattoo ingredients can be identified, they also should be tested. In this scenario, recall reactions may occur; testing with the tattoo paste should be avoided if the prior reaction was severe. Importantly, patients with a PPD allergy should be counseled to avoid hair dyes that contain PPD. Many patients who are sensitized to PPD have strong reactions on patch testing and are at risk for severe reactions if PPD or PPD-related compounds are encountered in hair dye.

Patch testing for ACD to permanent tattoos is complex. In most cases, patch testing is of limited utility because many of the chemicals that have been reported to cause ACD are not commercially available. Additionally, a 2014 study of 90 patients with chronic tattoo reactions found that the majority had negative patch testing to the European baseline series (66%), disperse dyes (87%), and tattoo inks (87%–92%). The investigators theorized that the allergens causing tattoo reactions are formed by haptenization of “parent” chemicals in the dermis, meaning application of chemicals present in the original tattoo ink may not identify the relevant allergen.²⁶ If patch testing is performed, it is most ideal if individual pigment ingredients can be identified. Allergens to be considered for testing include azo dyes, aromatic amines, iron oxide, barium, zinc, copper, molybdenum, titanium, gold sodium thiosulfate, nickel sulfate, carbon, shellac, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), quinophthalone (yellow) dyes, mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal, many of which are not commercially available for purchase.

Final Interpretation

As tattoos become increasingly trendy, tattoo ACD should be recognized by the astute dermatologist. The most common allergen associated with tattoo ACD is PPD, but other potential allergens include azo dyes and newer pigments. Unlike tattoos of the past, today’s inks are unlikely to contain toxic metals. Diagnosing ACD caused by permanent tattoo inks requires a high degree of suspicion, as patch testing may be of limited utility.

Sometimes regrettable yet increasingly common, tattoos are an ancient art form used in modern times as a mark of artistic and cultural expression. Allergic contact dermatitis (ACD) to tattoo ink is rare, but the popularity of tattoos makes ACD an increasingly recognized occurrence. In a retrospective study of 38,543 patch-tested patients, only 29 (0.08%) had tattoo-related ACD, with the majority of patients being female and young adults. The most common contact allergy was to paraphenylenediamine (PPD), which occurred in 22 (76%) patients.¹ In this article, we will walk you through the rainbow of tattoo ACD, covering hypersensitivity reactions to both temporary and permanent tattoo inks.

Temporary Tattoo Inks

Henna is the most common temporary tattoo ink. Derived from the plant Lawsonia inermis, henna is an orange dye that has been used in many parts of the world, particularly in Islamic and Hindu cultures, to dye skin, hair, and fabrics. Application of henna tattoos is common for weddings and other celebrations, and brides may wear elaborate henna patterns. To create these tattoos, henna powder is mixed with water and sometimes essential oils and is then applied to the skin for several hours. After application, the henna pigment lawsone (2-hydroxy-1,4-naphthoquinone) interacts with keratin and leaves a red-orange stain on the skin²; longer application time leads to a deeper color. Most traditional cutaneous henna designs fade in 2 to 6 weeks, but some last longer. Red henna generally is considered safe with low incidence of contact allergy. What is referred to as black henna usually is red henna mixed with PPD, a black dye, which is added to deepen the color. Paraphenylenediamine is highly sensitizing; patients can become sensitized to the PPD in the tattoo itself.² One study confirmed the presence of PPD in black henna tattoos, with chemical analysis of common preparations revealing concentrations ranging from less than 1% to 30%.² Patients who undergo patch testing for tattoo reactions often are strongly positive to PPD and have concomitant reactions to azo dyes, black rubber, and anesthetics. Other aromatic amines including aminophenols have been identified in black henna tattoo ink, and these chemicals also may contribute to ACD.³ Less common sources of contact allergy from temporary black henna tattoos include resorcinol,⁴ para-tertiary butylphenol formaldehyde resin,⁵ and fragrance.⁶

Clinically, ACD to PPD in temporary tattoos presents 1 to 3 days after application if the patient is already sensitized or 4 to 14 days if the patient is sensitized by the tattoo ink.² Most patients notice erythema, edema, vesicles, papules, and/or bullae, but other less common reactions including generalized dermatitis, systemic symptoms, urticaria, and pustules have been described.² Postinflammatory hypopigmentation or hyperpigmentation also can occur.

Because of the sensitizing nature of black henna tattoos, consumers are turning to natural temporary tattoos. Jagua temporary tattoos, with pigment derived from the sap of fruit from the Genipa americana tree, have been associated with ACD.⁷ This black dye is applied and washed off in a similar fashion to henna tattoos. Importantly, a recent analysis of jagua dye identified no PPD. In one case, a patient who developed ACD to a jagua tattoo was patch tested to components of the dye and had a positive reaction to genipin, a component of the fruit extract.⁷ Thus, jagua tattoos often are marketed as safe but are an emerging source of contact dermatitis to temporary tattoos.

Permanent Tattoo Inks

Permanent tattoos are created by injecting small amounts of ink into the dermis. As the name suggests, these tattoos are permanent. Tattoos are common; nearly one-third of Americans have at least 1 tattoo.¹ Historically, tattoos were created using black pigment composed of amorphous carbon or black iron oxides.^8,9 Metallic pigments (eg, mercury, chromium, cobalt, cadmium) were once used to add color to tattoos, but these metals are now only rarely used; in fact, a 2019 study of tattoo ink components identified 44 distinct pigments in 1416 permanent inks, with an average of 3 pigments per ink.⁸ Of the 44 pigments, 10 had metallic components including iron, barium, zinc, copper, molybdenum, and titanium. The remaining 34 pigments contained carbon, azo, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), or quinophthalone (yellow) dyes. The authors noted that nearly one-quarter of the tattoo pigments identified in their study had been reported as contact allergens.⁸

Typically, reactions to permanent tattoo inks manifest as an eczematous dermatitis occurring weeks to years after tattoo application.^9,10 The dermatitis usually is locally confined to the tattoo and may be limited to particular colors; occasionally, a new tattoo reaction may trigger concurrent inflammation in older tattoos. Many tattoo reactions occur as a response to red pigment but also have occurred with other tattoo ink components.⁹ Many researchers have speculated as to whether the reaction is related to the ink component itself or from the photochemical breakdown of the ink by exposure to UV radiation and/or laser therapy.⁹

Red Pigment
Red ink is the most common color reported to cause tattoo hypersensitivity reactions. Historically, red tattoo pigments include mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal,¹¹ but today’s tattoo inks primarily are composed of other pigments, such as quinacridone and azo dyes.¹² Several cases of red tattoo ink hypersensitivity reactions exist in the literature, many without completion of patch tests or without positive patch tests to relevant red pigments.^11-15

Black Pigment
In general, reactions to permanent black tattoo ink are rare; however, a few case reports exist. Black pigment can be created with India ink (carbon), logwood (chrome), iron oxide, and titanium.^16,17 Shellac can be used as a binding agent in tattoo ink; there is at least one report of a reaction to black tattoo ink with a positive patch test to shellac and the original black ink.¹⁸

Azo Pigments
Azo pigments frequently are used in modern tattoos due to their vibrant colors. One case of hypersensitivity to azo pigment involved an eczematous ulcerated plaque overlying yellow, red, and green ink in a recently applied tattoo. Patch testing with the inks originally used in the tattoo was negative. The authors noted that the 3 problematic ink colors all contained pigment yellow 65—an azo pigment—and attributed the reaction to this dye.²² In another azo reaction, a patient had erythema and pruritus overlying a tattoo applied 1 month prior. Patch testing was positive for aminoazobenzene, an azo pigment that was present in the orange ink of the tattoo.²³

Management of Tattoo Hypersensitivity Reactions

Hypersensitivity reactions to temporary tattoos are just that—temporary. Topical steroids and time generally will allow these reactions to resolve. In the setting of vigorous reactions, patients may develop postinflammatory hypopigmentation or hyperpigmentation that may last for months. Unfortunately, bullous tattoo reactions can lead to scarring and keloid formation, requiring more aggressive therapy.

Management of reactions to permanent tattoos is more challenging. High-potency topical steroids under occlusion or intralesional corticosteroid injections may aid in treating pruritus or discomfort. For severe reactions, oral corticosteroids may be required. Patients also may consider laser tattoo removal; however, providers should be aware that there have been rare reports of systemic urticarial reactions from this procedure.^24,25 Obviously limited by location and size, excision also may be offered.

Patch Testing for Tattoo Ink Contact Allergy

When patients present for evaluation and management of tattoo ACD, it is important to also consider other causes, including granulomatous tattoo reaction, pseudolymphoma, and lichenoid tattoo reaction. A biopsy can be helpful if the diagnosis is in question.

Patch testing for contact allergy to temporary tattoo inks should include PPD, fragrance, aminophenols, resorcinol, para-tertiary butylphenol formaldehyde, and essential oils. Jagua currently is not available for commercial purchase but also should be considered if the patient has the original product or in research settings. If the individual tattoo ingredients can be identified, they also should be tested. In this scenario, recall reactions may occur; testing with the tattoo paste should be avoided if the prior reaction was severe. Importantly, patients with a PPD allergy should be counseled to avoid hair dyes that contain PPD. Many patients who are sensitized to PPD have strong reactions on patch testing and are at risk for severe reactions if PPD or PPD-related compounds are encountered in hair dye.

Patch testing for ACD to permanent tattoos is complex. In most cases, patch testing is of limited utility because many of the chemicals that have been reported to cause ACD are not commercially available. Additionally, a 2014 study of 90 patients with chronic tattoo reactions found that the majority had negative patch testing to the European baseline series (66%), disperse dyes (87%), and tattoo inks (87%–92%). The investigators theorized that the allergens causing tattoo reactions are formed by haptenization of “parent” chemicals in the dermis, meaning application of chemicals present in the original tattoo ink may not identify the relevant allergen.²⁶ If patch testing is performed, it is most ideal if individual pigment ingredients can be identified. Allergens to be considered for testing include azo dyes, aromatic amines, iron oxide, barium, zinc, copper, molybdenum, titanium, gold sodium thiosulfate, nickel sulfate, carbon, shellac, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine (purple), quinophthalone (yellow) dyes, mercuric sulfide (vermilion, cinnabar), scarlet lake, cadmium red, carmine, and cochineal, many of which are not commercially available for purchase.

Final Interpretation

As tattoos become increasingly trendy, tattoo ACD should be recognized by the astute dermatologist. The most common allergen associated with tattoo ACD is PPD, but other potential allergens include azo dyes and newer pigments. Unlike tattoos of the past, today’s inks are unlikely to contain toxic metals. Diagnosing ACD caused by permanent tattoo inks requires a high degree of suspicion, as patch testing may be of limited utility.

The top three contact allergens in patients younger than 18 years of age are hydroperoxides of linalool, nickel sulfate, and methylisothiazolinone, according to an analysis of data from the Pediatric Allergic Contact Dermatitis Registry.

The registry is the first multicenter prospective database in the United States with a focus on pediatric allergic contact dermatitis. JiaDe (Jeff) Yu, MD, a dermatologist at Massachusetts General Hospital, Boston, was awarded a Dermatology Foundation Career Development Grant and formed the registry in 2018 “in an effort to gain a better understanding of allergic contact dermatitis in children,” Idy Tam, MS, said during the virtual annual meeting of the Society for Pediatric Dermatology. “There is currently limited data regarding the pediatric allergic contact dermatitis in the U.S., despite as many as 20% of children having allergic contact dermatitis.”

To date, the Pediatric Allergic Contact Dermatitis Registry consists of 10 academic medical centers with high volume pediatric patch testing across the United States: Massachusetts General Hospital, Boston; Brigham and Women’s Hospital, Boston; the University of Missouri–Columbia; Stanford (Calif.) University; the Medical University of South Carolina, Charleston; Texas Children’s Hospital, Houston; Northwestern University, Chicago; Emory University, Atlanta; Washington University, St. Louis; and the University of California, San Diego.

For the current analysis, Ms. Tam, a research fellow in the department of dermatology at Massachusetts General Hospital, and colleagues collected data on 218 patients under age 18 who were referred for an evaluation of allergic contact dermatitis at one of the 10 participating sites between January 2016 and June 2020.

The mean age of children at the time of their patch testing was 10 years, 62% were girls, and 66% had a history of atopic dermatitis (AD). Most (75%) were White, 14% were Black, 6% were Asian, the rest were from other racial backgrounds. The distribution of dermatitis varied; the top five most commonly affected sites were the face (62%), arms (35%), legs (29%), hands (27%), and neck (20%).

Ms. Tam reported that the mean number of allergens patch tested per child was 78. In all, 81% of children had one or more positive patch test reactions, with a similar rate among those with and without a history of AD (80% vs. 82%, respectively; P = .21). The five most common allergens were hydroperoxides of linalool (22%), nickel sulfate (19%), methylisothiazolinone (17%), cobalt chloride (13%), and fragrance mix I (12%).

The top two treatments at the time of patch testing were a topical corticosteroid (78%) and a topical calcineurin inhibitor (26%).

“This study has allowed for the increased collaboration among dermatologists with expertise in pediatric dermatology and allergic contact dermatitis,” concluded Ms. Tam, a fourth-year medical student at Tufts University, Boston. “We continue to actively seek further collaboration with a goal of creating the most comprehensive pediatric allergic contact dermatitis registry, which can improve our understanding of this condition in children and hopefully guide future research in this field.”

The work was recognized as one of the top poster abstracts at the meeting. The researchers reported having no relevant disclosures.

[email protected]

The top three contact allergens in patients younger than 18 years of age are hydroperoxides of linalool, nickel sulfate, and methylisothiazolinone, according to an analysis of data from the Pediatric Allergic Contact Dermatitis Registry.

The registry is the first multicenter prospective database in the United States with a focus on pediatric allergic contact dermatitis. JiaDe (Jeff) Yu, MD, a dermatologist at Massachusetts General Hospital, Boston, was awarded a Dermatology Foundation Career Development Grant and formed the registry in 2018 “in an effort to gain a better understanding of allergic contact dermatitis in children,” Idy Tam, MS, said during the virtual annual meeting of the Society for Pediatric Dermatology. “There is currently limited data regarding the pediatric allergic contact dermatitis in the U.S., despite as many as 20% of children having allergic contact dermatitis.”

To date, the Pediatric Allergic Contact Dermatitis Registry consists of 10 academic medical centers with high volume pediatric patch testing across the United States: Massachusetts General Hospital, Boston; Brigham and Women’s Hospital, Boston; the University of Missouri–Columbia; Stanford (Calif.) University; the Medical University of South Carolina, Charleston; Texas Children’s Hospital, Houston; Northwestern University, Chicago; Emory University, Atlanta; Washington University, St. Louis; and the University of California, San Diego.

For the current analysis, Ms. Tam, a research fellow in the department of dermatology at Massachusetts General Hospital, and colleagues collected data on 218 patients under age 18 who were referred for an evaluation of allergic contact dermatitis at one of the 10 participating sites between January 2016 and June 2020.

The mean age of children at the time of their patch testing was 10 years, 62% were girls, and 66% had a history of atopic dermatitis (AD). Most (75%) were White, 14% were Black, 6% were Asian, the rest were from other racial backgrounds. The distribution of dermatitis varied; the top five most commonly affected sites were the face (62%), arms (35%), legs (29%), hands (27%), and neck (20%).

Ms. Tam reported that the mean number of allergens patch tested per child was 78. In all, 81% of children had one or more positive patch test reactions, with a similar rate among those with and without a history of AD (80% vs. 82%, respectively; P = .21). The five most common allergens were hydroperoxides of linalool (22%), nickel sulfate (19%), methylisothiazolinone (17%), cobalt chloride (13%), and fragrance mix I (12%).

The top two treatments at the time of patch testing were a topical corticosteroid (78%) and a topical calcineurin inhibitor (26%).

“This study has allowed for the increased collaboration among dermatologists with expertise in pediatric dermatology and allergic contact dermatitis,” concluded Ms. Tam, a fourth-year medical student at Tufts University, Boston. “We continue to actively seek further collaboration with a goal of creating the most comprehensive pediatric allergic contact dermatitis registry, which can improve our understanding of this condition in children and hopefully guide future research in this field.”

The work was recognized as one of the top poster abstracts at the meeting. The researchers reported having no relevant disclosures.

[email protected]

The top three contact allergens in patients younger than 18 years of age are hydroperoxides of linalool, nickel sulfate, and methylisothiazolinone, according to an analysis of data from the Pediatric Allergic Contact Dermatitis Registry.

The registry is the first multicenter prospective database in the United States with a focus on pediatric allergic contact dermatitis. JiaDe (Jeff) Yu, MD, a dermatologist at Massachusetts General Hospital, Boston, was awarded a Dermatology Foundation Career Development Grant and formed the registry in 2018 “in an effort to gain a better understanding of allergic contact dermatitis in children,” Idy Tam, MS, said during the virtual annual meeting of the Society for Pediatric Dermatology. “There is currently limited data regarding the pediatric allergic contact dermatitis in the U.S., despite as many as 20% of children having allergic contact dermatitis.”

To date, the Pediatric Allergic Contact Dermatitis Registry consists of 10 academic medical centers with high volume pediatric patch testing across the United States: Massachusetts General Hospital, Boston; Brigham and Women’s Hospital, Boston; the University of Missouri–Columbia; Stanford (Calif.) University; the Medical University of South Carolina, Charleston; Texas Children’s Hospital, Houston; Northwestern University, Chicago; Emory University, Atlanta; Washington University, St. Louis; and the University of California, San Diego.

For the current analysis, Ms. Tam, a research fellow in the department of dermatology at Massachusetts General Hospital, and colleagues collected data on 218 patients under age 18 who were referred for an evaluation of allergic contact dermatitis at one of the 10 participating sites between January 2016 and June 2020.

The mean age of children at the time of their patch testing was 10 years, 62% were girls, and 66% had a history of atopic dermatitis (AD). Most (75%) were White, 14% were Black, 6% were Asian, the rest were from other racial backgrounds. The distribution of dermatitis varied; the top five most commonly affected sites were the face (62%), arms (35%), legs (29%), hands (27%), and neck (20%).

Ms. Tam reported that the mean number of allergens patch tested per child was 78. In all, 81% of children had one or more positive patch test reactions, with a similar rate among those with and without a history of AD (80% vs. 82%, respectively; P = .21). The five most common allergens were hydroperoxides of linalool (22%), nickel sulfate (19%), methylisothiazolinone (17%), cobalt chloride (13%), and fragrance mix I (12%).

The top two treatments at the time of patch testing were a topical corticosteroid (78%) and a topical calcineurin inhibitor (26%).

“This study has allowed for the increased collaboration among dermatologists with expertise in pediatric dermatology and allergic contact dermatitis,” concluded Ms. Tam, a fourth-year medical student at Tufts University, Boston. “We continue to actively seek further collaboration with a goal of creating the most comprehensive pediatric allergic contact dermatitis registry, which can improve our understanding of this condition in children and hopefully guide future research in this field.”

The work was recognized as one of the top poster abstracts at the meeting. The researchers reported having no relevant disclosures.

[email protected]

In the clinical experience of Kari L. Martin, MD, incorporating patch testing into your existing practice requires careful thought and planning.

“Time needs to be allocated for a patch test consultation, placement, removal, and reading,” she said at the virtual annual meeting of the Society for Pediatric Dermatology. “You will need more time in the day that you’re reading the patch test for patient education. However, your staff will need more time on the front end of the patch test process for application. Also, if they are customizing patch tests, they’ll need time to make the patch tests along with access to a refrigerator and plenty of counter space.”

Other factors to consider are the site of service, your payer mix, and if you need to complete prior authorizations for patch testing.

Dr. Martin, associate professor of dermatology and child health at the University of Missouri–Columbia, said that the diagnosis of allergic contact dermatitis (ACD) crosses her mind when she sees a patient with new dermatitis, especially in an older child; if the dermatitis is patterned or regional; if there’s exacerbation of an underlying, previously stable skin disease; or if it’s a pattern known to be associated with systemic contact dermatitis. “In fact, 13%-25% of healthy, asymptomatic kids have allergen sensitization,” she said. “If you take that a step further and look at kids who are suspected of having allergic contact dermatitis, 25%-96% have allergen sensitization. Still, that doesn’t mean that those tests are relevant to the dermatitis that’s going on. If you take kids who are referred to tertiary centers for patch testing, about half will have relevant patch test results.”

Pediatric ACD differs from adult ACD in three ways, Dr. Martin said. First, children have a different clinical morphology and distribution on presentation, compared with adults. “In adults, the most common clinical presentation is hand dermatitis, while kids more often present with a scattered generalized morphology of dermatitis,” she said. “This occurs in about one-third of children with ACD. Their patterns of allergen exposure are also different. For the most part, adults are in control of their own environments and what is placed on their skin, whereas kids are not. When thinking about what you might need to patch test a child to if you’re considering ACD, it’s important to think about not only what the parent or caregiver puts directly on the child’s skin but also any connubial or consort allergen exposure – the most common ones coming from the caregivers themselves, such as fragrance or hair dyes that are transferred to a young child.”

The third factor that differs between pediatric and adult ACD is the allergen source. Dr. Martin noted that children and adults use different personal care products, wear different types of clothing, and spend different amounts of time in play versus work. “Children have many more hobbies in general that are unfortunately lost as many of us age,” she said. That means “thinking through the child’s entire day and how the seasons differ for them, such as what sports they’re in and what protective equipment may be involved with where their dermatitis is, or what musical instruments they play.”

Applying the T.R.U.E. patch test panel or a customized patch test panel to young children poses certain challenges, considering their limited body surface area and propensity to squirm. Dr. Martin often employs distraction techniques when placing patches on young patients, including the use of bubbles, music, movies, and games. “The goal is always to get as much of the patches on the back or the flanks as possible,” she said. “If you need additional space you can use the upper outer arms, the abdomen, or the anterior lateral thighs. Another thing to consider is how to set up your week for pediatric patch testing. There’s a standardized process for adults where we place the patches on day 0, read them on day 2, with removal of the patches at that time, and then perform a delayed read between day 4-7.”

The process is similar for postpubescent children, despite the lack of clear guidelines in the medical literature. “There is much controversy and different practices between different pediatric patch test centers,” Dr. Martin said. “There is more consensus between the older kids and the prepubescent group ages 6-12. Most clinicians will still do a similar placement on day 0 with removal and initial read on day 2, with a delayed read on day 4-7. However, some groups will remove patches at 24 hours, especially in those with atopic dermatitis (AD) or a generalized dermatitis, to reduce irritant reactions. Others will also use half-strength concentrations of allergens.”

The most controversy lies with children younger than 6 years, she said. For those aged 3-6 years, who do not have AD, most practices use a standardized pediatric tray with a 24- to 48-hour contact time. However, patch testing can be “very challenging” for children who are under 3 years of age, and children with AD who are under 6 years, “so there needs to be a very high degree of suspicion for ACD and very careful selection of the allergens and contact time that is used in those particular cases,” she noted.

The most common allergens in children are nickel, fragrance mix I, cobalt, balsam of Peru, neomycin, and bacitracin, which largely match the common allergens seen in adults. However, allergens more common in children, compared with adults, include gold, propylene glycol, 2-Bromo-2-nitropropane-1,3-diol, and cocamidopropyl betaine. “If the child presents with a regional dermatitis or a patterned dermatitis, sometimes you can hone in on your suspected allergens and only test for a few,” Dr. Martin said. “In a child with eyelid dermatitis, you’re going to worry more about cocamidopropyl betaine in their shampoos and cleansers. Also, a metal allergen could be transferred from their hands from toys or coins, specifically nickel and cobalt. They also may have different sports gear such as goggles that may be affecting their eyelid dermatitis, which you would not necessarily see in an adult.”

Periorificial contact dermatitis can also differ in presentation between children and adults. “In kids, think about musical instruments, flavored lip balms, gum, and pacifiers,” she said. “For ACD on the buttocks and posterior thighs, think about toilet seat allergens, especially those in the potty training ages, and the nickel bolts on school chairs.”

In 2018, Dr. Martin and her colleagues on the Pediatric Contact Dermatitis Workgroup published a pediatric baseline patch test series as a way to expand on the T.R.U.E. test (Dermatitis. 2018;29[4]:206-12). “It’s nice to have this panel available as a baseline screening tool when you’re unsure of possible triggers of the dermatitis but you still have high suspicion of allergic dermatitis,” Dr. Martin said. “This also is helpful for patients who present with generalized dermatitis. It’s still not perfect. We are collecting prospective data to fine-tune this baseline series.”

She reported having no financial disclosures.

[email protected]

In the clinical experience of Kari L. Martin, MD, incorporating patch testing into your existing practice requires careful thought and planning.

“Time needs to be allocated for a patch test consultation, placement, removal, and reading,” she said at the virtual annual meeting of the Society for Pediatric Dermatology. “You will need more time in the day that you’re reading the patch test for patient education. However, your staff will need more time on the front end of the patch test process for application. Also, if they are customizing patch tests, they’ll need time to make the patch tests along with access to a refrigerator and plenty of counter space.”

Other factors to consider are the site of service, your payer mix, and if you need to complete prior authorizations for patch testing.

Dr. Martin, associate professor of dermatology and child health at the University of Missouri–Columbia, said that the diagnosis of allergic contact dermatitis (ACD) crosses her mind when she sees a patient with new dermatitis, especially in an older child; if the dermatitis is patterned or regional; if there’s exacerbation of an underlying, previously stable skin disease; or if it’s a pattern known to be associated with systemic contact dermatitis. “In fact, 13%-25% of healthy, asymptomatic kids have allergen sensitization,” she said. “If you take that a step further and look at kids who are suspected of having allergic contact dermatitis, 25%-96% have allergen sensitization. Still, that doesn’t mean that those tests are relevant to the dermatitis that’s going on. If you take kids who are referred to tertiary centers for patch testing, about half will have relevant patch test results.”

Pediatric ACD differs from adult ACD in three ways, Dr. Martin said. First, children have a different clinical morphology and distribution on presentation, compared with adults. “In adults, the most common clinical presentation is hand dermatitis, while kids more often present with a scattered generalized morphology of dermatitis,” she said. “This occurs in about one-third of children with ACD. Their patterns of allergen exposure are also different. For the most part, adults are in control of their own environments and what is placed on their skin, whereas kids are not. When thinking about what you might need to patch test a child to if you’re considering ACD, it’s important to think about not only what the parent or caregiver puts directly on the child’s skin but also any connubial or consort allergen exposure – the most common ones coming from the caregivers themselves, such as fragrance or hair dyes that are transferred to a young child.”

The third factor that differs between pediatric and adult ACD is the allergen source. Dr. Martin noted that children and adults use different personal care products, wear different types of clothing, and spend different amounts of time in play versus work. “Children have many more hobbies in general that are unfortunately lost as many of us age,” she said. That means “thinking through the child’s entire day and how the seasons differ for them, such as what sports they’re in and what protective equipment may be involved with where their dermatitis is, or what musical instruments they play.”

Applying the T.R.U.E. patch test panel or a customized patch test panel to young children poses certain challenges, considering their limited body surface area and propensity to squirm. Dr. Martin often employs distraction techniques when placing patches on young patients, including the use of bubbles, music, movies, and games. “The goal is always to get as much of the patches on the back or the flanks as possible,” she said. “If you need additional space you can use the upper outer arms, the abdomen, or the anterior lateral thighs. Another thing to consider is how to set up your week for pediatric patch testing. There’s a standardized process for adults where we place the patches on day 0, read them on day 2, with removal of the patches at that time, and then perform a delayed read between day 4-7.”

The process is similar for postpubescent children, despite the lack of clear guidelines in the medical literature. “There is much controversy and different practices between different pediatric patch test centers,” Dr. Martin said. “There is more consensus between the older kids and the prepubescent group ages 6-12. Most clinicians will still do a similar placement on day 0 with removal and initial read on day 2, with a delayed read on day 4-7. However, some groups will remove patches at 24 hours, especially in those with atopic dermatitis (AD) or a generalized dermatitis, to reduce irritant reactions. Others will also use half-strength concentrations of allergens.”

The most controversy lies with children younger than 6 years, she said. For those aged 3-6 years, who do not have AD, most practices use a standardized pediatric tray with a 24- to 48-hour contact time. However, patch testing can be “very challenging” for children who are under 3 years of age, and children with AD who are under 6 years, “so there needs to be a very high degree of suspicion for ACD and very careful selection of the allergens and contact time that is used in those particular cases,” she noted.

The most common allergens in children are nickel, fragrance mix I, cobalt, balsam of Peru, neomycin, and bacitracin, which largely match the common allergens seen in adults. However, allergens more common in children, compared with adults, include gold, propylene glycol, 2-Bromo-2-nitropropane-1,3-diol, and cocamidopropyl betaine. “If the child presents with a regional dermatitis or a patterned dermatitis, sometimes you can hone in on your suspected allergens and only test for a few,” Dr. Martin said. “In a child with eyelid dermatitis, you’re going to worry more about cocamidopropyl betaine in their shampoos and cleansers. Also, a metal allergen could be transferred from their hands from toys or coins, specifically nickel and cobalt. They also may have different sports gear such as goggles that may be affecting their eyelid dermatitis, which you would not necessarily see in an adult.”

Periorificial contact dermatitis can also differ in presentation between children and adults. “In kids, think about musical instruments, flavored lip balms, gum, and pacifiers,” she said. “For ACD on the buttocks and posterior thighs, think about toilet seat allergens, especially those in the potty training ages, and the nickel bolts on school chairs.”

In 2018, Dr. Martin and her colleagues on the Pediatric Contact Dermatitis Workgroup published a pediatric baseline patch test series as a way to expand on the T.R.U.E. test (Dermatitis. 2018;29[4]:206-12). “It’s nice to have this panel available as a baseline screening tool when you’re unsure of possible triggers of the dermatitis but you still have high suspicion of allergic dermatitis,” Dr. Martin said. “This also is helpful for patients who present with generalized dermatitis. It’s still not perfect. We are collecting prospective data to fine-tune this baseline series.”

She reported having no financial disclosures.

[email protected]

In the clinical experience of Kari L. Martin, MD, incorporating patch testing into your existing practice requires careful thought and planning.

“Time needs to be allocated for a patch test consultation, placement, removal, and reading,” she said at the virtual annual meeting of the Society for Pediatric Dermatology. “You will need more time in the day that you’re reading the patch test for patient education. However, your staff will need more time on the front end of the patch test process for application. Also, if they are customizing patch tests, they’ll need time to make the patch tests along with access to a refrigerator and plenty of counter space.”

Other factors to consider are the site of service, your payer mix, and if you need to complete prior authorizations for patch testing.

Dr. Martin, associate professor of dermatology and child health at the University of Missouri–Columbia, said that the diagnosis of allergic contact dermatitis (ACD) crosses her mind when she sees a patient with new dermatitis, especially in an older child; if the dermatitis is patterned or regional; if there’s exacerbation of an underlying, previously stable skin disease; or if it’s a pattern known to be associated with systemic contact dermatitis. “In fact, 13%-25% of healthy, asymptomatic kids have allergen sensitization,” she said. “If you take that a step further and look at kids who are suspected of having allergic contact dermatitis, 25%-96% have allergen sensitization. Still, that doesn’t mean that those tests are relevant to the dermatitis that’s going on. If you take kids who are referred to tertiary centers for patch testing, about half will have relevant patch test results.”

Pediatric ACD differs from adult ACD in three ways, Dr. Martin said. First, children have a different clinical morphology and distribution on presentation, compared with adults. “In adults, the most common clinical presentation is hand dermatitis, while kids more often present with a scattered generalized morphology of dermatitis,” she said. “This occurs in about one-third of children with ACD. Their patterns of allergen exposure are also different. For the most part, adults are in control of their own environments and what is placed on their skin, whereas kids are not. When thinking about what you might need to patch test a child to if you’re considering ACD, it’s important to think about not only what the parent or caregiver puts directly on the child’s skin but also any connubial or consort allergen exposure – the most common ones coming from the caregivers themselves, such as fragrance or hair dyes that are transferred to a young child.”

The third factor that differs between pediatric and adult ACD is the allergen source. Dr. Martin noted that children and adults use different personal care products, wear different types of clothing, and spend different amounts of time in play versus work. “Children have many more hobbies in general that are unfortunately lost as many of us age,” she said. That means “thinking through the child’s entire day and how the seasons differ for them, such as what sports they’re in and what protective equipment may be involved with where their dermatitis is, or what musical instruments they play.”

Applying the T.R.U.E. patch test panel or a customized patch test panel to young children poses certain challenges, considering their limited body surface area and propensity to squirm. Dr. Martin often employs distraction techniques when placing patches on young patients, including the use of bubbles, music, movies, and games. “The goal is always to get as much of the patches on the back or the flanks as possible,” she said. “If you need additional space you can use the upper outer arms, the abdomen, or the anterior lateral thighs. Another thing to consider is how to set up your week for pediatric patch testing. There’s a standardized process for adults where we place the patches on day 0, read them on day 2, with removal of the patches at that time, and then perform a delayed read between day 4-7.”

The process is similar for postpubescent children, despite the lack of clear guidelines in the medical literature. “There is much controversy and different practices between different pediatric patch test centers,” Dr. Martin said. “There is more consensus between the older kids and the prepubescent group ages 6-12. Most clinicians will still do a similar placement on day 0 with removal and initial read on day 2, with a delayed read on day 4-7. However, some groups will remove patches at 24 hours, especially in those with atopic dermatitis (AD) or a generalized dermatitis, to reduce irritant reactions. Others will also use half-strength concentrations of allergens.”

The most controversy lies with children younger than 6 years, she said. For those aged 3-6 years, who do not have AD, most practices use a standardized pediatric tray with a 24- to 48-hour contact time. However, patch testing can be “very challenging” for children who are under 3 years of age, and children with AD who are under 6 years, “so there needs to be a very high degree of suspicion for ACD and very careful selection of the allergens and contact time that is used in those particular cases,” she noted.

The most common allergens in children are nickel, fragrance mix I, cobalt, balsam of Peru, neomycin, and bacitracin, which largely match the common allergens seen in adults. However, allergens more common in children, compared with adults, include gold, propylene glycol, 2-Bromo-2-nitropropane-1,3-diol, and cocamidopropyl betaine. “If the child presents with a regional dermatitis or a patterned dermatitis, sometimes you can hone in on your suspected allergens and only test for a few,” Dr. Martin said. “In a child with eyelid dermatitis, you’re going to worry more about cocamidopropyl betaine in their shampoos and cleansers. Also, a metal allergen could be transferred from their hands from toys or coins, specifically nickel and cobalt. They also may have different sports gear such as goggles that may be affecting their eyelid dermatitis, which you would not necessarily see in an adult.”

Periorificial contact dermatitis can also differ in presentation between children and adults. “In kids, think about musical instruments, flavored lip balms, gum, and pacifiers,” she said. “For ACD on the buttocks and posterior thighs, think about toilet seat allergens, especially those in the potty training ages, and the nickel bolts on school chairs.”

In 2018, Dr. Martin and her colleagues on the Pediatric Contact Dermatitis Workgroup published a pediatric baseline patch test series as a way to expand on the T.R.U.E. test (Dermatitis. 2018;29[4]:206-12). “It’s nice to have this panel available as a baseline screening tool when you’re unsure of possible triggers of the dermatitis but you still have high suspicion of allergic dermatitis,” Dr. Martin said. “This also is helpful for patients who present with generalized dermatitis. It’s still not perfect. We are collecting prospective data to fine-tune this baseline series.”

She reported having no financial disclosures.

[email protected]

To the Editor: 

A 61-year-old man presented to the emergency department with a rash on the right leg, generalized pruritus, and chest pain. The patient described intermittent exertional pressure-like chest pain over the last few days but had no known prior cardiac history. He also noted worsening edema of the right leg with erythema. Three months prior he had been hospitalized for a similar presentation and was diagnosed with cellulitis of the right leg. The patient was treated with a course of trimethoprim-sulfamethoxazole and permethrin cream for presumed scabies and followed up with dermatology for the persistent generalized pruritic rash and cellulitis. At that time, he was diagnosed with stasis dermatitis with dermatitis neglecta and excoriations. He was educated on general hygiene and treated with triamcinolone, hydrophilic ointment, and pramoxine lotion for pruritus. He also was empirically treated again for scabies.  

At the current presentation, preliminary investigation showed profound anemia with a hemoglobin level of 6.2 g/dL (baseline hemoglobin level 3 months prior, 13.1 g/dL). He was subsequently admitted to the general medicine ward for further investigation of severe symptomatic anemia. A medical history revealed moderate chronic obstructive pulmonary disease, hypertension, gastroesophageal reflux disease, xerosis, and fracture of the right ankle following open reduction internal fixation 6 years prior to admission. There was no history of blood loss, antiplatelet agents, or anticoagulants. He was on disability and lived in a single-room occupancy hotel. He did not report any high-risk sexual behaviors or abuse of alcohol or drugs. He actively smoked 1.5 packs of cigarettes per day for the last 30 years. He denied any allergies. 

Physical examination revealed the patient was afebrile, nontoxic, disheveled, and in no acute distress. He had anicteric sclera and pale conjunctiva. The right leg appeared more erythematous and edematous compared to the left leg but without warmth or tenderness to palpation. He had innumerable 4- to 5-mm, erythematous, excoriated papules on the skin (Figure). His bed sheets were noted to have multiple rusty-black specks thought to be related to the crusted lesions. Physical examination was otherwise unremarkable.  

Laboratory workup revealed severe iron-deficiency anemia without any evidence of hemolysis, marrow suppression, infection, or immune compromise (Table). He had a vitamin B12 deficiency (197 pg/mL [reference range, 239-931 pg/mL]), but we felt it was very unlikely to be responsible for his profound, sudden-onset microcytic anemia. Further evaluation for occult bleeding revealed an unremarkable upper endoscopy with push enteroscopy and colonoscopy. An alternate etiology of the anemia could not be identified.     

Subsequently, he reported multiple pruritic bug bites sustained at the hotel room where he resided and continued to note pruritus while hospitalized. Pest control inspected the hospital room and identified bedbugs, Cimex lectularius, among his belongings. Upon further review, his clothes and walker were found to be completely infested with these organisms in different stages of development. Treatment included blood transfusions, iron supplementation, and environmental control of the infested living space both in the hospital and at his residence, with subsequent resolution of symptoms and anemia. Two weeks following discharge, the patient no longer reported pruritus, and his hemoglobin level had returned to baseline.  

Over the last decade there has been an exponential resurgence in C lectularius infestations in developed countries attributed to increasing global travel, growing pesticide resistance, lack of public awareness, and inadequate pest control programs. This re-emergence has resulted in a public health problem. Although bedbugs are not known to transmit infectious diseases, severe infestation can result in notable dermatitis, iron-deficiency anemia from chronic blood loss, superinfection, allergic reactions including anaphylaxis in rare cases, and psychologic distress. 

Iron-deficiency anemia caused by excessive bedbug biting in infants and children has been documented as early as the 1960s.¹ Our knowledge of severe anemia due to bedbug infestation is limited to only 4 cases in the literature, according to a PubMed search of articles indexed for MEDLINE using the terms bedbugs anemia and cimex anemia.^1-4 All cases reported bedbug infestations involving personal clothing, belongings, and/or living spaces. Patient concerns at presentation ranged from lethargy and fatigue with pruritic rash to chest pain and syncope with findings of severe microcytic or normocytic anemia (hemoglobin level, 5-8 g/dL). All cases were treated supportively with blood transfusion and iron supplementation, with hemoglobin recovery after several weeks. Environmental extermination also was required to prevent recurrence.^1-4 Given that each bedbug blood meal is on average 7 mm3, one would have to incur a minimum of 143,000 bites to experience a blood loss of 1 L.³  

The differential diagnosis for a patient with generalized pruritus should be broad and includes dermatologic conditions (eg, xerosis, atopic dermatitis, contact dermatitis, urticaria, dermatophytosis, lichen simplex chronicus, psoriasis, scabies, pediculosis corporis and pubis, other arthropod bites, bullous pemphigoid), systemic disorders (eg, renal disease, diabetes mellitus, thyroid disease, cholestasis, human immunodeficiency virus), malignancy, connective tissue disease, medication side effects, and psychogenic and neuropathic itch.     

The diagnosis of C lectularius infestation is confirmed by finding the wingless, reddish brown, flat and ovular arthropod, with adult lengths of 4 to 7 mm, approximately the size of an apple seed.^5-11 Bedbugs typically are active at night and feed for 3 to 10 minutes. After their feed or during the day, bedbugs will return to their nest in furniture, mattresses, beds, walls, and floors. Bedbug bites appear as small clusters or lines of pruritic erythematous papules with a central hemorrhagic puncta. Other cutaneous symptoms include isolated pruritus, papules, nodules, and bullous eruptions.⁷ Additional signs of bedbug infestation include black fecal stains in areas of inhabitation as well as actual bedbugs feeding during the day due to overcrowding.  

Treatment of pruritic localized cutaneous reactions is supportive and includes antipruritic agents, topical steroids, topical anesthetics, antihistamines, or topical or systemic antibiotics for secondary infections.^5-11 Systemic reactions, including anaphylaxis, are treated with epinephrine, antihistamines, and/or corticosteroids, while severe anemia is treated supportively with blood transfusions and iron supplementation.^5-11 To prevent reoccurrence, environmental control in the form of nonchemical and chemical treatments is crucial in controlling bedbug infestations.^5-11  

This case highlights the relevance of a rare but notable morbidity associated with bedbug infestation and the adverse effects of bedbugs on public health. This patient's living situation in a single-room occupancy hotel, poor hygiene, and possible cognitive impairment from his multiple medical conditions may have increased his risk for extreme bedbug infestation. With a good history, physical examination, proper inspection of the patient's belongings, and provider awareness of this epidemic, the severity of this patient's anemia may have been circumvented on the prior hospital admission and follow-up office visit. Once such an infestation is confirmed, a multidisciplinary approach including social work assistance, health services, and pest control is needed to appropriately treat the patient and the environment. Methods in preventing and managing this growing public health problem include improving hygiene, avoiding secondhand goods, and increasing awareness in the identification and proper elimination of bedbugs.^5-7  

To the Editor: 

A 61-year-old man presented to the emergency department with a rash on the right leg, generalized pruritus, and chest pain. The patient described intermittent exertional pressure-like chest pain over the last few days but had no known prior cardiac history. He also noted worsening edema of the right leg with erythema. Three months prior he had been hospitalized for a similar presentation and was diagnosed with cellulitis of the right leg. The patient was treated with a course of trimethoprim-sulfamethoxazole and permethrin cream for presumed scabies and followed up with dermatology for the persistent generalized pruritic rash and cellulitis. At that time, he was diagnosed with stasis dermatitis with dermatitis neglecta and excoriations. He was educated on general hygiene and treated with triamcinolone, hydrophilic ointment, and pramoxine lotion for pruritus. He also was empirically treated again for scabies.  

At the current presentation, preliminary investigation showed profound anemia with a hemoglobin level of 6.2 g/dL (baseline hemoglobin level 3 months prior, 13.1 g/dL). He was subsequently admitted to the general medicine ward for further investigation of severe symptomatic anemia. A medical history revealed moderate chronic obstructive pulmonary disease, hypertension, gastroesophageal reflux disease, xerosis, and fracture of the right ankle following open reduction internal fixation 6 years prior to admission. There was no history of blood loss, antiplatelet agents, or anticoagulants. He was on disability and lived in a single-room occupancy hotel. He did not report any high-risk sexual behaviors or abuse of alcohol or drugs. He actively smoked 1.5 packs of cigarettes per day for the last 30 years. He denied any allergies. 

Physical examination revealed the patient was afebrile, nontoxic, disheveled, and in no acute distress. He had anicteric sclera and pale conjunctiva. The right leg appeared more erythematous and edematous compared to the left leg but without warmth or tenderness to palpation. He had innumerable 4- to 5-mm, erythematous, excoriated papules on the skin (Figure). His bed sheets were noted to have multiple rusty-black specks thought to be related to the crusted lesions. Physical examination was otherwise unremarkable.  

Laboratory workup revealed severe iron-deficiency anemia without any evidence of hemolysis, marrow suppression, infection, or immune compromise (Table). He had a vitamin B12 deficiency (197 pg/mL [reference range, 239-931 pg/mL]), but we felt it was very unlikely to be responsible for his profound, sudden-onset microcytic anemia. Further evaluation for occult bleeding revealed an unremarkable upper endoscopy with push enteroscopy and colonoscopy. An alternate etiology of the anemia could not be identified.     

Subsequently, he reported multiple pruritic bug bites sustained at the hotel room where he resided and continued to note pruritus while hospitalized. Pest control inspected the hospital room and identified bedbugs, Cimex lectularius, among his belongings. Upon further review, his clothes and walker were found to be completely infested with these organisms in different stages of development. Treatment included blood transfusions, iron supplementation, and environmental control of the infested living space both in the hospital and at his residence, with subsequent resolution of symptoms and anemia. Two weeks following discharge, the patient no longer reported pruritus, and his hemoglobin level had returned to baseline.  

Over the last decade there has been an exponential resurgence in C lectularius infestations in developed countries attributed to increasing global travel, growing pesticide resistance, lack of public awareness, and inadequate pest control programs. This re-emergence has resulted in a public health problem. Although bedbugs are not known to transmit infectious diseases, severe infestation can result in notable dermatitis, iron-deficiency anemia from chronic blood loss, superinfection, allergic reactions including anaphylaxis in rare cases, and psychologic distress. 

Iron-deficiency anemia caused by excessive bedbug biting in infants and children has been documented as early as the 1960s.¹ Our knowledge of severe anemia due to bedbug infestation is limited to only 4 cases in the literature, according to a PubMed search of articles indexed for MEDLINE using the terms bedbugs anemia and cimex anemia.^1-4 All cases reported bedbug infestations involving personal clothing, belongings, and/or living spaces. Patient concerns at presentation ranged from lethargy and fatigue with pruritic rash to chest pain and syncope with findings of severe microcytic or normocytic anemia (hemoglobin level, 5-8 g/dL). All cases were treated supportively with blood transfusion and iron supplementation, with hemoglobin recovery after several weeks. Environmental extermination also was required to prevent recurrence.^1-4 Given that each bedbug blood meal is on average 7 mm3, one would have to incur a minimum of 143,000 bites to experience a blood loss of 1 L.³  

The differential diagnosis for a patient with generalized pruritus should be broad and includes dermatologic conditions (eg, xerosis, atopic dermatitis, contact dermatitis, urticaria, dermatophytosis, lichen simplex chronicus, psoriasis, scabies, pediculosis corporis and pubis, other arthropod bites, bullous pemphigoid), systemic disorders (eg, renal disease, diabetes mellitus, thyroid disease, cholestasis, human immunodeficiency virus), malignancy, connective tissue disease, medication side effects, and psychogenic and neuropathic itch.     

The diagnosis of C lectularius infestation is confirmed by finding the wingless, reddish brown, flat and ovular arthropod, with adult lengths of 4 to 7 mm, approximately the size of an apple seed.^5-11 Bedbugs typically are active at night and feed for 3 to 10 minutes. After their feed or during the day, bedbugs will return to their nest in furniture, mattresses, beds, walls, and floors. Bedbug bites appear as small clusters or lines of pruritic erythematous papules with a central hemorrhagic puncta. Other cutaneous symptoms include isolated pruritus, papules, nodules, and bullous eruptions.⁷ Additional signs of bedbug infestation include black fecal stains in areas of inhabitation as well as actual bedbugs feeding during the day due to overcrowding.  

Treatment of pruritic localized cutaneous reactions is supportive and includes antipruritic agents, topical steroids, topical anesthetics, antihistamines, or topical or systemic antibiotics for secondary infections.^5-11 Systemic reactions, including anaphylaxis, are treated with epinephrine, antihistamines, and/or corticosteroids, while severe anemia is treated supportively with blood transfusions and iron supplementation.^5-11 To prevent reoccurrence, environmental control in the form of nonchemical and chemical treatments is crucial in controlling bedbug infestations.^5-11  

This case highlights the relevance of a rare but notable morbidity associated with bedbug infestation and the adverse effects of bedbugs on public health. This patient's living situation in a single-room occupancy hotel, poor hygiene, and possible cognitive impairment from his multiple medical conditions may have increased his risk for extreme bedbug infestation. With a good history, physical examination, proper inspection of the patient's belongings, and provider awareness of this epidemic, the severity of this patient's anemia may have been circumvented on the prior hospital admission and follow-up office visit. Once such an infestation is confirmed, a multidisciplinary approach including social work assistance, health services, and pest control is needed to appropriately treat the patient and the environment. Methods in preventing and managing this growing public health problem include improving hygiene, avoiding secondhand goods, and increasing awareness in the identification and proper elimination of bedbugs.^5-7  

To the Editor: 

A 61-year-old man presented to the emergency department with a rash on the right leg, generalized pruritus, and chest pain. The patient described intermittent exertional pressure-like chest pain over the last few days but had no known prior cardiac history. He also noted worsening edema of the right leg with erythema. Three months prior he had been hospitalized for a similar presentation and was diagnosed with cellulitis of the right leg. The patient was treated with a course of trimethoprim-sulfamethoxazole and permethrin cream for presumed scabies and followed up with dermatology for the persistent generalized pruritic rash and cellulitis. At that time, he was diagnosed with stasis dermatitis with dermatitis neglecta and excoriations. He was educated on general hygiene and treated with triamcinolone, hydrophilic ointment, and pramoxine lotion for pruritus. He also was empirically treated again for scabies.  

At the current presentation, preliminary investigation showed profound anemia with a hemoglobin level of 6.2 g/dL (baseline hemoglobin level 3 months prior, 13.1 g/dL). He was subsequently admitted to the general medicine ward for further investigation of severe symptomatic anemia. A medical history revealed moderate chronic obstructive pulmonary disease, hypertension, gastroesophageal reflux disease, xerosis, and fracture of the right ankle following open reduction internal fixation 6 years prior to admission. There was no history of blood loss, antiplatelet agents, or anticoagulants. He was on disability and lived in a single-room occupancy hotel. He did not report any high-risk sexual behaviors or abuse of alcohol or drugs. He actively smoked 1.5 packs of cigarettes per day for the last 30 years. He denied any allergies. 

Physical examination revealed the patient was afebrile, nontoxic, disheveled, and in no acute distress. He had anicteric sclera and pale conjunctiva. The right leg appeared more erythematous and edematous compared to the left leg but without warmth or tenderness to palpation. He had innumerable 4- to 5-mm, erythematous, excoriated papules on the skin (Figure). His bed sheets were noted to have multiple rusty-black specks thought to be related to the crusted lesions. Physical examination was otherwise unremarkable.  

Laboratory workup revealed severe iron-deficiency anemia without any evidence of hemolysis, marrow suppression, infection, or immune compromise (Table). He had a vitamin B12 deficiency (197 pg/mL [reference range, 239-931 pg/mL]), but we felt it was very unlikely to be responsible for his profound, sudden-onset microcytic anemia. Further evaluation for occult bleeding revealed an unremarkable upper endoscopy with push enteroscopy and colonoscopy. An alternate etiology of the anemia could not be identified.     

Subsequently, he reported multiple pruritic bug bites sustained at the hotel room where he resided and continued to note pruritus while hospitalized. Pest control inspected the hospital room and identified bedbugs, Cimex lectularius, among his belongings. Upon further review, his clothes and walker were found to be completely infested with these organisms in different stages of development. Treatment included blood transfusions, iron supplementation, and environmental control of the infested living space both in the hospital and at his residence, with subsequent resolution of symptoms and anemia. Two weeks following discharge, the patient no longer reported pruritus, and his hemoglobin level had returned to baseline.  

Over the last decade there has been an exponential resurgence in C lectularius infestations in developed countries attributed to increasing global travel, growing pesticide resistance, lack of public awareness, and inadequate pest control programs. This re-emergence has resulted in a public health problem. Although bedbugs are not known to transmit infectious diseases, severe infestation can result in notable dermatitis, iron-deficiency anemia from chronic blood loss, superinfection, allergic reactions including anaphylaxis in rare cases, and psychologic distress. 

Iron-deficiency anemia caused by excessive bedbug biting in infants and children has been documented as early as the 1960s.¹ Our knowledge of severe anemia due to bedbug infestation is limited to only 4 cases in the literature, according to a PubMed search of articles indexed for MEDLINE using the terms bedbugs anemia and cimex anemia.^1-4 All cases reported bedbug infestations involving personal clothing, belongings, and/or living spaces. Patient concerns at presentation ranged from lethargy and fatigue with pruritic rash to chest pain and syncope with findings of severe microcytic or normocytic anemia (hemoglobin level, 5-8 g/dL). All cases were treated supportively with blood transfusion and iron supplementation, with hemoglobin recovery after several weeks. Environmental extermination also was required to prevent recurrence.^1-4 Given that each bedbug blood meal is on average 7 mm3, one would have to incur a minimum of 143,000 bites to experience a blood loss of 1 L.³  

The differential diagnosis for a patient with generalized pruritus should be broad and includes dermatologic conditions (eg, xerosis, atopic dermatitis, contact dermatitis, urticaria, dermatophytosis, lichen simplex chronicus, psoriasis, scabies, pediculosis corporis and pubis, other arthropod bites, bullous pemphigoid), systemic disorders (eg, renal disease, diabetes mellitus, thyroid disease, cholestasis, human immunodeficiency virus), malignancy, connective tissue disease, medication side effects, and psychogenic and neuropathic itch.     

The diagnosis of C lectularius infestation is confirmed by finding the wingless, reddish brown, flat and ovular arthropod, with adult lengths of 4 to 7 mm, approximately the size of an apple seed.^5-11 Bedbugs typically are active at night and feed for 3 to 10 minutes. After their feed or during the day, bedbugs will return to their nest in furniture, mattresses, beds, walls, and floors. Bedbug bites appear as small clusters or lines of pruritic erythematous papules with a central hemorrhagic puncta. Other cutaneous symptoms include isolated pruritus, papules, nodules, and bullous eruptions.⁷ Additional signs of bedbug infestation include black fecal stains in areas of inhabitation as well as actual bedbugs feeding during the day due to overcrowding.  

Treatment of pruritic localized cutaneous reactions is supportive and includes antipruritic agents, topical steroids, topical anesthetics, antihistamines, or topical or systemic antibiotics for secondary infections.^5-11 Systemic reactions, including anaphylaxis, are treated with epinephrine, antihistamines, and/or corticosteroids, while severe anemia is treated supportively with blood transfusions and iron supplementation.^5-11 To prevent reoccurrence, environmental control in the form of nonchemical and chemical treatments is crucial in controlling bedbug infestations.^5-11  

This case highlights the relevance of a rare but notable morbidity associated with bedbug infestation and the adverse effects of bedbugs on public health. This patient's living situation in a single-room occupancy hotel, poor hygiene, and possible cognitive impairment from his multiple medical conditions may have increased his risk for extreme bedbug infestation. With a good history, physical examination, proper inspection of the patient's belongings, and provider awareness of this epidemic, the severity of this patient's anemia may have been circumvented on the prior hospital admission and follow-up office visit. Once such an infestation is confirmed, a multidisciplinary approach including social work assistance, health services, and pest control is needed to appropriately treat the patient and the environment. Methods in preventing and managing this growing public health problem include improving hygiene, avoiding secondhand goods, and increasing awareness in the identification and proper elimination of bedbugs.^5-7  

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.