Cutis

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Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

Myth: Psoriasis Is Only a Skin Problem

Psoriasis is predominantly regarded as a skin disease because of the outward clinical presentation of the condition. However, psoriasis is a disorder of the immune system and its damage may be more than skin deep.

Psoriasis commonly presents on the skin and nails, but a growing body of evidence has suggested that psoriasis is associated with systemic comorbidities. Up to 25% of psoriasis patients develop joint inflammation, and psoriatic arthritis (PsA) may precede skin involvement. There also is a risk for cardiovascular complications. Because of the emotional distress caused by psoriasis, patients may develop psychosocial disorders. Other conditions in patients with psoriasis include diabetes mellitus, high blood pressure, Crohn disease, and the metabolic syndrome.

Results from surveys conducted by the National Psoriasis Foundation from 2003 to 2011 found that the diagnosis of psoriasis preceded PsA in the majority of patients by a mean period of 14.6 years. Patients with moderate to severe psoriasis were more likely to develop PsA than patients with mild psoriasis. Furthermore, patients with severe psoriasis were more likely to develop diabetes mellitus and cardiovascular disease.

In a Cutis editorial, Dr. Jeffrey Weinberg emphasizes that the role of the dermatologist “is to identify and educate patients with psoriasis who are at risk of systemic complications and ensure appropriate follow-up for their treatment and overall health.” An infographic created by the American Academy of Dermatology illustrates areas of the body that may be impacted by psoriasis beyond the skin; for example, patients may develop eye problems, weight gain, or mood changes. Consider distributing this infographic to patients to show how psoriasis can affect more than their skin.

More Cutis content is available on psoriasis comorbidities:

• Do Psoriasis Patients Engage In Vigorous Physical Activity?
• The Role of Biologic Therapy for Psoriasis in Cardiovascular Risk Reduction
• VIDEO: Psoriasis and Internal Disease
• Uveitis and Psoriasis
• VIDEO: Update on Psoriasis Comorbidities

To the Editor:

Although relatively uncommon, hypersensitivity reactions to tattoo pigment are on the rise due to the increasing popularity and prevalence of tattoos.¹ Multiple adverse events have been described in association with tattoos, including inflammatory, infectious, and neoplastic responses.² An id reaction (also known as autoeczematization or autosensitization) develops distant to an initial site of infection or sensitization. We describe a unique case of an id reaction and subsequent development of prurigo nodules associated with contact allergy to red tattoo ink.

A 40-year-old woman was referred to the New York University Skin and Cancer Unit (New York, New York) for evaluation of a pruritic eruption arising on and near sites of tattooed skin on the right foot and right upper arm of 8 months’ duration. The patient reported that she had obtained a polychromatic tattoo on the right dorsal foot 9 months prior to the current presentation. Approximately 1 month later, she developed pruritic papulonodular lesions localized to the red-pigmented areas of the tattoo. Concomitantly, the patient developed a similar eruption confined to areas of red pigment in a polychromatic tattoo on the right upper arm that she had obtained 10 years prior. She was treated with intralesional triamcinolone to several of the lesions on the right dorsal foot with some benefit; however, a few days later she developed a generalized, erythematous, pruritic eruption on the back, abdomen, arms, and legs. Her medical history was remarkable only for mild iron-deficiency anemia. She had no known drug allergies or history of atopy and was not taking any medications prior to the onset of the eruption.

Skin examination revealed multiple, well-demarcated, eczematous papulonodules with surrounding erythema confined to the red-pigmented areas of the tattoo on the right dorsal foot, with several similar lesions on the surrounding nontattooed skin (Figure 1). Linear, well-demarcated, eczematous, hyperpigmented plaques also were noted on the red-pigmented areas of the tattoo on the patient’s right upper arm (Figure 2). Eczematous plaques and scattered excoriations were noted on the back, abdomen, flanks, arms, and legs.

Patch testing with the North American Standard Series, metal series, and samples of the red pigments used in the tattoo on the foot were negative. A punch biopsy of a lesion on the dorsal right foot showed a psoriasiform spongiotic dermatitis with eosinophils (Figure 3). Periodic acid–Schiff staining with diastase failed to reveal fungal hyphae. The histologic findings were consistent with allergic contact dermatitis. A punch biopsy of the eczematous reaction on nontattooed skin on the trunk demonstrated a perivascular dermatitis with eosinophils and subtle spongiosis consistent with an id reaction.

The patient was treated with fluocinonide ointment for several months with no effect. Subsequently, she received several short courses of oral prednisone, after which the affected areas of the tattoo on the arm and foot flattened and the id reaction resolved; however, after several months, the red-pigmented areas of the tattoo on the foot again became elevated and pruritic, and the patient developed widespread prurigo nodules on nontattooed skin on the trunk, arms, and legs. She was subsequently referred to a laser specialist for a trial of fractional laser treatment to cautiously remove the red tattoo pigment. After 2 treatments, the pruritus improved and the papular lesions appeared slightly flatter; however, the prurigo nodules remained. The tattoo on the patient’s foot was surgically removed; however, the prurigo nodules remained. Ultimately, the lesions cleared with a several-month course of mycophenolate mofetil.

Systemic allergic reactions to tattoo ink are rare but can cause considerable morbidity. An id reaction, also known as autoeczematization or autosensitization, is a reaction that develops distant to an initial site of infection or sensitization. Although the pathogenesis of this reaction is not certain, it has been hypothesized that autoimmunity to skin antigens might play a role.³ Autologous epidermal cells are thought to become antigenic in the presence of acute inflammation at the primary cutaneous site. These antigenic autologous epidermal cells are postulated to enter the circulation and cause secondary eczematous lesions at distant sites. This proposed mechanism is supported by the development of positive skin reactions to autologous extracts of epidermal scaling in patients with active id reaction.³

Hematogenous dissemination of cytokines has been implicated in id reactions.⁴ Keratinocytes produce cytokines in response to conditions that are known to trigger id reactions.⁵ Epidermal cytokines released from the primary site of sensitization are thought to heighten sensitivity at distant skin areas.⁴ These cytokines regulate both cell-mediated and humoral cutaneous immune responses. Increased levels of activated HLA-DR isotype–positive T cells in patients with active autoeczemization favors a cellular-mediated immune mechanism. The presence of activated antigen-specific T cells also supports the role of allergic contact dermatitis in triggering id reactions.⁶

Allergic contact dermatitis is the most common hypersensitivity reaction to tattoo ink, with red pigments representing the most common cause of tattoo-related allergic contact dermatitis. Historically, cinnabar (mercuric sulfide) has been the most common red pigment to cause allergic contact dermatitis.⁷ More recently, mercury-free organic pigments (eg, azo dyes) have been used in polychromatic tattoos due to their ability to retain color over long periods of time⁸; however, these organic red tattoo pigments also have been implicated in allergic reactions.^8-11 The composition of these new organic red tattoo pigments varies, but chemical analysis has revealed a mixture of aromatic azo compounds (eg, quinacridone),¹⁰ heavy metals (eg, aluminum, lead, cadmium, chromium, cobalt, iron, titanium),^9,12 and intermediate reactive compounds (eg, naphthalene, 2-naphthol, chlorobenzene, benzene).⁸ Allergic contact dermatitis to red tattoo ink is well documented^8,13; however, a PubMed search of articles indexed for MEDLINE using the terms tattoo and dermatitis, tattoo and allergy, tattoo and autosensitization, tattoo and id reaction, and tattoo and autoeczematization yielded only 3 other reports of a concomitant id reaction.^11,14,15

The diagnosis of id reaction associated with allergic contact dermatitis is made on the basis of clinical history, physical examination, and histopathology. Patch testing usually is not positive in cases of tattoo allergy; it is thought that the allergen is a tattoo ink byproduct possibly caused by photoinduced or metabolic change of the tattoo pigment and a haptenization process.^1,8,16 Histologically, variable reaction patterns, including eczematous, lichenoid, granulomatous, and pseudolymphomatous reactions have been reported in association with delayed-type inflammatory reactions to tattoo pigments, but the lichenoid pattern is most commonly observed.⁸

Treatment options for allergic contact dermatitis to tattoo ink include topical, intralesional, and oral steroids; topical calcineurin inhibitors; and surgical excision of the tattoo. Q-switched lasers—ruby, Nd:YAG, and alexandrite—are the gold standard for removing tattoo pigments¹⁷; however, these lasers remove tattoo pigment by selective photothermolysis, resulting in extracellular extravasation of pigment, which can precipitate a heightened immune response that can lead to localized and generalized allergic reactions.¹⁸ Therefore, Q-switched lasers should be avoided in the setting of an allergic reaction to tattoo ink. Fractional ablative laser resurfacing may be a safer alternative for removal of tattoos in the setting of an allergic reaction.¹⁷ Further studies are needed to confirm the safety and efficacy of this modality for allergic tattoo ink removal.^17,18

Our case illustrates a rare cause of id reaction and the subsequent development of prurigo nodules associated with contact allergy to red tattoo ink. We present this case to raise awareness of the potential health and iatrogenic risks associated with tattoo placement. Further investigation of these color additives is warranted to better elucidate ink components responsible for these cutaneous allergic reactions.

Acknowledgments
We would like to thank Vitaly Terushkin, MD (West Orange, New Jersey, and New York, New York), and Arielle Kauvar, MD (New York, New York), for their contributions to the patient’s clinical care.

To the Editor:

Although relatively uncommon, hypersensitivity reactions to tattoo pigment are on the rise due to the increasing popularity and prevalence of tattoos.¹ Multiple adverse events have been described in association with tattoos, including inflammatory, infectious, and neoplastic responses.² An id reaction (also known as autoeczematization or autosensitization) develops distant to an initial site of infection or sensitization. We describe a unique case of an id reaction and subsequent development of prurigo nodules associated with contact allergy to red tattoo ink.

A 40-year-old woman was referred to the New York University Skin and Cancer Unit (New York, New York) for evaluation of a pruritic eruption arising on and near sites of tattooed skin on the right foot and right upper arm of 8 months’ duration. The patient reported that she had obtained a polychromatic tattoo on the right dorsal foot 9 months prior to the current presentation. Approximately 1 month later, she developed pruritic papulonodular lesions localized to the red-pigmented areas of the tattoo. Concomitantly, the patient developed a similar eruption confined to areas of red pigment in a polychromatic tattoo on the right upper arm that she had obtained 10 years prior. She was treated with intralesional triamcinolone to several of the lesions on the right dorsal foot with some benefit; however, a few days later she developed a generalized, erythematous, pruritic eruption on the back, abdomen, arms, and legs. Her medical history was remarkable only for mild iron-deficiency anemia. She had no known drug allergies or history of atopy and was not taking any medications prior to the onset of the eruption.

Skin examination revealed multiple, well-demarcated, eczematous papulonodules with surrounding erythema confined to the red-pigmented areas of the tattoo on the right dorsal foot, with several similar lesions on the surrounding nontattooed skin (Figure 1). Linear, well-demarcated, eczematous, hyperpigmented plaques also were noted on the red-pigmented areas of the tattoo on the patient’s right upper arm (Figure 2). Eczematous plaques and scattered excoriations were noted on the back, abdomen, flanks, arms, and legs.

Patch testing with the North American Standard Series, metal series, and samples of the red pigments used in the tattoo on the foot were negative. A punch biopsy of a lesion on the dorsal right foot showed a psoriasiform spongiotic dermatitis with eosinophils (Figure 3). Periodic acid–Schiff staining with diastase failed to reveal fungal hyphae. The histologic findings were consistent with allergic contact dermatitis. A punch biopsy of the eczematous reaction on nontattooed skin on the trunk demonstrated a perivascular dermatitis with eosinophils and subtle spongiosis consistent with an id reaction.

The patient was treated with fluocinonide ointment for several months with no effect. Subsequently, she received several short courses of oral prednisone, after which the affected areas of the tattoo on the arm and foot flattened and the id reaction resolved; however, after several months, the red-pigmented areas of the tattoo on the foot again became elevated and pruritic, and the patient developed widespread prurigo nodules on nontattooed skin on the trunk, arms, and legs. She was subsequently referred to a laser specialist for a trial of fractional laser treatment to cautiously remove the red tattoo pigment. After 2 treatments, the pruritus improved and the papular lesions appeared slightly flatter; however, the prurigo nodules remained. The tattoo on the patient’s foot was surgically removed; however, the prurigo nodules remained. Ultimately, the lesions cleared with a several-month course of mycophenolate mofetil.

Systemic allergic reactions to tattoo ink are rare but can cause considerable morbidity. An id reaction, also known as autoeczematization or autosensitization, is a reaction that develops distant to an initial site of infection or sensitization. Although the pathogenesis of this reaction is not certain, it has been hypothesized that autoimmunity to skin antigens might play a role.³ Autologous epidermal cells are thought to become antigenic in the presence of acute inflammation at the primary cutaneous site. These antigenic autologous epidermal cells are postulated to enter the circulation and cause secondary eczematous lesions at distant sites. This proposed mechanism is supported by the development of positive skin reactions to autologous extracts of epidermal scaling in patients with active id reaction.³

Hematogenous dissemination of cytokines has been implicated in id reactions.⁴ Keratinocytes produce cytokines in response to conditions that are known to trigger id reactions.⁵ Epidermal cytokines released from the primary site of sensitization are thought to heighten sensitivity at distant skin areas.⁴ These cytokines regulate both cell-mediated and humoral cutaneous immune responses. Increased levels of activated HLA-DR isotype–positive T cells in patients with active autoeczemization favors a cellular-mediated immune mechanism. The presence of activated antigen-specific T cells also supports the role of allergic contact dermatitis in triggering id reactions.⁶

Allergic contact dermatitis is the most common hypersensitivity reaction to tattoo ink, with red pigments representing the most common cause of tattoo-related allergic contact dermatitis. Historically, cinnabar (mercuric sulfide) has been the most common red pigment to cause allergic contact dermatitis.⁷ More recently, mercury-free organic pigments (eg, azo dyes) have been used in polychromatic tattoos due to their ability to retain color over long periods of time⁸; however, these organic red tattoo pigments also have been implicated in allergic reactions.^8-11 The composition of these new organic red tattoo pigments varies, but chemical analysis has revealed a mixture of aromatic azo compounds (eg, quinacridone),¹⁰ heavy metals (eg, aluminum, lead, cadmium, chromium, cobalt, iron, titanium),^9,12 and intermediate reactive compounds (eg, naphthalene, 2-naphthol, chlorobenzene, benzene).⁸ Allergic contact dermatitis to red tattoo ink is well documented^8,13; however, a PubMed search of articles indexed for MEDLINE using the terms tattoo and dermatitis, tattoo and allergy, tattoo and autosensitization, tattoo and id reaction, and tattoo and autoeczematization yielded only 3 other reports of a concomitant id reaction.^11,14,15

The diagnosis of id reaction associated with allergic contact dermatitis is made on the basis of clinical history, physical examination, and histopathology. Patch testing usually is not positive in cases of tattoo allergy; it is thought that the allergen is a tattoo ink byproduct possibly caused by photoinduced or metabolic change of the tattoo pigment and a haptenization process.^1,8,16 Histologically, variable reaction patterns, including eczematous, lichenoid, granulomatous, and pseudolymphomatous reactions have been reported in association with delayed-type inflammatory reactions to tattoo pigments, but the lichenoid pattern is most commonly observed.⁸

Treatment options for allergic contact dermatitis to tattoo ink include topical, intralesional, and oral steroids; topical calcineurin inhibitors; and surgical excision of the tattoo. Q-switched lasers—ruby, Nd:YAG, and alexandrite—are the gold standard for removing tattoo pigments¹⁷; however, these lasers remove tattoo pigment by selective photothermolysis, resulting in extracellular extravasation of pigment, which can precipitate a heightened immune response that can lead to localized and generalized allergic reactions.¹⁸ Therefore, Q-switched lasers should be avoided in the setting of an allergic reaction to tattoo ink. Fractional ablative laser resurfacing may be a safer alternative for removal of tattoos in the setting of an allergic reaction.¹⁷ Further studies are needed to confirm the safety and efficacy of this modality for allergic tattoo ink removal.^17,18

Our case illustrates a rare cause of id reaction and the subsequent development of prurigo nodules associated with contact allergy to red tattoo ink. We present this case to raise awareness of the potential health and iatrogenic risks associated with tattoo placement. Further investigation of these color additives is warranted to better elucidate ink components responsible for these cutaneous allergic reactions.

Acknowledgments
We would like to thank Vitaly Terushkin, MD (West Orange, New Jersey, and New York, New York), and Arielle Kauvar, MD (New York, New York), for their contributions to the patient’s clinical care.

To the Editor:

Although relatively uncommon, hypersensitivity reactions to tattoo pigment are on the rise due to the increasing popularity and prevalence of tattoos.¹ Multiple adverse events have been described in association with tattoos, including inflammatory, infectious, and neoplastic responses.² An id reaction (also known as autoeczematization or autosensitization) develops distant to an initial site of infection or sensitization. We describe a unique case of an id reaction and subsequent development of prurigo nodules associated with contact allergy to red tattoo ink.

A 40-year-old woman was referred to the New York University Skin and Cancer Unit (New York, New York) for evaluation of a pruritic eruption arising on and near sites of tattooed skin on the right foot and right upper arm of 8 months’ duration. The patient reported that she had obtained a polychromatic tattoo on the right dorsal foot 9 months prior to the current presentation. Approximately 1 month later, she developed pruritic papulonodular lesions localized to the red-pigmented areas of the tattoo. Concomitantly, the patient developed a similar eruption confined to areas of red pigment in a polychromatic tattoo on the right upper arm that she had obtained 10 years prior. She was treated with intralesional triamcinolone to several of the lesions on the right dorsal foot with some benefit; however, a few days later she developed a generalized, erythematous, pruritic eruption on the back, abdomen, arms, and legs. Her medical history was remarkable only for mild iron-deficiency anemia. She had no known drug allergies or history of atopy and was not taking any medications prior to the onset of the eruption.

Skin examination revealed multiple, well-demarcated, eczematous papulonodules with surrounding erythema confined to the red-pigmented areas of the tattoo on the right dorsal foot, with several similar lesions on the surrounding nontattooed skin (Figure 1). Linear, well-demarcated, eczematous, hyperpigmented plaques also were noted on the red-pigmented areas of the tattoo on the patient’s right upper arm (Figure 2). Eczematous plaques and scattered excoriations were noted on the back, abdomen, flanks, arms, and legs.

Patch testing with the North American Standard Series, metal series, and samples of the red pigments used in the tattoo on the foot were negative. A punch biopsy of a lesion on the dorsal right foot showed a psoriasiform spongiotic dermatitis with eosinophils (Figure 3). Periodic acid–Schiff staining with diastase failed to reveal fungal hyphae. The histologic findings were consistent with allergic contact dermatitis. A punch biopsy of the eczematous reaction on nontattooed skin on the trunk demonstrated a perivascular dermatitis with eosinophils and subtle spongiosis consistent with an id reaction.

The patient was treated with fluocinonide ointment for several months with no effect. Subsequently, she received several short courses of oral prednisone, after which the affected areas of the tattoo on the arm and foot flattened and the id reaction resolved; however, after several months, the red-pigmented areas of the tattoo on the foot again became elevated and pruritic, and the patient developed widespread prurigo nodules on nontattooed skin on the trunk, arms, and legs. She was subsequently referred to a laser specialist for a trial of fractional laser treatment to cautiously remove the red tattoo pigment. After 2 treatments, the pruritus improved and the papular lesions appeared slightly flatter; however, the prurigo nodules remained. The tattoo on the patient’s foot was surgically removed; however, the prurigo nodules remained. Ultimately, the lesions cleared with a several-month course of mycophenolate mofetil.

Systemic allergic reactions to tattoo ink are rare but can cause considerable morbidity. An id reaction, also known as autoeczematization or autosensitization, is a reaction that develops distant to an initial site of infection or sensitization. Although the pathogenesis of this reaction is not certain, it has been hypothesized that autoimmunity to skin antigens might play a role.³ Autologous epidermal cells are thought to become antigenic in the presence of acute inflammation at the primary cutaneous site. These antigenic autologous epidermal cells are postulated to enter the circulation and cause secondary eczematous lesions at distant sites. This proposed mechanism is supported by the development of positive skin reactions to autologous extracts of epidermal scaling in patients with active id reaction.³

Hematogenous dissemination of cytokines has been implicated in id reactions.⁴ Keratinocytes produce cytokines in response to conditions that are known to trigger id reactions.⁵ Epidermal cytokines released from the primary site of sensitization are thought to heighten sensitivity at distant skin areas.⁴ These cytokines regulate both cell-mediated and humoral cutaneous immune responses. Increased levels of activated HLA-DR isotype–positive T cells in patients with active autoeczemization favors a cellular-mediated immune mechanism. The presence of activated antigen-specific T cells also supports the role of allergic contact dermatitis in triggering id reactions.⁶

Allergic contact dermatitis is the most common hypersensitivity reaction to tattoo ink, with red pigments representing the most common cause of tattoo-related allergic contact dermatitis. Historically, cinnabar (mercuric sulfide) has been the most common red pigment to cause allergic contact dermatitis.⁷ More recently, mercury-free organic pigments (eg, azo dyes) have been used in polychromatic tattoos due to their ability to retain color over long periods of time⁸; however, these organic red tattoo pigments also have been implicated in allergic reactions.^8-11 The composition of these new organic red tattoo pigments varies, but chemical analysis has revealed a mixture of aromatic azo compounds (eg, quinacridone),¹⁰ heavy metals (eg, aluminum, lead, cadmium, chromium, cobalt, iron, titanium),^9,12 and intermediate reactive compounds (eg, naphthalene, 2-naphthol, chlorobenzene, benzene).⁸ Allergic contact dermatitis to red tattoo ink is well documented^8,13; however, a PubMed search of articles indexed for MEDLINE using the terms tattoo and dermatitis, tattoo and allergy, tattoo and autosensitization, tattoo and id reaction, and tattoo and autoeczematization yielded only 3 other reports of a concomitant id reaction.^11,14,15

The diagnosis of id reaction associated with allergic contact dermatitis is made on the basis of clinical history, physical examination, and histopathology. Patch testing usually is not positive in cases of tattoo allergy; it is thought that the allergen is a tattoo ink byproduct possibly caused by photoinduced or metabolic change of the tattoo pigment and a haptenization process.^1,8,16 Histologically, variable reaction patterns, including eczematous, lichenoid, granulomatous, and pseudolymphomatous reactions have been reported in association with delayed-type inflammatory reactions to tattoo pigments, but the lichenoid pattern is most commonly observed.⁸

Treatment options for allergic contact dermatitis to tattoo ink include topical, intralesional, and oral steroids; topical calcineurin inhibitors; and surgical excision of the tattoo. Q-switched lasers—ruby, Nd:YAG, and alexandrite—are the gold standard for removing tattoo pigments¹⁷; however, these lasers remove tattoo pigment by selective photothermolysis, resulting in extracellular extravasation of pigment, which can precipitate a heightened immune response that can lead to localized and generalized allergic reactions.¹⁸ Therefore, Q-switched lasers should be avoided in the setting of an allergic reaction to tattoo ink. Fractional ablative laser resurfacing may be a safer alternative for removal of tattoos in the setting of an allergic reaction.¹⁷ Further studies are needed to confirm the safety and efficacy of this modality for allergic tattoo ink removal.^17,18

Our case illustrates a rare cause of id reaction and the subsequent development of prurigo nodules associated with contact allergy to red tattoo ink. We present this case to raise awareness of the potential health and iatrogenic risks associated with tattoo placement. Further investigation of these color additives is warranted to better elucidate ink components responsible for these cutaneous allergic reactions.

Acknowledgments
We would like to thank Vitaly Terushkin, MD (West Orange, New Jersey, and New York, New York), and Arielle Kauvar, MD (New York, New York), for their contributions to the patient’s clinical care.

To the Editor:

Disseminated cryptococcosis is a well-known opportunistic infection in patients with advanced human immunodeficiency virus (HIV) infection, but it is not frequently seen as a primary infection of the skin in immunocompetent hosts. We report a case of primary cutaneous cryptococcosis (PCC) of the lower legs in an immunocompetent Iraq War veteran.

A 28-year-old female service member presented to the dermatology clinic with progressively enlarging plaquelike lesions on the shins of 6 months’ duration. The patient had resided and worked as a deployed soldier in the lower level of a bullet hole–laden, pigeon-infested observation tower in southern Iraq 9 months prior to the current presentation. During her 7-month deployment, she reported daily exposure to pigeon excreta on equipment and frequently sustained superficial abrasions and lacerations to the legs due to the cramped and hazardous working environment. The patient noticed intensely pruritic, bugbitelike papular lesions on the shins and calves 1 month after residing in the observation tower. She sought medical treatment and was given hydrocortisone cream 1% and calamine lotion for a presumed irritant dermatitis. Over the ensuing 3 months, the pruritus worsened, and the primary lesions coalesced into annular erythematous plaques (Figure).

After returning to the United States, the patient presented again for medical care and was given ketoconazole cream 1% for presumed tinea corporis, which resulted in no improvement. A dermatologic consultation and evaluation ensued with subsequent microbial workup showing no bacterial growth on wound culture and no fungal elements on a potassium hydroxide preparation. Hematoxylin and eosin, periodic acid–Schiff, and Grocott-Gomori methenamine-silver staining did not demonstrate any organisms. Tissue cultures for bacteria and acid-fast bacilli showed no growth. A fungal tissue culture ultimately confirmed the presence of Cryptococcus neoformans. A lumbar puncture showed no evidence of Cryptococcus on DNA probe testing. Serologic testing for HIV was negative, and brain magnetic resonance imaging showed no lesions. Sputum culture and staining showed no fungal elements, and a chest radiograph was normal. A diagnosis of PCC was made and therapy with oral fluconazole 200 mg twice daily was initiated, with the intention of completing a 6-month course. During the treatment, the pruritus resolved within 3 weeks and the lesions involuted over 3 months. From the time of onset of the lesions throughout treatment, the patient showed no pulmonary, neurologic, or other systemic symptoms. She currently is healthy with no evidence of recurrence.

Primary cutaneous cryptococcosis mainly affects individuals with underlying immunosuppression, most commonly due to advanced HIV, prolonged treatment with immunosuppressive medications, or organ transplantation.¹ The most common route of inoculation is by inhalation of Cryptococcus spores with subsequent hematogenous dissemination.² Primary cutaneous cryptococcosis with skin lesions and no concomitant systemic involvement has rarely been reported, and when encountered, it usually is associated with environments that predispose patients to skin wounds with simultaneous exposure to soil or vegetative debris contaminated with bird excreta.³ Primary cutaneous cryptococcosis can present in a myriad of ways, including papules, nodules, plaques, and even necrotizing fasciitis–like skin lesions.^4,5 This variable presentation often creates clinical confusion and diagnostic delay; therefore, a high index of suspicion is required for timely diagnosis.

Due to the worldwide deployment of US military service members, exotic cutaneous infectious diseases such as PCC may be encountered in dermatology practice. Prompt clinical and histologic diagnosis is imperative to assess for systemic disease and avoid cutaneous spread and morbidity in US service members and travelers returning home from the Middle East.

To the Editor:

Disseminated cryptococcosis is a well-known opportunistic infection in patients with advanced human immunodeficiency virus (HIV) infection, but it is not frequently seen as a primary infection of the skin in immunocompetent hosts. We report a case of primary cutaneous cryptococcosis (PCC) of the lower legs in an immunocompetent Iraq War veteran.

A 28-year-old female service member presented to the dermatology clinic with progressively enlarging plaquelike lesions on the shins of 6 months’ duration. The patient had resided and worked as a deployed soldier in the lower level of a bullet hole–laden, pigeon-infested observation tower in southern Iraq 9 months prior to the current presentation. During her 7-month deployment, she reported daily exposure to pigeon excreta on equipment and frequently sustained superficial abrasions and lacerations to the legs due to the cramped and hazardous working environment. The patient noticed intensely pruritic, bugbitelike papular lesions on the shins and calves 1 month after residing in the observation tower. She sought medical treatment and was given hydrocortisone cream 1% and calamine lotion for a presumed irritant dermatitis. Over the ensuing 3 months, the pruritus worsened, and the primary lesions coalesced into annular erythematous plaques (Figure).

After returning to the United States, the patient presented again for medical care and was given ketoconazole cream 1% for presumed tinea corporis, which resulted in no improvement. A dermatologic consultation and evaluation ensued with subsequent microbial workup showing no bacterial growth on wound culture and no fungal elements on a potassium hydroxide preparation. Hematoxylin and eosin, periodic acid–Schiff, and Grocott-Gomori methenamine-silver staining did not demonstrate any organisms. Tissue cultures for bacteria and acid-fast bacilli showed no growth. A fungal tissue culture ultimately confirmed the presence of Cryptococcus neoformans. A lumbar puncture showed no evidence of Cryptococcus on DNA probe testing. Serologic testing for HIV was negative, and brain magnetic resonance imaging showed no lesions. Sputum culture and staining showed no fungal elements, and a chest radiograph was normal. A diagnosis of PCC was made and therapy with oral fluconazole 200 mg twice daily was initiated, with the intention of completing a 6-month course. During the treatment, the pruritus resolved within 3 weeks and the lesions involuted over 3 months. From the time of onset of the lesions throughout treatment, the patient showed no pulmonary, neurologic, or other systemic symptoms. She currently is healthy with no evidence of recurrence.

Primary cutaneous cryptococcosis mainly affects individuals with underlying immunosuppression, most commonly due to advanced HIV, prolonged treatment with immunosuppressive medications, or organ transplantation.¹ The most common route of inoculation is by inhalation of Cryptococcus spores with subsequent hematogenous dissemination.² Primary cutaneous cryptococcosis with skin lesions and no concomitant systemic involvement has rarely been reported, and when encountered, it usually is associated with environments that predispose patients to skin wounds with simultaneous exposure to soil or vegetative debris contaminated with bird excreta.³ Primary cutaneous cryptococcosis can present in a myriad of ways, including papules, nodules, plaques, and even necrotizing fasciitis–like skin lesions.^4,5 This variable presentation often creates clinical confusion and diagnostic delay; therefore, a high index of suspicion is required for timely diagnosis.

Due to the worldwide deployment of US military service members, exotic cutaneous infectious diseases such as PCC may be encountered in dermatology practice. Prompt clinical and histologic diagnosis is imperative to assess for systemic disease and avoid cutaneous spread and morbidity in US service members and travelers returning home from the Middle East.

To the Editor:

Disseminated cryptococcosis is a well-known opportunistic infection in patients with advanced human immunodeficiency virus (HIV) infection, but it is not frequently seen as a primary infection of the skin in immunocompetent hosts. We report a case of primary cutaneous cryptococcosis (PCC) of the lower legs in an immunocompetent Iraq War veteran.

A 28-year-old female service member presented to the dermatology clinic with progressively enlarging plaquelike lesions on the shins of 6 months’ duration. The patient had resided and worked as a deployed soldier in the lower level of a bullet hole–laden, pigeon-infested observation tower in southern Iraq 9 months prior to the current presentation. During her 7-month deployment, she reported daily exposure to pigeon excreta on equipment and frequently sustained superficial abrasions and lacerations to the legs due to the cramped and hazardous working environment. The patient noticed intensely pruritic, bugbitelike papular lesions on the shins and calves 1 month after residing in the observation tower. She sought medical treatment and was given hydrocortisone cream 1% and calamine lotion for a presumed irritant dermatitis. Over the ensuing 3 months, the pruritus worsened, and the primary lesions coalesced into annular erythematous plaques (Figure).

After returning to the United States, the patient presented again for medical care and was given ketoconazole cream 1% for presumed tinea corporis, which resulted in no improvement. A dermatologic consultation and evaluation ensued with subsequent microbial workup showing no bacterial growth on wound culture and no fungal elements on a potassium hydroxide preparation. Hematoxylin and eosin, periodic acid–Schiff, and Grocott-Gomori methenamine-silver staining did not demonstrate any organisms. Tissue cultures for bacteria and acid-fast bacilli showed no growth. A fungal tissue culture ultimately confirmed the presence of Cryptococcus neoformans. A lumbar puncture showed no evidence of Cryptococcus on DNA probe testing. Serologic testing for HIV was negative, and brain magnetic resonance imaging showed no lesions. Sputum culture and staining showed no fungal elements, and a chest radiograph was normal. A diagnosis of PCC was made and therapy with oral fluconazole 200 mg twice daily was initiated, with the intention of completing a 6-month course. During the treatment, the pruritus resolved within 3 weeks and the lesions involuted over 3 months. From the time of onset of the lesions throughout treatment, the patient showed no pulmonary, neurologic, or other systemic symptoms. She currently is healthy with no evidence of recurrence.

Primary cutaneous cryptococcosis mainly affects individuals with underlying immunosuppression, most commonly due to advanced HIV, prolonged treatment with immunosuppressive medications, or organ transplantation.¹ The most common route of inoculation is by inhalation of Cryptococcus spores with subsequent hematogenous dissemination.² Primary cutaneous cryptococcosis with skin lesions and no concomitant systemic involvement has rarely been reported, and when encountered, it usually is associated with environments that predispose patients to skin wounds with simultaneous exposure to soil or vegetative debris contaminated with bird excreta.³ Primary cutaneous cryptococcosis can present in a myriad of ways, including papules, nodules, plaques, and even necrotizing fasciitis–like skin lesions.^4,5 This variable presentation often creates clinical confusion and diagnostic delay; therefore, a high index of suspicion is required for timely diagnosis.

Due to the worldwide deployment of US military service members, exotic cutaneous infectious diseases such as PCC may be encountered in dermatology practice. Prompt clinical and histologic diagnosis is imperative to assess for systemic disease and avoid cutaneous spread and morbidity in US service members and travelers returning home from the Middle East.

The Diagnosis: Tinea Faciei

Given the morphology of the plaque, a potassium hydroxide preparation was performed and was positive for hyphal elements consistent with dermatophyte infection (Figure).

Tinea faciei is a fungal infection of the face caused by a dermatophyte that invades the stratum corneum.¹ It is transmitted through direct contact with an infected individual or fomite.² Infections typically are characterized by annular or serpiginous erythematous plaques with a scaly appearance and advancing edge. There may be associated vesicles, papules, or pustules with crusting around the advancing border.³ Tinea faciei can occur concomitantly with other dermatophytic infections and frequently presents atypically due to different characteristics of facial anatomy when compared to other tinea infections. As a result, it often is misdiagnosed.¹

Tinea faciei represents roughly 19% of all superficial fungal infections and occurs more commonly in temperate humid regions.⁴ It can occur at any age but has bimodal peaks in incidence during childhood and early adulthood.⁵ The most common causative dermatophytes are Trichophyton tonsurans, Microsporum canis, Trichophyton mentagrophytes, and Trichophyton rubrum.¹ Transmission is mainly through direct contact with infected individuals, animals, or soil, which likely occurred during the close quarters and exercises our patient experienced during basic training in the military.

Tinea faciei often is misdiagnosed and treated with topical corticosteroids. The steroids can give a false impression that the rash is resolving by initially decreasing the inflammatory component and reducing scale, which is referred to as tinea incognito. Once the steroid is stopped, however, the fungal infection often returns worse than the original presentation. The differential diagnosis includes subacute cutaneous lupus erythematosus, periorificial dermatitis, seborrheic dermatitis, psoriasis, rosacea, erythema annulare centrifugum, granuloma annulare, sarcoidosis, and contact dermatitis.^1,3,6

Diagnosis of tinea faciei is best made with skin scraping of the active border of the lesion. The scraping is treated with potassium hydroxide 10%. Visualizing branching or curving hyphae confirms the diagnosis. Fungal speciation often is not performed due to the long time needed to culture. Wood lamp may fluoresce blue-green if tinea faciei is caused by Microsporum species; however, diagnosis in this manner is limited because other common species do not fluoresce.⁷

Options for treatment of tinea faciei include topical antifungals for 2 to 6 weeks for localized disease or oral antifungals for more extensive or unresponsive infections for 1 to 8 weeks depending on the agent that is used. If fungal folliculitis is present, oral medication should be given.¹ Our patient was treated with oral terbinafine 250 mg once daily for 4 weeks with follow-up after that time to ensure resolution.

The Diagnosis: Tinea Faciei

Given the morphology of the plaque, a potassium hydroxide preparation was performed and was positive for hyphal elements consistent with dermatophyte infection (Figure).

Tinea faciei is a fungal infection of the face caused by a dermatophyte that invades the stratum corneum.¹ It is transmitted through direct contact with an infected individual or fomite.² Infections typically are characterized by annular or serpiginous erythematous plaques with a scaly appearance and advancing edge. There may be associated vesicles, papules, or pustules with crusting around the advancing border.³ Tinea faciei can occur concomitantly with other dermatophytic infections and frequently presents atypically due to different characteristics of facial anatomy when compared to other tinea infections. As a result, it often is misdiagnosed.¹

Tinea faciei represents roughly 19% of all superficial fungal infections and occurs more commonly in temperate humid regions.⁴ It can occur at any age but has bimodal peaks in incidence during childhood and early adulthood.⁵ The most common causative dermatophytes are Trichophyton tonsurans, Microsporum canis, Trichophyton mentagrophytes, and Trichophyton rubrum.¹ Transmission is mainly through direct contact with infected individuals, animals, or soil, which likely occurred during the close quarters and exercises our patient experienced during basic training in the military.

Tinea faciei often is misdiagnosed and treated with topical corticosteroids. The steroids can give a false impression that the rash is resolving by initially decreasing the inflammatory component and reducing scale, which is referred to as tinea incognito. Once the steroid is stopped, however, the fungal infection often returns worse than the original presentation. The differential diagnosis includes subacute cutaneous lupus erythematosus, periorificial dermatitis, seborrheic dermatitis, psoriasis, rosacea, erythema annulare centrifugum, granuloma annulare, sarcoidosis, and contact dermatitis.^1,3,6

Diagnosis of tinea faciei is best made with skin scraping of the active border of the lesion. The scraping is treated with potassium hydroxide 10%. Visualizing branching or curving hyphae confirms the diagnosis. Fungal speciation often is not performed due to the long time needed to culture. Wood lamp may fluoresce blue-green if tinea faciei is caused by Microsporum species; however, diagnosis in this manner is limited because other common species do not fluoresce.⁷

Options for treatment of tinea faciei include topical antifungals for 2 to 6 weeks for localized disease or oral antifungals for more extensive or unresponsive infections for 1 to 8 weeks depending on the agent that is used. If fungal folliculitis is present, oral medication should be given.¹ Our patient was treated with oral terbinafine 250 mg once daily for 4 weeks with follow-up after that time to ensure resolution.

The Diagnosis: Tinea Faciei

Given the morphology of the plaque, a potassium hydroxide preparation was performed and was positive for hyphal elements consistent with dermatophyte infection (Figure).

Tinea faciei is a fungal infection of the face caused by a dermatophyte that invades the stratum corneum.¹ It is transmitted through direct contact with an infected individual or fomite.² Infections typically are characterized by annular or serpiginous erythematous plaques with a scaly appearance and advancing edge. There may be associated vesicles, papules, or pustules with crusting around the advancing border.³ Tinea faciei can occur concomitantly with other dermatophytic infections and frequently presents atypically due to different characteristics of facial anatomy when compared to other tinea infections. As a result, it often is misdiagnosed.¹

Tinea faciei represents roughly 19% of all superficial fungal infections and occurs more commonly in temperate humid regions.⁴ It can occur at any age but has bimodal peaks in incidence during childhood and early adulthood.⁵ The most common causative dermatophytes are Trichophyton tonsurans, Microsporum canis, Trichophyton mentagrophytes, and Trichophyton rubrum.¹ Transmission is mainly through direct contact with infected individuals, animals, or soil, which likely occurred during the close quarters and exercises our patient experienced during basic training in the military.

Tinea faciei often is misdiagnosed and treated with topical corticosteroids. The steroids can give a false impression that the rash is resolving by initially decreasing the inflammatory component and reducing scale, which is referred to as tinea incognito. Once the steroid is stopped, however, the fungal infection often returns worse than the original presentation. The differential diagnosis includes subacute cutaneous lupus erythematosus, periorificial dermatitis, seborrheic dermatitis, psoriasis, rosacea, erythema annulare centrifugum, granuloma annulare, sarcoidosis, and contact dermatitis.^1,3,6

Diagnosis of tinea faciei is best made with skin scraping of the active border of the lesion. The scraping is treated with potassium hydroxide 10%. Visualizing branching or curving hyphae confirms the diagnosis. Fungal speciation often is not performed due to the long time needed to culture. Wood lamp may fluoresce blue-green if tinea faciei is caused by Microsporum species; however, diagnosis in this manner is limited because other common species do not fluoresce.⁷

Options for treatment of tinea faciei include topical antifungals for 2 to 6 weeks for localized disease or oral antifungals for more extensive or unresponsive infections for 1 to 8 weeks depending on the agent that is used. If fungal folliculitis is present, oral medication should be given.¹ Our patient was treated with oral terbinafine 250 mg once daily for 4 weeks with follow-up after that time to ensure resolution.

To the Editor:

A 22-year-old Somali woman presented to our institution with oral lesions of 2 years’ duration. The lesions started as small papules in the corners of the mouth that gradually continued to spread to the mucosal lips and gums. The lesions did not drain any material. The patient reported that they were not painful and had not regressed. She was concerned about the cosmetic appearance of the lesions. The patient believed the lesions had developed from working in a chicken factory and was concerned that they appeared possibly due to contact with a substance in the factory. Additionally, she noted that her voice had become hoarse. She was otherwise healthy and denied any sexual contact or ever having a blood transfusion.

Physical examination revealed 10 to 15 flesh-colored papules measuring 2 to 3 mm in diameter on the vermilion, mucosal surfaces of the lips, and upper and lower gingivae (Figure 1). No lesions were seen on the hard and soft palate, tongue, buccal mucosa, or posterior pharynx.

Skin biopsy of the left lower mucosal lip revealed parakeratosis, acanthosis, superficial koilocytes, and atypical keratinocytes with frequent mitoses (Figures 2A–2C). In situ hybridization testing for human papillomavirus (HPV) was negative for low-risk types 6 and 11 but positive for high-risk types 16 and 18 (Figure 2D). Laboratory investigations including complete blood cell count, electrolyte panel, and liver function studies were normal, and serum was negative for syphilis and human immunodeficiency virus antibodies.

The combined clinical and histologic findings were diagnostic of oral bowenoid papulosis. Gynecologic evaluation showed that the patient had undergone female circumcision, and she had a normal Papanicolaou test. The patient was referred to both the ear, nose, and throat clinic as well as the dermatologic surgery department to discuss treatment options, but she was lost to follow-up.

Bowenoid papulosis is triggered by HPV infection and manifests clinically as solitary or multiple verrucous papules and plaques that are usually located on the genitalia.¹ Only a few cases of bowenoid papulosis have been reported in the oral cavity.^1-5 Because this disease is sexually transmitted, the mean age of onset of bowenoid papulosis is 31 years.² There is a small risk (2%–3%) of developing invasive carcinoma in bowenoid papulosis.^1-3,6 Most lesions are associated with HPV type 16; however, bowenoid papulosis also has been associated with HPV types 18, 31, 32, 35, and 39.²

Some investigators consider bowenoid papulosis and Bowen disease (a type of squamous cell carcinoma [SCC] in situ) to be histologically identical^1,6; however, some histologic differences have been reported.^1-3,6 Bowenoid papulosis has more dilated and tortuous dermal capillaries and less atypia and dyskeratosis than Bowen disease.^1,6 In contrast to bowenoid papulosis, Bowen disease is characterized clinically as well-defined scaly plaques on sun-exposed areas of the skin in older adults. Invasive SCC can be seen in 5% of skin lesions and 30% of penile lesions associated with Bowen disease.² Risk factors for Bowen disease include sun exposure; arsenic poisoning; and infection with HPV types 2, 16, 18, 31, 33, 52, and 67.^1,6

Oral bowenoid papulosis is rare. A PubMed search of articles indexed for MEDLINE using the term oral bowenoid papulosis yielded 7 additional cases, which are summarized in the Table. In 1987 Lookingbill et al² described one of the first reported cases of oral disease in a 33-year-old immunosuppressed man receiving prednisone therapy for systemic lupus erythematosus who had both mouth and genital lesions. All lesions were positive for HPV type 16. The patient subsequently developed SCC of the tongue.² Since then, 7 other cases of oral bowenoid papulosis have been described including the current case.^1,3-5 Four (57%) cases in total were associated with immunosuppression and genital lesions.^2-5

The risk for progression of oral bowenoid papulosis to invasive SCC is not known. Our search yielded only 1 case of this occurrence.²

Two of 3 cases of solitary lip lesions in oral bowenoid papulosis were treated with surgical excision.¹ Other treatment options include CO₂ laser therapy, cryotherapy, 5-fluorouracil, bleomycin, intralesional interferon alfa, and imiquimod.^1-3,5,6

Our case represents a rare report of oral bowenoid papulosis. Recognition of this unusual presentation is important for the diagnosis and management of this disease.

To the Editor:

A 22-year-old Somali woman presented to our institution with oral lesions of 2 years’ duration. The lesions started as small papules in the corners of the mouth that gradually continued to spread to the mucosal lips and gums. The lesions did not drain any material. The patient reported that they were not painful and had not regressed. She was concerned about the cosmetic appearance of the lesions. The patient believed the lesions had developed from working in a chicken factory and was concerned that they appeared possibly due to contact with a substance in the factory. Additionally, she noted that her voice had become hoarse. She was otherwise healthy and denied any sexual contact or ever having a blood transfusion.

Physical examination revealed 10 to 15 flesh-colored papules measuring 2 to 3 mm in diameter on the vermilion, mucosal surfaces of the lips, and upper and lower gingivae (Figure 1). No lesions were seen on the hard and soft palate, tongue, buccal mucosa, or posterior pharynx.

Skin biopsy of the left lower mucosal lip revealed parakeratosis, acanthosis, superficial koilocytes, and atypical keratinocytes with frequent mitoses (Figures 2A–2C). In situ hybridization testing for human papillomavirus (HPV) was negative for low-risk types 6 and 11 but positive for high-risk types 16 and 18 (Figure 2D). Laboratory investigations including complete blood cell count, electrolyte panel, and liver function studies were normal, and serum was negative for syphilis and human immunodeficiency virus antibodies.

The combined clinical and histologic findings were diagnostic of oral bowenoid papulosis. Gynecologic evaluation showed that the patient had undergone female circumcision, and she had a normal Papanicolaou test. The patient was referred to both the ear, nose, and throat clinic as well as the dermatologic surgery department to discuss treatment options, but she was lost to follow-up.

Bowenoid papulosis is triggered by HPV infection and manifests clinically as solitary or multiple verrucous papules and plaques that are usually located on the genitalia.¹ Only a few cases of bowenoid papulosis have been reported in the oral cavity.^1-5 Because this disease is sexually transmitted, the mean age of onset of bowenoid papulosis is 31 years.² There is a small risk (2%–3%) of developing invasive carcinoma in bowenoid papulosis.^1-3,6 Most lesions are associated with HPV type 16; however, bowenoid papulosis also has been associated with HPV types 18, 31, 32, 35, and 39.²

Some investigators consider bowenoid papulosis and Bowen disease (a type of squamous cell carcinoma [SCC] in situ) to be histologically identical^1,6; however, some histologic differences have been reported.^1-3,6 Bowenoid papulosis has more dilated and tortuous dermal capillaries and less atypia and dyskeratosis than Bowen disease.^1,6 In contrast to bowenoid papulosis, Bowen disease is characterized clinically as well-defined scaly plaques on sun-exposed areas of the skin in older adults. Invasive SCC can be seen in 5% of skin lesions and 30% of penile lesions associated with Bowen disease.² Risk factors for Bowen disease include sun exposure; arsenic poisoning; and infection with HPV types 2, 16, 18, 31, 33, 52, and 67.^1,6

Oral bowenoid papulosis is rare. A PubMed search of articles indexed for MEDLINE using the term oral bowenoid papulosis yielded 7 additional cases, which are summarized in the Table. In 1987 Lookingbill et al² described one of the first reported cases of oral disease in a 33-year-old immunosuppressed man receiving prednisone therapy for systemic lupus erythematosus who had both mouth and genital lesions. All lesions were positive for HPV type 16. The patient subsequently developed SCC of the tongue.² Since then, 7 other cases of oral bowenoid papulosis have been described including the current case.^1,3-5 Four (57%) cases in total were associated with immunosuppression and genital lesions.^2-5

The risk for progression of oral bowenoid papulosis to invasive SCC is not known. Our search yielded only 1 case of this occurrence.²

Two of 3 cases of solitary lip lesions in oral bowenoid papulosis were treated with surgical excision.¹ Other treatment options include CO₂ laser therapy, cryotherapy, 5-fluorouracil, bleomycin, intralesional interferon alfa, and imiquimod.^1-3,5,6

Our case represents a rare report of oral bowenoid papulosis. Recognition of this unusual presentation is important for the diagnosis and management of this disease.

To the Editor:

A 22-year-old Somali woman presented to our institution with oral lesions of 2 years’ duration. The lesions started as small papules in the corners of the mouth that gradually continued to spread to the mucosal lips and gums. The lesions did not drain any material. The patient reported that they were not painful and had not regressed. She was concerned about the cosmetic appearance of the lesions. The patient believed the lesions had developed from working in a chicken factory and was concerned that they appeared possibly due to contact with a substance in the factory. Additionally, she noted that her voice had become hoarse. She was otherwise healthy and denied any sexual contact or ever having a blood transfusion.

Physical examination revealed 10 to 15 flesh-colored papules measuring 2 to 3 mm in diameter on the vermilion, mucosal surfaces of the lips, and upper and lower gingivae (Figure 1). No lesions were seen on the hard and soft palate, tongue, buccal mucosa, or posterior pharynx.

Skin biopsy of the left lower mucosal lip revealed parakeratosis, acanthosis, superficial koilocytes, and atypical keratinocytes with frequent mitoses (Figures 2A–2C). In situ hybridization testing for human papillomavirus (HPV) was negative for low-risk types 6 and 11 but positive for high-risk types 16 and 18 (Figure 2D). Laboratory investigations including complete blood cell count, electrolyte panel, and liver function studies were normal, and serum was negative for syphilis and human immunodeficiency virus antibodies.

The combined clinical and histologic findings were diagnostic of oral bowenoid papulosis. Gynecologic evaluation showed that the patient had undergone female circumcision, and she had a normal Papanicolaou test. The patient was referred to both the ear, nose, and throat clinic as well as the dermatologic surgery department to discuss treatment options, but she was lost to follow-up.

Bowenoid papulosis is triggered by HPV infection and manifests clinically as solitary or multiple verrucous papules and plaques that are usually located on the genitalia.¹ Only a few cases of bowenoid papulosis have been reported in the oral cavity.^1-5 Because this disease is sexually transmitted, the mean age of onset of bowenoid papulosis is 31 years.² There is a small risk (2%–3%) of developing invasive carcinoma in bowenoid papulosis.^1-3,6 Most lesions are associated with HPV type 16; however, bowenoid papulosis also has been associated with HPV types 18, 31, 32, 35, and 39.²

Some investigators consider bowenoid papulosis and Bowen disease (a type of squamous cell carcinoma [SCC] in situ) to be histologically identical^1,6; however, some histologic differences have been reported.^1-3,6 Bowenoid papulosis has more dilated and tortuous dermal capillaries and less atypia and dyskeratosis than Bowen disease.^1,6 In contrast to bowenoid papulosis, Bowen disease is characterized clinically as well-defined scaly plaques on sun-exposed areas of the skin in older adults. Invasive SCC can be seen in 5% of skin lesions and 30% of penile lesions associated with Bowen disease.² Risk factors for Bowen disease include sun exposure; arsenic poisoning; and infection with HPV types 2, 16, 18, 31, 33, 52, and 67.^1,6

Oral bowenoid papulosis is rare. A PubMed search of articles indexed for MEDLINE using the term oral bowenoid papulosis yielded 7 additional cases, which are summarized in the Table. In 1987 Lookingbill et al² described one of the first reported cases of oral disease in a 33-year-old immunosuppressed man receiving prednisone therapy for systemic lupus erythematosus who had both mouth and genital lesions. All lesions were positive for HPV type 16. The patient subsequently developed SCC of the tongue.² Since then, 7 other cases of oral bowenoid papulosis have been described including the current case.^1,3-5 Four (57%) cases in total were associated with immunosuppression and genital lesions.^2-5

The risk for progression of oral bowenoid papulosis to invasive SCC is not known. Our search yielded only 1 case of this occurrence.²

Two of 3 cases of solitary lip lesions in oral bowenoid papulosis were treated with surgical excision.¹ Other treatment options include CO₂ laser therapy, cryotherapy, 5-fluorouracil, bleomycin, intralesional interferon alfa, and imiquimod.^1-3,5,6

Our case represents a rare report of oral bowenoid papulosis. Recognition of this unusual presentation is important for the diagnosis and management of this disease.

Perniosis, or chilblain, is characterized by localized, tender, erythematous skin lesions that occur as an abnormal reaction to exposure to cold and damp conditions. Although the lesions favor the distal extremities, perniosis may present anywhere on the body. Lesions can develop within hours to days following exposure to temperature less than 10°C or damp environments with greater than 60% humidity.¹ Acute cases may lead to pruritus and tenderness, whereas chronic cases may involve lesions that blister or ulcerate and can take weeks to heal. We report an unusual case of erythematous plaques arising on the buttocks of a 73-year-old woman using ice pack treatments for chronic low back pain.

Case Report

A 73-year-old woman presented with recurrent tender lesions on the buttocks of 5 years’ duration. Her medical history was remarkable for hypertension, hypothyroidism, and lumbar spinal fusion surgery 5 years prior. Physical examination revealed indurated erythematous plaques with areas of erosions on the left buttock with some involvement of the right buttock (Figure 1).

After a trial of oral valacyclovir for presumed herpes simplex infection provided no relief, a punch biopsy of the left buttock was performed, which revealed a cell-poor interface dermatitis with superficial and deep perivascular and periadnexal lymphocytic infiltrates (Figure 2). Perieccrine lymphocytes were present in a small portion of the reticular dermis (Figure 3). The patient revealed she had been sitting on ice packs for several hours daily since the lumbar spinal fusion surgery 5 years prior to alleviate chronic low back pain.

Based on the clinicopathologic correlation, a diagnosis of perniosis secondary to ice pack therapy was made. An evaluation for concomitant or underlying connective tissue disease (CTD) including a complete blood cell count with sedimentation rate, antinuclear antibodies (ANAs), serum protein electrophoresis, and serum levels of cryoglobulins and complement components was unremarkable. Our patient was treated with simple analgesia and was encouraged to avoid direct contact with ice packs for extended periods of time. Because of her low back pain, she continued to use ice packs but readjusted them sporadically and decreased frequency of use. She had complete resolution of the lesions at 6-month follow-up.

Comment

Perniosis is a self-limited condition, manifesting as erythematous plaques or nodules following exposure to cold and damp conditions. It was first reported in 1902 by Hochsinger² as tender submental plaques occurring in children after exposure to cold weather. Since then, reports of perniosis have been described in equestrians and long-distance cyclists as well as in the context of other outdoor activities.^3-5 In all cases, patients developed perniosis at sites of exposure to cold or damp conditions.

Perniosis arising in patients using ice pack therapy is a rare and recent phenomenon, with only 3 other known reported cases.^6,7 In all cases, including ours, patients reported treating chronic low back pain with ice packs for more than 2 hours per day. Clinical presentations included erythematous to purpuric plaques with ulceration on the lower back or buttocks that reoccurred with subsequent use of ice packs. No concomitant CTD was reported.⁶

Much controversy exists as to whether idiopathic perniosis (IP) increases susceptibility to acquiring an autoimmune disease or if IP is a form of CTD that follows a more indolent course.⁸ In a prospective study of 33 patients with underlying IP, no patients developed lupus erythematosus (LE), with a median follow-up of 38 months.⁹ A study by Crowson and Magro⁸ revealed that 18 of 39 patients with perniotic lesions had an associated systemic disease including LE, human immunodeficiency virus, viral hepatitis, rheumatoid arthritis, cryofibrinogenemia, hypergammaglobulinemia, iritis, or Crohn disease. Of the 21 other patients who had no underlying CTD or systemic disease, 10 had a positive ANA test but no systemic symptoms; therefore, all 21 of these patients were classified as cases of IP.⁸

Cutaneous biopsy to distinguish between IP and autoimmune perniosis remains controversial; perniotic lesions and discoid LE share histopathologic features,⁹ as was evident with our case, which demonstrated overlapping findings of vacuolar change with superficial and deep perivascular and periadnexal lymphoid infiltrates. Typical features of IP include thrombosed capillaries in the papillary dermis and lymphocytic exocytosis localized to the acrosyringia, whereas secondary perniosis has superficial and deep perivascular and perieccrine lymphocytic infiltrates with vascular thrombosis in the reticular dermis. Vascular ectasia, dermal mucinosis, basement membrane zone thickening, and erythrocyte extravasation are not reliable and may be seen in both cases.⁸ One study revealed the only significant difference between both entities was the perieccrine distribution of lymphocytic infiltrate in cases of IP (P=.007), whereas an absence of perieccrine involvement was noted in autoimmune cases.⁹

Direct immunofluorescence (DIF) may help differentiate IP from autoimmune perniosis. In a prospective study by Viguier et al,⁹ 6 of 9 patients with IP had negative DIF and 3 had slight nonspecific C3 immunoreactivity of dermal vessels. Conversely, in patients with autoimmune perniosis, positive DIF with the lupus band test was seen in 3 of 7 patients, all who had a positive ANA test⁹; however, positive ANA levels also were reported in patients with autoimmune perniosis but negative DIF, suggesting that DIF lacks specificity in diagnosing autoimmune perniosis.

Although histopathologic findings bear similarities to LE, there are no guidelines to suggest for or against laboratory testing for CTD in patients presenting with perniosis. Some investigators have suggested that any patient with clinical features suggestive of perniosis should undergo laboratory evaluation including a complete blood cell count and assessment for antibodies to Ro, ANA, rheumatoid factor, cryofibrinogens, and antiphospholipid antibodies.⁹ Serum protein electrophoresis and immunofixation electrophoresis may be done to exclude monoclonal gammopathy.

For idiopathic cases, treatment is aimed at limiting or removing cold exposure. Patients should be advised regarding the use of long-term ice pack use and the potential development of perniosis. For chronic perniosis lasting beyond several weeks, a combination of a slow taper of oral prednisone, hydroxychloroquine, and quinacrine has been successful in patients with persistent lesions despite making environmental modifications.³ Intralesional triamcinolone acetonide and nifedipine also have been effective in perniotic hand lesions.¹⁰

Conclusion

We report a rare case of perniosis on the buttocks that arose in a patient who utilized ice packs for treatment of chronic low back pain. Ice pack–induced perniosis may be an underreported entity. Histopathologic examination is nondescript, as overlapping features of perniosis and LE have been observed with no underlying CTD present. Correlation with patient history and clinical examination is paramount in diagnosis and management.

Perniosis, or chilblain, is characterized by localized, tender, erythematous skin lesions that occur as an abnormal reaction to exposure to cold and damp conditions. Although the lesions favor the distal extremities, perniosis may present anywhere on the body. Lesions can develop within hours to days following exposure to temperature less than 10°C or damp environments with greater than 60% humidity.¹ Acute cases may lead to pruritus and tenderness, whereas chronic cases may involve lesions that blister or ulcerate and can take weeks to heal. We report an unusual case of erythematous plaques arising on the buttocks of a 73-year-old woman using ice pack treatments for chronic low back pain.

Case Report

A 73-year-old woman presented with recurrent tender lesions on the buttocks of 5 years’ duration. Her medical history was remarkable for hypertension, hypothyroidism, and lumbar spinal fusion surgery 5 years prior. Physical examination revealed indurated erythematous plaques with areas of erosions on the left buttock with some involvement of the right buttock (Figure 1).

After a trial of oral valacyclovir for presumed herpes simplex infection provided no relief, a punch biopsy of the left buttock was performed, which revealed a cell-poor interface dermatitis with superficial and deep perivascular and periadnexal lymphocytic infiltrates (Figure 2). Perieccrine lymphocytes were present in a small portion of the reticular dermis (Figure 3). The patient revealed she had been sitting on ice packs for several hours daily since the lumbar spinal fusion surgery 5 years prior to alleviate chronic low back pain.

Based on the clinicopathologic correlation, a diagnosis of perniosis secondary to ice pack therapy was made. An evaluation for concomitant or underlying connective tissue disease (CTD) including a complete blood cell count with sedimentation rate, antinuclear antibodies (ANAs), serum protein electrophoresis, and serum levels of cryoglobulins and complement components was unremarkable. Our patient was treated with simple analgesia and was encouraged to avoid direct contact with ice packs for extended periods of time. Because of her low back pain, she continued to use ice packs but readjusted them sporadically and decreased frequency of use. She had complete resolution of the lesions at 6-month follow-up.

Comment

Perniosis is a self-limited condition, manifesting as erythematous plaques or nodules following exposure to cold and damp conditions. It was first reported in 1902 by Hochsinger² as tender submental plaques occurring in children after exposure to cold weather. Since then, reports of perniosis have been described in equestrians and long-distance cyclists as well as in the context of other outdoor activities.^3-5 In all cases, patients developed perniosis at sites of exposure to cold or damp conditions.

Perniosis arising in patients using ice pack therapy is a rare and recent phenomenon, with only 3 other known reported cases.^6,7 In all cases, including ours, patients reported treating chronic low back pain with ice packs for more than 2 hours per day. Clinical presentations included erythematous to purpuric plaques with ulceration on the lower back or buttocks that reoccurred with subsequent use of ice packs. No concomitant CTD was reported.⁶

Much controversy exists as to whether idiopathic perniosis (IP) increases susceptibility to acquiring an autoimmune disease or if IP is a form of CTD that follows a more indolent course.⁸ In a prospective study of 33 patients with underlying IP, no patients developed lupus erythematosus (LE), with a median follow-up of 38 months.⁹ A study by Crowson and Magro⁸ revealed that 18 of 39 patients with perniotic lesions had an associated systemic disease including LE, human immunodeficiency virus, viral hepatitis, rheumatoid arthritis, cryofibrinogenemia, hypergammaglobulinemia, iritis, or Crohn disease. Of the 21 other patients who had no underlying CTD or systemic disease, 10 had a positive ANA test but no systemic symptoms; therefore, all 21 of these patients were classified as cases of IP.⁸

Cutaneous biopsy to distinguish between IP and autoimmune perniosis remains controversial; perniotic lesions and discoid LE share histopathologic features,⁹ as was evident with our case, which demonstrated overlapping findings of vacuolar change with superficial and deep perivascular and periadnexal lymphoid infiltrates. Typical features of IP include thrombosed capillaries in the papillary dermis and lymphocytic exocytosis localized to the acrosyringia, whereas secondary perniosis has superficial and deep perivascular and perieccrine lymphocytic infiltrates with vascular thrombosis in the reticular dermis. Vascular ectasia, dermal mucinosis, basement membrane zone thickening, and erythrocyte extravasation are not reliable and may be seen in both cases.⁸ One study revealed the only significant difference between both entities was the perieccrine distribution of lymphocytic infiltrate in cases of IP (P=.007), whereas an absence of perieccrine involvement was noted in autoimmune cases.⁹

Direct immunofluorescence (DIF) may help differentiate IP from autoimmune perniosis. In a prospective study by Viguier et al,⁹ 6 of 9 patients with IP had negative DIF and 3 had slight nonspecific C3 immunoreactivity of dermal vessels. Conversely, in patients with autoimmune perniosis, positive DIF with the lupus band test was seen in 3 of 7 patients, all who had a positive ANA test⁹; however, positive ANA levels also were reported in patients with autoimmune perniosis but negative DIF, suggesting that DIF lacks specificity in diagnosing autoimmune perniosis.

Although histopathologic findings bear similarities to LE, there are no guidelines to suggest for or against laboratory testing for CTD in patients presenting with perniosis. Some investigators have suggested that any patient with clinical features suggestive of perniosis should undergo laboratory evaluation including a complete blood cell count and assessment for antibodies to Ro, ANA, rheumatoid factor, cryofibrinogens, and antiphospholipid antibodies.⁹ Serum protein electrophoresis and immunofixation electrophoresis may be done to exclude monoclonal gammopathy.

For idiopathic cases, treatment is aimed at limiting or removing cold exposure. Patients should be advised regarding the use of long-term ice pack use and the potential development of perniosis. For chronic perniosis lasting beyond several weeks, a combination of a slow taper of oral prednisone, hydroxychloroquine, and quinacrine has been successful in patients with persistent lesions despite making environmental modifications.³ Intralesional triamcinolone acetonide and nifedipine also have been effective in perniotic hand lesions.¹⁰

Conclusion

We report a rare case of perniosis on the buttocks that arose in a patient who utilized ice packs for treatment of chronic low back pain. Ice pack–induced perniosis may be an underreported entity. Histopathologic examination is nondescript, as overlapping features of perniosis and LE have been observed with no underlying CTD present. Correlation with patient history and clinical examination is paramount in diagnosis and management.

Perniosis, or chilblain, is characterized by localized, tender, erythematous skin lesions that occur as an abnormal reaction to exposure to cold and damp conditions. Although the lesions favor the distal extremities, perniosis may present anywhere on the body. Lesions can develop within hours to days following exposure to temperature less than 10°C or damp environments with greater than 60% humidity.¹ Acute cases may lead to pruritus and tenderness, whereas chronic cases may involve lesions that blister or ulcerate and can take weeks to heal. We report an unusual case of erythematous plaques arising on the buttocks of a 73-year-old woman using ice pack treatments for chronic low back pain.

Case Report

A 73-year-old woman presented with recurrent tender lesions on the buttocks of 5 years’ duration. Her medical history was remarkable for hypertension, hypothyroidism, and lumbar spinal fusion surgery 5 years prior. Physical examination revealed indurated erythematous plaques with areas of erosions on the left buttock with some involvement of the right buttock (Figure 1).

After a trial of oral valacyclovir for presumed herpes simplex infection provided no relief, a punch biopsy of the left buttock was performed, which revealed a cell-poor interface dermatitis with superficial and deep perivascular and periadnexal lymphocytic infiltrates (Figure 2). Perieccrine lymphocytes were present in a small portion of the reticular dermis (Figure 3). The patient revealed she had been sitting on ice packs for several hours daily since the lumbar spinal fusion surgery 5 years prior to alleviate chronic low back pain.

Based on the clinicopathologic correlation, a diagnosis of perniosis secondary to ice pack therapy was made. An evaluation for concomitant or underlying connective tissue disease (CTD) including a complete blood cell count with sedimentation rate, antinuclear antibodies (ANAs), serum protein electrophoresis, and serum levels of cryoglobulins and complement components was unremarkable. Our patient was treated with simple analgesia and was encouraged to avoid direct contact with ice packs for extended periods of time. Because of her low back pain, she continued to use ice packs but readjusted them sporadically and decreased frequency of use. She had complete resolution of the lesions at 6-month follow-up.

Comment

Perniosis is a self-limited condition, manifesting as erythematous plaques or nodules following exposure to cold and damp conditions. It was first reported in 1902 by Hochsinger² as tender submental plaques occurring in children after exposure to cold weather. Since then, reports of perniosis have been described in equestrians and long-distance cyclists as well as in the context of other outdoor activities.^3-5 In all cases, patients developed perniosis at sites of exposure to cold or damp conditions.

Perniosis arising in patients using ice pack therapy is a rare and recent phenomenon, with only 3 other known reported cases.^6,7 In all cases, including ours, patients reported treating chronic low back pain with ice packs for more than 2 hours per day. Clinical presentations included erythematous to purpuric plaques with ulceration on the lower back or buttocks that reoccurred with subsequent use of ice packs. No concomitant CTD was reported.⁶

Much controversy exists as to whether idiopathic perniosis (IP) increases susceptibility to acquiring an autoimmune disease or if IP is a form of CTD that follows a more indolent course.⁸ In a prospective study of 33 patients with underlying IP, no patients developed lupus erythematosus (LE), with a median follow-up of 38 months.⁹ A study by Crowson and Magro⁸ revealed that 18 of 39 patients with perniotic lesions had an associated systemic disease including LE, human immunodeficiency virus, viral hepatitis, rheumatoid arthritis, cryofibrinogenemia, hypergammaglobulinemia, iritis, or Crohn disease. Of the 21 other patients who had no underlying CTD or systemic disease, 10 had a positive ANA test but no systemic symptoms; therefore, all 21 of these patients were classified as cases of IP.⁸

Cutaneous biopsy to distinguish between IP and autoimmune perniosis remains controversial; perniotic lesions and discoid LE share histopathologic features,⁹ as was evident with our case, which demonstrated overlapping findings of vacuolar change with superficial and deep perivascular and periadnexal lymphoid infiltrates. Typical features of IP include thrombosed capillaries in the papillary dermis and lymphocytic exocytosis localized to the acrosyringia, whereas secondary perniosis has superficial and deep perivascular and perieccrine lymphocytic infiltrates with vascular thrombosis in the reticular dermis. Vascular ectasia, dermal mucinosis, basement membrane zone thickening, and erythrocyte extravasation are not reliable and may be seen in both cases.⁸ One study revealed the only significant difference between both entities was the perieccrine distribution of lymphocytic infiltrate in cases of IP (P=.007), whereas an absence of perieccrine involvement was noted in autoimmune cases.⁹

Direct immunofluorescence (DIF) may help differentiate IP from autoimmune perniosis. In a prospective study by Viguier et al,⁹ 6 of 9 patients with IP had negative DIF and 3 had slight nonspecific C3 immunoreactivity of dermal vessels. Conversely, in patients with autoimmune perniosis, positive DIF with the lupus band test was seen in 3 of 7 patients, all who had a positive ANA test⁹; however, positive ANA levels also were reported in patients with autoimmune perniosis but negative DIF, suggesting that DIF lacks specificity in diagnosing autoimmune perniosis.

Although histopathologic findings bear similarities to LE, there are no guidelines to suggest for or against laboratory testing for CTD in patients presenting with perniosis. Some investigators have suggested that any patient with clinical features suggestive of perniosis should undergo laboratory evaluation including a complete blood cell count and assessment for antibodies to Ro, ANA, rheumatoid factor, cryofibrinogens, and antiphospholipid antibodies.⁹ Serum protein electrophoresis and immunofixation electrophoresis may be done to exclude monoclonal gammopathy.

For idiopathic cases, treatment is aimed at limiting or removing cold exposure. Patients should be advised regarding the use of long-term ice pack use and the potential development of perniosis. For chronic perniosis lasting beyond several weeks, a combination of a slow taper of oral prednisone, hydroxychloroquine, and quinacrine has been successful in patients with persistent lesions despite making environmental modifications.³ Intralesional triamcinolone acetonide and nifedipine also have been effective in perniotic hand lesions.¹⁰

Conclusion

We report a rare case of perniosis on the buttocks that arose in a patient who utilized ice packs for treatment of chronic low back pain. Ice pack–induced perniosis may be an underreported entity. Histopathologic examination is nondescript, as overlapping features of perniosis and LE have been observed with no underlying CTD present. Correlation with patient history and clinical examination is paramount in diagnosis and management.

To the Editor:

Gemcitabine is a nucleoside analogue used to treat a variety of solid and hematologic malignancies. Cutaneous toxicities include radiation recall dermatitis and erysipelaslike reactions that occur in areas not previously treated with radiation. Often referred to as pseudocellulitis, these reactions generally have been reported in areas of lymphedema in patients with solid malignancies.^1-6 Herein, we report a rare case of gemcitabine-induced pseudocellulitis on the legs in a patient with a history of hematologic malignancy and total body irradiation (TBI).

A 61-year-old woman with history of peripheral T-cell lymphoma presented to the emergency department at our institution with acute-onset redness, tenderness, and swelling of the legs that was concerning for cellulitis. The patient’s history was notable for receiving gemcitabine 1000 mg/m² for treatment of refractory lymphoma (12 and 4 days prior to presentation) as well as lymphedema of the legs. Her complete treatment course included multiple rounds of chemotherapy and matched unrelated donor nonmyeloablative allogeneic stem cell transplantation with a single dose of TBI at 200 cGy at our institution. Her transplant was complicated only by mild cutaneous graft-versus-host disease, which resolved with prednisone and tacrolimus.

On physical examination, the patient was afebrile with symmetric erythema and induration extending from the bilateral knees to the dorsal feet. A complete blood cell count was notable for a white blood cell count of 5400/µL (reference range, 4500–11,000/µL) and a platelet count of 96,000/µL (reference range, 150,000–400,000/µL). Plain film radiographs of the bilateral ankles were remarkable only for moderate subcutaneous edema. She received vancomycin in the emergency department and was admitted to the oncology service. Blood cultures drawn on admission were negative. Dermatology was consulted on admission, and a diagnosis of pseudocellulitis was made in conjunction with oncology (Figure). Antibiotics were held, and the patient was treated symptomatically with ibuprofen and was discharged 1 day after admission. The reaction resolved after 1 week with the use of diphenhydramine, nonsteroidal anti-inflammatory drugs, and compression. The patient was not rechallenged with gemcitabine.

Gemcitabine-induced pseudocellulitis is a rare cutaneous side effect of gemcitabine therapy. Reported cases have suggested key characteristics of pseudocellulitis (Table). The reaction is characterized by localized erythema, edema, and tenderness of the skin, with onset generally 48 hours to 1 week after receiving gemcitabine.^1-6 Lymphedema appears to be a risk factor.^1,3-5 Six cases (including the current case) demonstrated confinement of these findings to areas of prior lymphedema.^1,4,6 Infectious workup is negative, and rechallenging with gemcitabine likely will reproduce the reaction. Unlike radiation recall dermatitis, there is no prior localized radiation exposure.

Our patient had a history of hematologic malignancy and a one-time low-dose TBI of 200 cGy, unlike the other reported cases described in the Table. It is difficult to attribute our patient’s localized eruption to radiation recall given the history of TBI. The clinical examination, laboratory findings, and time frame of the reaction were consistent with gemcitabine-induced pseudocellulitis.

It is important to be aware of pseudocellulitis as a possible complication of gemcitabine therapy in patients without history of localized radiation. Early recognition of pseudocellulitis may prevent unnecessary exposure to broad-spectrum antibiotics. Patients’ temperature, white blood cell count, clinical examination, and potentially ancillary studies (eg, vascular studies, inflammatory markers) should be reviewed carefully to determine whether there is an infectious or alternate etiology. In patients with known prior lymphedema, it may be beneficial to educate clinicians and patients alike about this potential adverse effect of gemcitabine and the high likelihood of recurrence on re-exposure.

To the Editor:

Gemcitabine is a nucleoside analogue used to treat a variety of solid and hematologic malignancies. Cutaneous toxicities include radiation recall dermatitis and erysipelaslike reactions that occur in areas not previously treated with radiation. Often referred to as pseudocellulitis, these reactions generally have been reported in areas of lymphedema in patients with solid malignancies.^1-6 Herein, we report a rare case of gemcitabine-induced pseudocellulitis on the legs in a patient with a history of hematologic malignancy and total body irradiation (TBI).

A 61-year-old woman with history of peripheral T-cell lymphoma presented to the emergency department at our institution with acute-onset redness, tenderness, and swelling of the legs that was concerning for cellulitis. The patient’s history was notable for receiving gemcitabine 1000 mg/m² for treatment of refractory lymphoma (12 and 4 days prior to presentation) as well as lymphedema of the legs. Her complete treatment course included multiple rounds of chemotherapy and matched unrelated donor nonmyeloablative allogeneic stem cell transplantation with a single dose of TBI at 200 cGy at our institution. Her transplant was complicated only by mild cutaneous graft-versus-host disease, which resolved with prednisone and tacrolimus.

On physical examination, the patient was afebrile with symmetric erythema and induration extending from the bilateral knees to the dorsal feet. A complete blood cell count was notable for a white blood cell count of 5400/µL (reference range, 4500–11,000/µL) and a platelet count of 96,000/µL (reference range, 150,000–400,000/µL). Plain film radiographs of the bilateral ankles were remarkable only for moderate subcutaneous edema. She received vancomycin in the emergency department and was admitted to the oncology service. Blood cultures drawn on admission were negative. Dermatology was consulted on admission, and a diagnosis of pseudocellulitis was made in conjunction with oncology (Figure). Antibiotics were held, and the patient was treated symptomatically with ibuprofen and was discharged 1 day after admission. The reaction resolved after 1 week with the use of diphenhydramine, nonsteroidal anti-inflammatory drugs, and compression. The patient was not rechallenged with gemcitabine.

Gemcitabine-induced pseudocellulitis is a rare cutaneous side effect of gemcitabine therapy. Reported cases have suggested key characteristics of pseudocellulitis (Table). The reaction is characterized by localized erythema, edema, and tenderness of the skin, with onset generally 48 hours to 1 week after receiving gemcitabine.^1-6 Lymphedema appears to be a risk factor.^1,3-5 Six cases (including the current case) demonstrated confinement of these findings to areas of prior lymphedema.^1,4,6 Infectious workup is negative, and rechallenging with gemcitabine likely will reproduce the reaction. Unlike radiation recall dermatitis, there is no prior localized radiation exposure.

Our patient had a history of hematologic malignancy and a one-time low-dose TBI of 200 cGy, unlike the other reported cases described in the Table. It is difficult to attribute our patient’s localized eruption to radiation recall given the history of TBI. The clinical examination, laboratory findings, and time frame of the reaction were consistent with gemcitabine-induced pseudocellulitis.

It is important to be aware of pseudocellulitis as a possible complication of gemcitabine therapy in patients without history of localized radiation. Early recognition of pseudocellulitis may prevent unnecessary exposure to broad-spectrum antibiotics. Patients’ temperature, white blood cell count, clinical examination, and potentially ancillary studies (eg, vascular studies, inflammatory markers) should be reviewed carefully to determine whether there is an infectious or alternate etiology. In patients with known prior lymphedema, it may be beneficial to educate clinicians and patients alike about this potential adverse effect of gemcitabine and the high likelihood of recurrence on re-exposure.

To the Editor:

Gemcitabine is a nucleoside analogue used to treat a variety of solid and hematologic malignancies. Cutaneous toxicities include radiation recall dermatitis and erysipelaslike reactions that occur in areas not previously treated with radiation. Often referred to as pseudocellulitis, these reactions generally have been reported in areas of lymphedema in patients with solid malignancies.^1-6 Herein, we report a rare case of gemcitabine-induced pseudocellulitis on the legs in a patient with a history of hematologic malignancy and total body irradiation (TBI).

A 61-year-old woman with history of peripheral T-cell lymphoma presented to the emergency department at our institution with acute-onset redness, tenderness, and swelling of the legs that was concerning for cellulitis. The patient’s history was notable for receiving gemcitabine 1000 mg/m² for treatment of refractory lymphoma (12 and 4 days prior to presentation) as well as lymphedema of the legs. Her complete treatment course included multiple rounds of chemotherapy and matched unrelated donor nonmyeloablative allogeneic stem cell transplantation with a single dose of TBI at 200 cGy at our institution. Her transplant was complicated only by mild cutaneous graft-versus-host disease, which resolved with prednisone and tacrolimus.

On physical examination, the patient was afebrile with symmetric erythema and induration extending from the bilateral knees to the dorsal feet. A complete blood cell count was notable for a white blood cell count of 5400/µL (reference range, 4500–11,000/µL) and a platelet count of 96,000/µL (reference range, 150,000–400,000/µL). Plain film radiographs of the bilateral ankles were remarkable only for moderate subcutaneous edema. She received vancomycin in the emergency department and was admitted to the oncology service. Blood cultures drawn on admission were negative. Dermatology was consulted on admission, and a diagnosis of pseudocellulitis was made in conjunction with oncology (Figure). Antibiotics were held, and the patient was treated symptomatically with ibuprofen and was discharged 1 day after admission. The reaction resolved after 1 week with the use of diphenhydramine, nonsteroidal anti-inflammatory drugs, and compression. The patient was not rechallenged with gemcitabine.

Gemcitabine-induced pseudocellulitis is a rare cutaneous side effect of gemcitabine therapy. Reported cases have suggested key characteristics of pseudocellulitis (Table). The reaction is characterized by localized erythema, edema, and tenderness of the skin, with onset generally 48 hours to 1 week after receiving gemcitabine.^1-6 Lymphedema appears to be a risk factor.^1,3-5 Six cases (including the current case) demonstrated confinement of these findings to areas of prior lymphedema.^1,4,6 Infectious workup is negative, and rechallenging with gemcitabine likely will reproduce the reaction. Unlike radiation recall dermatitis, there is no prior localized radiation exposure.

Our patient had a history of hematologic malignancy and a one-time low-dose TBI of 200 cGy, unlike the other reported cases described in the Table. It is difficult to attribute our patient’s localized eruption to radiation recall given the history of TBI. The clinical examination, laboratory findings, and time frame of the reaction were consistent with gemcitabine-induced pseudocellulitis.

It is important to be aware of pseudocellulitis as a possible complication of gemcitabine therapy in patients without history of localized radiation. Early recognition of pseudocellulitis may prevent unnecessary exposure to broad-spectrum antibiotics. Patients’ temperature, white blood cell count, clinical examination, and potentially ancillary studies (eg, vascular studies, inflammatory markers) should be reviewed carefully to determine whether there is an infectious or alternate etiology. In patients with known prior lymphedema, it may be beneficial to educate clinicians and patients alike about this potential adverse effect of gemcitabine and the high likelihood of recurrence on re-exposure.

Click here to view the articles published in December 2018.

Click here to view the articles published in December 2018.

Click here to view the articles published in December 2018.

To improve patient care and outcomes, leading dermatologists from the Cutis Editorial Board answered 5 questions on nail care. Here’s what we found.

Do you routinely perform diagnostic testing before treating for onychomycosis?

Ninety-five percent of dermatologists perform diagnostic testing before treating onychomycosis. Of them, nearly two-thirds only test before treating with systemic antifungals, while one-third test before starting systemic or topical antifungals.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
A laboratory diagnosis of onychomycosis is an absolute necessity before treating for onychomycosis, and the vast majority of our board members are testing routinely. Diagnosis should ideally be performed before initiating both oral and topical therapy. Failure to do so may lead to incorrect treatment with progression of disease and missed diagnoses of malignancy (Lipner and Scher, 2016; Lipner and Scher, 2016).

Next page: Nail fungus

What diagnostic tests do you use to confirm the presence of a nail fungus?

More than 70% of respondents use histopathology or fungal culture to confirm the presence of a nail fungus. Direct microscopy is used by 38% and only 5% use polymerase chain reaction.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Options for diagnosis are potassium hydroxide preparation with microscopy, fungal culture, or nail plate clipping with histopathology. Polymerase chain reaction is another option that is available and covered by many insurance plans. Many of our board members use histopathology and fungal culture more often than other methods. Histopathology is advantageous for its high sensitivity and capacity to detect other nail diseases, such as nail psoriasis. A disadvantage is that the identity and viability of the infecting organism cannot be determined. While fungal culture can detect both identity and viability, the organism may take several weeks to grow and there is a high false-negative rate (Lipner and Scher, 2018 [Part 1]).

Next page: Laboratory monitoring with terbinafine

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Almost half of board members perform laboratory monitoring for patients taking terbinafine, which was reasonable prior to any published data on blood count and liver function tests in patients taking this drug. However, a new study on this topic should make us reconsider our practices. This study analyzed the rate of laboratory test abnormalities in 4985 patients taking terbinafine or griseofulvin for dermatophyte infections. Elevated alanine aminotransferase, aspartate aminotransferase, anemia, lymphopenia, and neutropenia were uncommon and similar to the baseline rates. Therefore, routine interval laboratory monitoring may be unnecessary in healthy patients taking oral terbinafine for onychomycosis (Stolmeier et al).

Next page: Biotin recommendations

Do you routinely recommend biotin to your patients?

Approximately half (52%) of dermatologists do not recommend biotin to their patients. However, 29% do recommend it for hair and nail disorders.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Biotin is an essential cofactor for mammalian carboxylase enzymes that are involved in important metabolic pathways in humans. Biotin supplementation is likely unnecessary for most individuals, as biotin intake is likely sufficient in a Western diet. There are limited data on biotin supplementation to treat dermatologic conditions, especially in patients with normal biotin levels. In addition, a recent warning issued by the US Food and Drug Administration reported that consumption of biotin may interfere with laboratory tests. Therefore, biotin should not be routinely recommended to patients without sufficient evidence that it would benefit their condition (Lipner, 2018).

Next page: Medication for onychomycosis

Which medication(s) do you prescribe most often for onychomycosis?

The top medications prescribed by dermatologists for onychomycosis were oral terbinafine (62%) and topical ciclopirox (52%), followed by oral fluconazole (29%), topical efinaconazole (24%), oral itraconazole (14%), and topical tavaborole (5%).

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Oral terbinafine is most frequently prescribed by our board, likely because it has the best efficacy, dosing regimen, and minimal potential for systemic side effects or drug-drug interactions. Efficacy with ciclopirox lacquer is quite low and the medication is difficult to apply. For toenail onychomycosis, application is daily with weekly clipping and removal and monthly debridement. Patients who are not candidates for terbinafine would likely benefit more from oral itraconazole, oral fluconazole (off label), efinaconazole, or tavaborole (Lipner and Scher, 2018 [Part II]).

Next page: More tips from derms

More Tips From Dermatologists

The dermatologists we polled had the following advice for their peers:

As with care in general in dermatology, the care and treatment of healthy nails and especially diseased nails is multifaceted and is optimized by using combination therapy. The combination of an oral antifungal and a topical that treats the local area and also provides protection and a healthy environment for nail growth and repair is ideal.—Fran E. Cook-Bolden, MD (New York, New York)

It’s important to culture for fungus before starting treatment. It seems many cultures turn out to be nondermatophytes, and terbinafine is not the best treatment.—Lawrence J. Green, MD (Washington, DC)

Nails do care. Diagnoses should be confirmed.—Richard K. Scher, MD (New York, New York)

About This Survey
The survey was fielded electronically to Cutis Editorial Board Members within the United States from October 22, 2018, to November 14, 2018. A total of 21 usable responses were received.

To improve patient care and outcomes, leading dermatologists from the Cutis Editorial Board answered 5 questions on nail care. Here’s what we found.

Do you routinely perform diagnostic testing before treating for onychomycosis?

Ninety-five percent of dermatologists perform diagnostic testing before treating onychomycosis. Of them, nearly two-thirds only test before treating with systemic antifungals, while one-third test before starting systemic or topical antifungals.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
A laboratory diagnosis of onychomycosis is an absolute necessity before treating for onychomycosis, and the vast majority of our board members are testing routinely. Diagnosis should ideally be performed before initiating both oral and topical therapy. Failure to do so may lead to incorrect treatment with progression of disease and missed diagnoses of malignancy (Lipner and Scher, 2016; Lipner and Scher, 2016).

Next page: Nail fungus

What diagnostic tests do you use to confirm the presence of a nail fungus?

More than 70% of respondents use histopathology or fungal culture to confirm the presence of a nail fungus. Direct microscopy is used by 38% and only 5% use polymerase chain reaction.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Options for diagnosis are potassium hydroxide preparation with microscopy, fungal culture, or nail plate clipping with histopathology. Polymerase chain reaction is another option that is available and covered by many insurance plans. Many of our board members use histopathology and fungal culture more often than other methods. Histopathology is advantageous for its high sensitivity and capacity to detect other nail diseases, such as nail psoriasis. A disadvantage is that the identity and viability of the infecting organism cannot be determined. While fungal culture can detect both identity and viability, the organism may take several weeks to grow and there is a high false-negative rate (Lipner and Scher, 2018 [Part 1]).

Next page: Laboratory monitoring with terbinafine

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Almost half of board members perform laboratory monitoring for patients taking terbinafine, which was reasonable prior to any published data on blood count and liver function tests in patients taking this drug. However, a new study on this topic should make us reconsider our practices. This study analyzed the rate of laboratory test abnormalities in 4985 patients taking terbinafine or griseofulvin for dermatophyte infections. Elevated alanine aminotransferase, aspartate aminotransferase, anemia, lymphopenia, and neutropenia were uncommon and similar to the baseline rates. Therefore, routine interval laboratory monitoring may be unnecessary in healthy patients taking oral terbinafine for onychomycosis (Stolmeier et al).

Next page: Biotin recommendations

Do you routinely recommend biotin to your patients?

Approximately half (52%) of dermatologists do not recommend biotin to their patients. However, 29% do recommend it for hair and nail disorders.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Biotin is an essential cofactor for mammalian carboxylase enzymes that are involved in important metabolic pathways in humans. Biotin supplementation is likely unnecessary for most individuals, as biotin intake is likely sufficient in a Western diet. There are limited data on biotin supplementation to treat dermatologic conditions, especially in patients with normal biotin levels. In addition, a recent warning issued by the US Food and Drug Administration reported that consumption of biotin may interfere with laboratory tests. Therefore, biotin should not be routinely recommended to patients without sufficient evidence that it would benefit their condition (Lipner, 2018).

Next page: Medication for onychomycosis

Which medication(s) do you prescribe most often for onychomycosis?

The top medications prescribed by dermatologists for onychomycosis were oral terbinafine (62%) and topical ciclopirox (52%), followed by oral fluconazole (29%), topical efinaconazole (24%), oral itraconazole (14%), and topical tavaborole (5%).

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Oral terbinafine is most frequently prescribed by our board, likely because it has the best efficacy, dosing regimen, and minimal potential for systemic side effects or drug-drug interactions. Efficacy with ciclopirox lacquer is quite low and the medication is difficult to apply. For toenail onychomycosis, application is daily with weekly clipping and removal and monthly debridement. Patients who are not candidates for terbinafine would likely benefit more from oral itraconazole, oral fluconazole (off label), efinaconazole, or tavaborole (Lipner and Scher, 2018 [Part II]).

Next page: More tips from derms

More Tips From Dermatologists

The dermatologists we polled had the following advice for their peers:

As with care in general in dermatology, the care and treatment of healthy nails and especially diseased nails is multifaceted and is optimized by using combination therapy. The combination of an oral antifungal and a topical that treats the local area and also provides protection and a healthy environment for nail growth and repair is ideal.—Fran E. Cook-Bolden, MD (New York, New York)

It’s important to culture for fungus before starting treatment. It seems many cultures turn out to be nondermatophytes, and terbinafine is not the best treatment.—Lawrence J. Green, MD (Washington, DC)

Nails do care. Diagnoses should be confirmed.—Richard K. Scher, MD (New York, New York)

About This Survey
The survey was fielded electronically to Cutis Editorial Board Members within the United States from October 22, 2018, to November 14, 2018. A total of 21 usable responses were received.

To improve patient care and outcomes, leading dermatologists from the Cutis Editorial Board answered 5 questions on nail care. Here’s what we found.

Do you routinely perform diagnostic testing before treating for onychomycosis?

Ninety-five percent of dermatologists perform diagnostic testing before treating onychomycosis. Of them, nearly two-thirds only test before treating with systemic antifungals, while one-third test before starting systemic or topical antifungals.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
A laboratory diagnosis of onychomycosis is an absolute necessity before treating for onychomycosis, and the vast majority of our board members are testing routinely. Diagnosis should ideally be performed before initiating both oral and topical therapy. Failure to do so may lead to incorrect treatment with progression of disease and missed diagnoses of malignancy (Lipner and Scher, 2016; Lipner and Scher, 2016).

Next page: Nail fungus

What diagnostic tests do you use to confirm the presence of a nail fungus?

More than 70% of respondents use histopathology or fungal culture to confirm the presence of a nail fungus. Direct microscopy is used by 38% and only 5% use polymerase chain reaction.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Options for diagnosis are potassium hydroxide preparation with microscopy, fungal culture, or nail plate clipping with histopathology. Polymerase chain reaction is another option that is available and covered by many insurance plans. Many of our board members use histopathology and fungal culture more often than other methods. Histopathology is advantageous for its high sensitivity and capacity to detect other nail diseases, such as nail psoriasis. A disadvantage is that the identity and viability of the infecting organism cannot be determined. While fungal culture can detect both identity and viability, the organism may take several weeks to grow and there is a high false-negative rate (Lipner and Scher, 2018 [Part 1]).

Next page: Laboratory monitoring with terbinafine

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Almost half of board members perform laboratory monitoring for patients taking terbinafine, which was reasonable prior to any published data on blood count and liver function tests in patients taking this drug. However, a new study on this topic should make us reconsider our practices. This study analyzed the rate of laboratory test abnormalities in 4985 patients taking terbinafine or griseofulvin for dermatophyte infections. Elevated alanine aminotransferase, aspartate aminotransferase, anemia, lymphopenia, and neutropenia were uncommon and similar to the baseline rates. Therefore, routine interval laboratory monitoring may be unnecessary in healthy patients taking oral terbinafine for onychomycosis (Stolmeier et al).

Next page: Biotin recommendations

Do you routinely recommend biotin to your patients?

Approximately half (52%) of dermatologists do not recommend biotin to their patients. However, 29% do recommend it for hair and nail disorders.

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Biotin is an essential cofactor for mammalian carboxylase enzymes that are involved in important metabolic pathways in humans. Biotin supplementation is likely unnecessary for most individuals, as biotin intake is likely sufficient in a Western diet. There are limited data on biotin supplementation to treat dermatologic conditions, especially in patients with normal biotin levels. In addition, a recent warning issued by the US Food and Drug Administration reported that consumption of biotin may interfere with laboratory tests. Therefore, biotin should not be routinely recommended to patients without sufficient evidence that it would benefit their condition (Lipner, 2018).

Next page: Medication for onychomycosis

Which medication(s) do you prescribe most often for onychomycosis?

The top medications prescribed by dermatologists for onychomycosis were oral terbinafine (62%) and topical ciclopirox (52%), followed by oral fluconazole (29%), topical efinaconazole (24%), oral itraconazole (14%), and topical tavaborole (5%).

Expert Commentary
Provided by Shari R. Lipner, MD, PhD (New York, New York)
Oral terbinafine is most frequently prescribed by our board, likely because it has the best efficacy, dosing regimen, and minimal potential for systemic side effects or drug-drug interactions. Efficacy with ciclopirox lacquer is quite low and the medication is difficult to apply. For toenail onychomycosis, application is daily with weekly clipping and removal and monthly debridement. Patients who are not candidates for terbinafine would likely benefit more from oral itraconazole, oral fluconazole (off label), efinaconazole, or tavaborole (Lipner and Scher, 2018 [Part II]).

Next page: More tips from derms

More Tips From Dermatologists

The dermatologists we polled had the following advice for their peers:

As with care in general in dermatology, the care and treatment of healthy nails and especially diseased nails is multifaceted and is optimized by using combination therapy. The combination of an oral antifungal and a topical that treats the local area and also provides protection and a healthy environment for nail growth and repair is ideal.—Fran E. Cook-Bolden, MD (New York, New York)

It’s important to culture for fungus before starting treatment. It seems many cultures turn out to be nondermatophytes, and terbinafine is not the best treatment.—Lawrence J. Green, MD (Washington, DC)

Nails do care. Diagnoses should be confirmed.—Richard K. Scher, MD (New York, New York)

About This Survey
The survey was fielded electronically to Cutis Editorial Board Members within the United States from October 22, 2018, to November 14, 2018. A total of 21 usable responses were received.