Cutis

The Diagnosis: Granuloma Faciale

A biopsy from a scalp lesion showed an intense mixed inflammatory infiltrate mainly consisting of eosinophils, but lymphocytes, histiocytes, neutrophils, and plasma cells also were present. A grenz zone was observed between the dermal infiltrate and epidermis. Perivascular infiltrates were penetrating vessel walls, and hyalinization of the vessel walls also was seen (Figure 1). Direct immunofluorescence demonstrated IgG positivity on vessel walls (Figure 2). A diagnosis of granuloma faciale with extrafacial lesions was made. Twice daily application of tacrolimus ointment 0.1% was started, but after a 10-month course of treatment, there was no notable difference in the lesions.

Granuloma faciale (GF) is an uncommon benign dermatosis of unknown pathogenesis characterized by erythematous, brown, or violaceous papules, plaques, or nodules. Granuloma faciale lesions can be solitary or multiple as well as disseminated and most often occur on the face. Predilection sites include the nose, periauricular area, cheeks, forehead, eyelids, and ears; however, lesions also have been reported to occur in extrafacial areas such as the trunk, arms, and legs.^1-4 In our patient, multiple plaques were seen on the scalp. Facial lesions usually precede extrafacial lesions, which may present months to several years after the appearance of facial disease; however, according to our patient's history his scalp lesions appeared before the facial lesions.

The differential diagnoses for GF mainly include erythema elevatum diutinum, cutaneous sarcoidosis, cutaneous lymphoma, lupus, basal cell carcinoma, and cutaneous pseudolymphoma.⁵ Diagnosis may be established based on a combination of clinical features and skin biopsy results. On histopathologic examination, small-vessel vasculitis usually is present with an infiltrate predominantly consisting of neutrophils and eosinophils.⁶

It has been suggested that actinic damage plays a role in the etiology of GF.⁷ The pathogenesis is uncertain, but it is thought that immunophenotypic and molecular analysis of the dermal infiltrate in GF reveals that most lymphocytes are clonally expanded and the process is mediated by interferon gamma.⁷ Tacrolimus acts by binding and inactivating calcineurin and thus blocking T-cell activation and proliferation, so it is not surprising that topical tacrolimus has been shown to be useful in the management of this condition.⁸

The Diagnosis: Granuloma Faciale

A biopsy from a scalp lesion showed an intense mixed inflammatory infiltrate mainly consisting of eosinophils, but lymphocytes, histiocytes, neutrophils, and plasma cells also were present. A grenz zone was observed between the dermal infiltrate and epidermis. Perivascular infiltrates were penetrating vessel walls, and hyalinization of the vessel walls also was seen (Figure 1). Direct immunofluorescence demonstrated IgG positivity on vessel walls (Figure 2). A diagnosis of granuloma faciale with extrafacial lesions was made. Twice daily application of tacrolimus ointment 0.1% was started, but after a 10-month course of treatment, there was no notable difference in the lesions.

Granuloma faciale (GF) is an uncommon benign dermatosis of unknown pathogenesis characterized by erythematous, brown, or violaceous papules, plaques, or nodules. Granuloma faciale lesions can be solitary or multiple as well as disseminated and most often occur on the face. Predilection sites include the nose, periauricular area, cheeks, forehead, eyelids, and ears; however, lesions also have been reported to occur in extrafacial areas such as the trunk, arms, and legs.^1-4 In our patient, multiple plaques were seen on the scalp. Facial lesions usually precede extrafacial lesions, which may present months to several years after the appearance of facial disease; however, according to our patient's history his scalp lesions appeared before the facial lesions.

The differential diagnoses for GF mainly include erythema elevatum diutinum, cutaneous sarcoidosis, cutaneous lymphoma, lupus, basal cell carcinoma, and cutaneous pseudolymphoma.⁵ Diagnosis may be established based on a combination of clinical features and skin biopsy results. On histopathologic examination, small-vessel vasculitis usually is present with an infiltrate predominantly consisting of neutrophils and eosinophils.⁶

It has been suggested that actinic damage plays a role in the etiology of GF.⁷ The pathogenesis is uncertain, but it is thought that immunophenotypic and molecular analysis of the dermal infiltrate in GF reveals that most lymphocytes are clonally expanded and the process is mediated by interferon gamma.⁷ Tacrolimus acts by binding and inactivating calcineurin and thus blocking T-cell activation and proliferation, so it is not surprising that topical tacrolimus has been shown to be useful in the management of this condition.⁸

The Diagnosis: Granuloma Faciale

A biopsy from a scalp lesion showed an intense mixed inflammatory infiltrate mainly consisting of eosinophils, but lymphocytes, histiocytes, neutrophils, and plasma cells also were present. A grenz zone was observed between the dermal infiltrate and epidermis. Perivascular infiltrates were penetrating vessel walls, and hyalinization of the vessel walls also was seen (Figure 1). Direct immunofluorescence demonstrated IgG positivity on vessel walls (Figure 2). A diagnosis of granuloma faciale with extrafacial lesions was made. Twice daily application of tacrolimus ointment 0.1% was started, but after a 10-month course of treatment, there was no notable difference in the lesions.

Granuloma faciale (GF) is an uncommon benign dermatosis of unknown pathogenesis characterized by erythematous, brown, or violaceous papules, plaques, or nodules. Granuloma faciale lesions can be solitary or multiple as well as disseminated and most often occur on the face. Predilection sites include the nose, periauricular area, cheeks, forehead, eyelids, and ears; however, lesions also have been reported to occur in extrafacial areas such as the trunk, arms, and legs.^1-4 In our patient, multiple plaques were seen on the scalp. Facial lesions usually precede extrafacial lesions, which may present months to several years after the appearance of facial disease; however, according to our patient's history his scalp lesions appeared before the facial lesions.

The differential diagnoses for GF mainly include erythema elevatum diutinum, cutaneous sarcoidosis, cutaneous lymphoma, lupus, basal cell carcinoma, and cutaneous pseudolymphoma.⁵ Diagnosis may be established based on a combination of clinical features and skin biopsy results. On histopathologic examination, small-vessel vasculitis usually is present with an infiltrate predominantly consisting of neutrophils and eosinophils.⁶

It has been suggested that actinic damage plays a role in the etiology of GF.⁷ The pathogenesis is uncertain, but it is thought that immunophenotypic and molecular analysis of the dermal infiltrate in GF reveals that most lymphocytes are clonally expanded and the process is mediated by interferon gamma.⁷ Tacrolimus acts by binding and inactivating calcineurin and thus blocking T-cell activation and proliferation, so it is not surprising that topical tacrolimus has been shown to be useful in the management of this condition.⁸

Tranexamic acid is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule. Although the US Food and Drug Administration–approved indications for tranexamic acid include treatment of patients with menorrhagia and reduction or prevention of hemorrhage in patients with hemophilia undergoing tooth extraction, the potential efficacy of tranexamic acid in the treatment of melasma has been consistently reported since the 1980s.¹

Tranexamic acid exerts effects on pigmentation via its inhibitory effects on UV light–induced plasminogen activator and plasmin activity.² UV radiation induces the synthesis of plasminogen activator by keratinocytes, which results in increased conversion of plasminogen to plasmin. Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.³ By inhibiting plasminogen activation, tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization. In treated guinea pig skin, application of topical tranexamic acid following UV radiation exposure inhibited the development of expected skin hyperpigmentation and also reduced tyrosinase activity.^4,5

The largest study on the use of oral tranexamic acid for treatment of melasma was a retrospective chart review of 561 melasma patients treated with tranexamic acid at a single center in Singapore.⁶ More than 90% of patients received prior treatment of their melasma, including bleaching creams and energy-based treatment. Among patients who received oral tranexamic acid over a 4-month period, 90% of patients demonstrated improvement in their melasma severity. Side effects were experienced by 7% of patients; the most common side effects were abdominal bloating and pain (experienced by 2% of patients). Notably, 1 patient developed deep vein thrombosis during treatment and subsequently was found to have protein S deficiency.⁶

Although the daily doses of tranexamic acid for the treatment of menorrhagia and perioperative hemophilia patients are 3900 mg and 30 to 40 mg/kg, respectively, effective daily doses reported for the treatment of melasma have ranged from the initial report of efficacy at 750 to 1500 mg to subsequent reports of improvement at daily doses of 500 mg.^1,2,6-8

Challenges to the use of tranexamic acid for melasma treatment in the United States include the medicolegal environment, specifically the risks associated with using a systemic procoagulant medication for a cosmetic indication. Patients should be screened and counseled on the risks of developing deep vein thrombosis and pulmonary embolism prior to initiating treatment. Cost and accessibility also may limit the use of tranexamic acid in the United States. Tranexamic acid is available for off-label use in the United States with a prescription in the form of 650-mg tablets that can be split by patients to approximate twice-daily 325 mg dosing. This cosmetic indication poses an out-of-pocket cost to patients of over $110 per month or as low as $48 per month with a coupon at the time of publication.⁹

Given the potential for serious adverse effects with the use of systemic tranexamic acid, there has been interest in formulating and evaluating topical tranexamic acid for cosmetic indications.^10-13 Topical tranexamic acid has been used alone and in conjunction with modalities to increase uptake, including intradermal injection, microneedling, and fractionated CO₂ laser.^12-14 Although these reports show initial promise, the currently available data are limited by small sample sizes, short treatment durations, lack of dose comparisons, and lack of short-term or long-term follow-up data. In addition to addressing these knowledge gaps in our understanding of topical tranexamic acid as a treatment option for melasma, further studies on the minimum systemic dose may address the downside of cost and potential for complications that may limit use of this medication in the United States.

The potential uses for tranexamic acid extend to the treatment of postinflammatory hyperpigmentation and rosacea. Melanocytes cultured in media conditioned by fractionated CO₂ laser–treated keratinocytes were found to have decreased tyrosinase activity and reduced melanin content when treated with tranexamic acid, suggesting the potential role for tranexamic acid to be used postprocedurally to reduce the risk for postinflammatory hyperpigmentation in prone skin types.¹⁵ Oral and topical tranexamic acid also have been reported to improve the appearance of erythematotelangiectatic rosacea, potentially relating to the inhibitory effects of tranexamic acid on neovascularization.^3,16,17 Although larger-scale controlled studies are required for further investigation of tranexamic acid for these indications, it has shown early promise as an adjunctive treatment for several dermatologic disorders, including melasma, and warrants further characterization as a potential therapeutic option.

Tranexamic acid is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule. Although the US Food and Drug Administration–approved indications for tranexamic acid include treatment of patients with menorrhagia and reduction or prevention of hemorrhage in patients with hemophilia undergoing tooth extraction, the potential efficacy of tranexamic acid in the treatment of melasma has been consistently reported since the 1980s.¹

Tranexamic acid exerts effects on pigmentation via its inhibitory effects on UV light–induced plasminogen activator and plasmin activity.² UV radiation induces the synthesis of plasminogen activator by keratinocytes, which results in increased conversion of plasminogen to plasmin. Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.³ By inhibiting plasminogen activation, tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization. In treated guinea pig skin, application of topical tranexamic acid following UV radiation exposure inhibited the development of expected skin hyperpigmentation and also reduced tyrosinase activity.^4,5

The largest study on the use of oral tranexamic acid for treatment of melasma was a retrospective chart review of 561 melasma patients treated with tranexamic acid at a single center in Singapore.⁶ More than 90% of patients received prior treatment of their melasma, including bleaching creams and energy-based treatment. Among patients who received oral tranexamic acid over a 4-month period, 90% of patients demonstrated improvement in their melasma severity. Side effects were experienced by 7% of patients; the most common side effects were abdominal bloating and pain (experienced by 2% of patients). Notably, 1 patient developed deep vein thrombosis during treatment and subsequently was found to have protein S deficiency.⁶

Although the daily doses of tranexamic acid for the treatment of menorrhagia and perioperative hemophilia patients are 3900 mg and 30 to 40 mg/kg, respectively, effective daily doses reported for the treatment of melasma have ranged from the initial report of efficacy at 750 to 1500 mg to subsequent reports of improvement at daily doses of 500 mg.^1,2,6-8

Challenges to the use of tranexamic acid for melasma treatment in the United States include the medicolegal environment, specifically the risks associated with using a systemic procoagulant medication for a cosmetic indication. Patients should be screened and counseled on the risks of developing deep vein thrombosis and pulmonary embolism prior to initiating treatment. Cost and accessibility also may limit the use of tranexamic acid in the United States. Tranexamic acid is available for off-label use in the United States with a prescription in the form of 650-mg tablets that can be split by patients to approximate twice-daily 325 mg dosing. This cosmetic indication poses an out-of-pocket cost to patients of over $110 per month or as low as $48 per month with a coupon at the time of publication.⁹

Given the potential for serious adverse effects with the use of systemic tranexamic acid, there has been interest in formulating and evaluating topical tranexamic acid for cosmetic indications.^10-13 Topical tranexamic acid has been used alone and in conjunction with modalities to increase uptake, including intradermal injection, microneedling, and fractionated CO₂ laser.^12-14 Although these reports show initial promise, the currently available data are limited by small sample sizes, short treatment durations, lack of dose comparisons, and lack of short-term or long-term follow-up data. In addition to addressing these knowledge gaps in our understanding of topical tranexamic acid as a treatment option for melasma, further studies on the minimum systemic dose may address the downside of cost and potential for complications that may limit use of this medication in the United States.

The potential uses for tranexamic acid extend to the treatment of postinflammatory hyperpigmentation and rosacea. Melanocytes cultured in media conditioned by fractionated CO₂ laser–treated keratinocytes were found to have decreased tyrosinase activity and reduced melanin content when treated with tranexamic acid, suggesting the potential role for tranexamic acid to be used postprocedurally to reduce the risk for postinflammatory hyperpigmentation in prone skin types.¹⁵ Oral and topical tranexamic acid also have been reported to improve the appearance of erythematotelangiectatic rosacea, potentially relating to the inhibitory effects of tranexamic acid on neovascularization.^3,16,17 Although larger-scale controlled studies are required for further investigation of tranexamic acid for these indications, it has shown early promise as an adjunctive treatment for several dermatologic disorders, including melasma, and warrants further characterization as a potential therapeutic option.

Tranexamic acid is a synthetic lysine derivative that inhibits plasminogen activation by blocking lysine-binding sites on the plasminogen molecule. Although the US Food and Drug Administration–approved indications for tranexamic acid include treatment of patients with menorrhagia and reduction or prevention of hemorrhage in patients with hemophilia undergoing tooth extraction, the potential efficacy of tranexamic acid in the treatment of melasma has been consistently reported since the 1980s.¹

Tranexamic acid exerts effects on pigmentation via its inhibitory effects on UV light–induced plasminogen activator and plasmin activity.² UV radiation induces the synthesis of plasminogen activator by keratinocytes, which results in increased conversion of plasminogen to plasmin. Plasminogen activator induces tyrosinase activity, resulting in increased melanin synthesis. The presence of plasmin results in increased production of both arachidonic acid and fibroblast growth factor, which stimulate melanogenesis and neovascularization, respectively.³ By inhibiting plasminogen activation, tranexamic acid mitigates UV radiation–induced melanogenesis and neovascularization. In treated guinea pig skin, application of topical tranexamic acid following UV radiation exposure inhibited the development of expected skin hyperpigmentation and also reduced tyrosinase activity.^4,5

The largest study on the use of oral tranexamic acid for treatment of melasma was a retrospective chart review of 561 melasma patients treated with tranexamic acid at a single center in Singapore.⁶ More than 90% of patients received prior treatment of their melasma, including bleaching creams and energy-based treatment. Among patients who received oral tranexamic acid over a 4-month period, 90% of patients demonstrated improvement in their melasma severity. Side effects were experienced by 7% of patients; the most common side effects were abdominal bloating and pain (experienced by 2% of patients). Notably, 1 patient developed deep vein thrombosis during treatment and subsequently was found to have protein S deficiency.⁶

Although the daily doses of tranexamic acid for the treatment of menorrhagia and perioperative hemophilia patients are 3900 mg and 30 to 40 mg/kg, respectively, effective daily doses reported for the treatment of melasma have ranged from the initial report of efficacy at 750 to 1500 mg to subsequent reports of improvement at daily doses of 500 mg.^1,2,6-8

Challenges to the use of tranexamic acid for melasma treatment in the United States include the medicolegal environment, specifically the risks associated with using a systemic procoagulant medication for a cosmetic indication. Patients should be screened and counseled on the risks of developing deep vein thrombosis and pulmonary embolism prior to initiating treatment. Cost and accessibility also may limit the use of tranexamic acid in the United States. Tranexamic acid is available for off-label use in the United States with a prescription in the form of 650-mg tablets that can be split by patients to approximate twice-daily 325 mg dosing. This cosmetic indication poses an out-of-pocket cost to patients of over $110 per month or as low as $48 per month with a coupon at the time of publication.⁹

Given the potential for serious adverse effects with the use of systemic tranexamic acid, there has been interest in formulating and evaluating topical tranexamic acid for cosmetic indications.^10-13 Topical tranexamic acid has been used alone and in conjunction with modalities to increase uptake, including intradermal injection, microneedling, and fractionated CO₂ laser.^12-14 Although these reports show initial promise, the currently available data are limited by small sample sizes, short treatment durations, lack of dose comparisons, and lack of short-term or long-term follow-up data. In addition to addressing these knowledge gaps in our understanding of topical tranexamic acid as a treatment option for melasma, further studies on the minimum systemic dose may address the downside of cost and potential for complications that may limit use of this medication in the United States.

The potential uses for tranexamic acid extend to the treatment of postinflammatory hyperpigmentation and rosacea. Melanocytes cultured in media conditioned by fractionated CO₂ laser–treated keratinocytes were found to have decreased tyrosinase activity and reduced melanin content when treated with tranexamic acid, suggesting the potential role for tranexamic acid to be used postprocedurally to reduce the risk for postinflammatory hyperpigmentation in prone skin types.¹⁵ Oral and topical tranexamic acid also have been reported to improve the appearance of erythematotelangiectatic rosacea, potentially relating to the inhibitory effects of tranexamic acid on neovascularization.^3,16,17 Although larger-scale controlled studies are required for further investigation of tranexamic acid for these indications, it has shown early promise as an adjunctive treatment for several dermatologic disorders, including melasma, and warrants further characterization as a potential therapeutic option.

Myth: Wearing makeup causes acne breakouts

Acne breakouts caused by makeup and other skin care products, known as acne cosmetica, typically resolve when patients stop using pore-clogging products; however, the overall impact of cosmetics on the development of acne lesions is considered to be negligible. Many cosmetics are not inherently comedogenic and can be used safely by patients in combination with proper skin care techniques.

Although dermatologists may be inclined to discourage makeup use during acne treatment or breakouts due to its potential to aggravate the patient’s condition, research has shown that treatment results and quality of life (QoL) scores associated with makeup use in acne patients may improve when patients receive instruction on how to use skin care products and cosmetics effectively. In one study of 50 female acne patients, 25 participants were instructed on how to use skin care products and cosmetics, and the other 25 participants received no specific instructions from dermatologists. After 4 weeks of treatment with conventional topical and/or oral acne medications, the investigators concluded that use of skin care products did not negatively impact acne treatment, and the group that received application instructions showed more notable improvements in QoL scores versus those who did not. In another study, the overall number of acne eruptions decreased over a 2- to 4-week period in female acne patients who were trained by a makeup artist to apply cosmetics while undergoing acne treatment. These results suggest that acne patients who wear makeup may benefit from a conversation with their dermatologist about what products and skin care techniques they can use to minimize exacerbation of or even improve their condition.

When choosing makeup that will not cause or exacerbate acne breakouts, patients should look for packaging that indicates the product will not clog pores and is oil-free, noncomedogenic, and/or nonacnegenic. Some makeup products are specifically formulated to help camouflage redness and pimples, which can help improve quality of life and self-esteem in acne patients who otherwise may be self-conscious about their appearance. Mineral-based cosmetics containing powdered formulas of silica, titanium dioxide, and zinc oxide can be used to absorb oil, camouflage redness, and prevent irritation. Anti-inflammatory ingredients and antioxidants also are used in some makeup products to reduce skin irritation and promote barrier repair. Additional cosmetic ingredients that can affect the mechanisms of acne pathogenesis and may contribute to a decrease in acne lesions include nicotinamide, lactic acid, triethyl acetate/ethyllineolate, and prebiotic plant extracts.

Makeup should be applied gently to avoid irritating the skin. It also is important to remind patients not to share their makeup brushes and applicators and to clean them weekly to ensure that bacteria, dead skin cells, and oil are not spread to the skin, which can lead to new breakouts. Although patients may be compelled to scrub the skin to remove makeup, a mild cleanser should be gently applied using the fingertips and rinsed off with lukewarm water to minimize skin irritation. Any makeup remaining on the skin after washing should be gently removed with an oil-free makeup remover.
 

Myth: Wearing makeup causes acne breakouts

Acne breakouts caused by makeup and other skin care products, known as acne cosmetica, typically resolve when patients stop using pore-clogging products; however, the overall impact of cosmetics on the development of acne lesions is considered to be negligible. Many cosmetics are not inherently comedogenic and can be used safely by patients in combination with proper skin care techniques.

Although dermatologists may be inclined to discourage makeup use during acne treatment or breakouts due to its potential to aggravate the patient’s condition, research has shown that treatment results and quality of life (QoL) scores associated with makeup use in acne patients may improve when patients receive instruction on how to use skin care products and cosmetics effectively. In one study of 50 female acne patients, 25 participants were instructed on how to use skin care products and cosmetics, and the other 25 participants received no specific instructions from dermatologists. After 4 weeks of treatment with conventional topical and/or oral acne medications, the investigators concluded that use of skin care products did not negatively impact acne treatment, and the group that received application instructions showed more notable improvements in QoL scores versus those who did not. In another study, the overall number of acne eruptions decreased over a 2- to 4-week period in female acne patients who were trained by a makeup artist to apply cosmetics while undergoing acne treatment. These results suggest that acne patients who wear makeup may benefit from a conversation with their dermatologist about what products and skin care techniques they can use to minimize exacerbation of or even improve their condition.

When choosing makeup that will not cause or exacerbate acne breakouts, patients should look for packaging that indicates the product will not clog pores and is oil-free, noncomedogenic, and/or nonacnegenic. Some makeup products are specifically formulated to help camouflage redness and pimples, which can help improve quality of life and self-esteem in acne patients who otherwise may be self-conscious about their appearance. Mineral-based cosmetics containing powdered formulas of silica, titanium dioxide, and zinc oxide can be used to absorb oil, camouflage redness, and prevent irritation. Anti-inflammatory ingredients and antioxidants also are used in some makeup products to reduce skin irritation and promote barrier repair. Additional cosmetic ingredients that can affect the mechanisms of acne pathogenesis and may contribute to a decrease in acne lesions include nicotinamide, lactic acid, triethyl acetate/ethyllineolate, and prebiotic plant extracts.

Makeup should be applied gently to avoid irritating the skin. It also is important to remind patients not to share their makeup brushes and applicators and to clean them weekly to ensure that bacteria, dead skin cells, and oil are not spread to the skin, which can lead to new breakouts. Although patients may be compelled to scrub the skin to remove makeup, a mild cleanser should be gently applied using the fingertips and rinsed off with lukewarm water to minimize skin irritation. Any makeup remaining on the skin after washing should be gently removed with an oil-free makeup remover.
 

Myth: Wearing makeup causes acne breakouts

Acne breakouts caused by makeup and other skin care products, known as acne cosmetica, typically resolve when patients stop using pore-clogging products; however, the overall impact of cosmetics on the development of acne lesions is considered to be negligible. Many cosmetics are not inherently comedogenic and can be used safely by patients in combination with proper skin care techniques.

Although dermatologists may be inclined to discourage makeup use during acne treatment or breakouts due to its potential to aggravate the patient’s condition, research has shown that treatment results and quality of life (QoL) scores associated with makeup use in acne patients may improve when patients receive instruction on how to use skin care products and cosmetics effectively. In one study of 50 female acne patients, 25 participants were instructed on how to use skin care products and cosmetics, and the other 25 participants received no specific instructions from dermatologists. After 4 weeks of treatment with conventional topical and/or oral acne medications, the investigators concluded that use of skin care products did not negatively impact acne treatment, and the group that received application instructions showed more notable improvements in QoL scores versus those who did not. In another study, the overall number of acne eruptions decreased over a 2- to 4-week period in female acne patients who were trained by a makeup artist to apply cosmetics while undergoing acne treatment. These results suggest that acne patients who wear makeup may benefit from a conversation with their dermatologist about what products and skin care techniques they can use to minimize exacerbation of or even improve their condition.

When choosing makeup that will not cause or exacerbate acne breakouts, patients should look for packaging that indicates the product will not clog pores and is oil-free, noncomedogenic, and/or nonacnegenic. Some makeup products are specifically formulated to help camouflage redness and pimples, which can help improve quality of life and self-esteem in acne patients who otherwise may be self-conscious about their appearance. Mineral-based cosmetics containing powdered formulas of silica, titanium dioxide, and zinc oxide can be used to absorb oil, camouflage redness, and prevent irritation. Anti-inflammatory ingredients and antioxidants also are used in some makeup products to reduce skin irritation and promote barrier repair. Additional cosmetic ingredients that can affect the mechanisms of acne pathogenesis and may contribute to a decrease in acne lesions include nicotinamide, lactic acid, triethyl acetate/ethyllineolate, and prebiotic plant extracts.

Makeup should be applied gently to avoid irritating the skin. It also is important to remind patients not to share their makeup brushes and applicators and to clean them weekly to ensure that bacteria, dead skin cells, and oil are not spread to the skin, which can lead to new breakouts. Although patients may be compelled to scrub the skin to remove makeup, a mild cleanser should be gently applied using the fingertips and rinsed off with lukewarm water to minimize skin irritation. Any makeup remaining on the skin after washing should be gently removed with an oil-free makeup remover.
 

The Diagnosis: Hypopigmented Mycosis Fungoides

The patient was started on clobetasol dipropionate cream 0.05% twice daily, which she did not tolerate due to a burning sensation on application. She then was started on narrowband UVB phototherapy 2 to 3 times weekly, and the hypopigmented areas began to improve. Narrowband UVB phototherapy was discontinued after 7 weeks due to the high cost to the patient, but the hypopigmented patches on the left thigh appeared to remit, and the patient did not return to the clinic for 6 months. She returned when the areas on the left thigh reappeared, along with new areas on the right buttock and right medial upper arm. Serial biopsies of the new patches also revealed a CD8⁺ atypical lymphocytic infiltrate consistent with hypopigmented patch-stage mycosis fungoides (MF). She was started on halobetasol ointment 0.05% twice daily to affected areas, which she tolerated well. Complete blood count and peripheral blood smear were unremarkable, and the patient continued to deny systemic symptoms. Over the next year, the patient's cutaneous findings continued to wax and wane with topical treatment, and she was referred to a regional cancer treatment center for a second opinion from a hematopathologist. Hematopathologic and dermatopathologic review of the case, including hematoxylin and eosin and immunohistochemical staining, was highly consistent with hypopigmented MF (Figures 1-3).

Mycosis fungoides is an uncommon disease characterized by atypical clonal T cells exhibiting epidermotropism. Most commonly, MF is characterized by a CD4⁺ lymphocytic infiltrate. Mycosis fungoides can be difficult to diagnose in its early stages, as it may resemble benign inflammatory conditions (eg, chronic atopic dermatitis, nummular eczema) and often requires biopsy and additional studies, such as immunohistochemistry, to secure a diagnosis. Hypopigmented MF is regarded as a subtype of MF, as it can exhibit different clinical and pathologic characteristics from classical MF. In particular, the lymphocytic phenotype in hypopigmented MF is more likely to be CD8⁺. 

In general, the progression of MF is characterized as stage IA (patches or plaques involving less than 10% body surface area [BSA]), IB (patches or plaques involving ≥10% BSA without lymph node or visceral involvement), IIA (patches or plaques of any percentage of BSA with lymph node involvement), IIB (cutaneous tumors with or without lymph node involvement), III (erythroderma with low blood tumor burden), or IV (erythroderma with high blood tumor burden with or without visceral involvement). Hypopigmented MF generally presents in early patch stage and rarely progresses past stage IB, and thus generally has a favorable prognosis.^1,2 Kim et al³ demonstrated that evolution from patch to plaque stage MF is accompanied by a shift in lymphocytes from the T helper 1 (Th1) to T helper 2 phenotype; therefore the Th1 phenotype, CD8⁺ T cells are associated with lower risk for disease progression. Other investigators also have hypothesized that predominance of Th1 phenotype, CD8⁺ T cells may have an immunoregulatory effect, thus preventing evolution of disease from patch to plaque stage and explaining why hypopigmented MF, with a predominantly CD8⁺ phenotype, confers better prognosis with less chance for disease progression than classical MF.^4,5 The patch- or plaque-stage lesions of classical MF have a predilection for non-sun exposed areas (eg, buttocks, medial thighs, breasts),² whereas hypopigmented MF tends to present with hypopigmented or depigmented lesions mainly distributed on the trunk, arms, and legs. These lesions may become more visible following sun exposure.¹ The size of the hypopigmented lesions can vary, and patients may complain of pruritus with variable intensity.

Hypopigmented MF presents more commonly in younger populations, in contrast to classical MF.^6-8 However, like classical MF, hypopigmented MF appears to more frequently affect individuals with darker Fitzpatrick skin types.^1,9,10 Although it generally is accepted that hypopigmented MF does not favor either sex, some studies suggest that hypopigmented MF has a female predominance.^6,10

Classical MF is characterized by an epidermotropic infiltrate of CD4⁺ T helper cells,¹⁰ whereas CD8⁺ epidermotropism is considered hallmark in hypopigmented MF.^10-12 The other typical histopathologic features of hypopigmented MF generally are identical to those of classical MF, with solitary or small groups of atypical haloed lymphocytes within the basal layer, exocytosis of lymphocytes out of proportion to spongiosis, and papillary dermal fibrosis. Immunohistochemistry generally is helpful in distinguishing between classical MF and hypopigmented MF.

The clinical differential diagnosis for hypopigmented MF includes the early (inflammatory) stage of vitiligo, postinflammatory hypopigmentation, lichen sclerosus, pityriasis alba, and leprosy.

First-line treatment for hypopigmented MF consists of phototherapy/photochemotherapy and topical steroids.^9,13 Narrowband UVB phototherapy has been used with good success in pediatric patients.¹⁴ However, narrowband UVB may not be as effective in darker-skinned individuals; it has been hypothesized that this lack of efficacy could be due to the protective effects of increased melanin in the skin.¹ Other topical therapies may include topical carmustine and topical nitrogen mustard.

The Diagnosis: Hypopigmented Mycosis Fungoides

The patient was started on clobetasol dipropionate cream 0.05% twice daily, which she did not tolerate due to a burning sensation on application. She then was started on narrowband UVB phototherapy 2 to 3 times weekly, and the hypopigmented areas began to improve. Narrowband UVB phototherapy was discontinued after 7 weeks due to the high cost to the patient, but the hypopigmented patches on the left thigh appeared to remit, and the patient did not return to the clinic for 6 months. She returned when the areas on the left thigh reappeared, along with new areas on the right buttock and right medial upper arm. Serial biopsies of the new patches also revealed a CD8⁺ atypical lymphocytic infiltrate consistent with hypopigmented patch-stage mycosis fungoides (MF). She was started on halobetasol ointment 0.05% twice daily to affected areas, which she tolerated well. Complete blood count and peripheral blood smear were unremarkable, and the patient continued to deny systemic symptoms. Over the next year, the patient's cutaneous findings continued to wax and wane with topical treatment, and she was referred to a regional cancer treatment center for a second opinion from a hematopathologist. Hematopathologic and dermatopathologic review of the case, including hematoxylin and eosin and immunohistochemical staining, was highly consistent with hypopigmented MF (Figures 1-3).

Mycosis fungoides is an uncommon disease characterized by atypical clonal T cells exhibiting epidermotropism. Most commonly, MF is characterized by a CD4⁺ lymphocytic infiltrate. Mycosis fungoides can be difficult to diagnose in its early stages, as it may resemble benign inflammatory conditions (eg, chronic atopic dermatitis, nummular eczema) and often requires biopsy and additional studies, such as immunohistochemistry, to secure a diagnosis. Hypopigmented MF is regarded as a subtype of MF, as it can exhibit different clinical and pathologic characteristics from classical MF. In particular, the lymphocytic phenotype in hypopigmented MF is more likely to be CD8⁺. 

In general, the progression of MF is characterized as stage IA (patches or plaques involving less than 10% body surface area [BSA]), IB (patches or plaques involving ≥10% BSA without lymph node or visceral involvement), IIA (patches or plaques of any percentage of BSA with lymph node involvement), IIB (cutaneous tumors with or without lymph node involvement), III (erythroderma with low blood tumor burden), or IV (erythroderma with high blood tumor burden with or without visceral involvement). Hypopigmented MF generally presents in early patch stage and rarely progresses past stage IB, and thus generally has a favorable prognosis.^1,2 Kim et al³ demonstrated that evolution from patch to plaque stage MF is accompanied by a shift in lymphocytes from the T helper 1 (Th1) to T helper 2 phenotype; therefore the Th1 phenotype, CD8⁺ T cells are associated with lower risk for disease progression. Other investigators also have hypothesized that predominance of Th1 phenotype, CD8⁺ T cells may have an immunoregulatory effect, thus preventing evolution of disease from patch to plaque stage and explaining why hypopigmented MF, with a predominantly CD8⁺ phenotype, confers better prognosis with less chance for disease progression than classical MF.^4,5 The patch- or plaque-stage lesions of classical MF have a predilection for non-sun exposed areas (eg, buttocks, medial thighs, breasts),² whereas hypopigmented MF tends to present with hypopigmented or depigmented lesions mainly distributed on the trunk, arms, and legs. These lesions may become more visible following sun exposure.¹ The size of the hypopigmented lesions can vary, and patients may complain of pruritus with variable intensity.

Hypopigmented MF presents more commonly in younger populations, in contrast to classical MF.^6-8 However, like classical MF, hypopigmented MF appears to more frequently affect individuals with darker Fitzpatrick skin types.^1,9,10 Although it generally is accepted that hypopigmented MF does not favor either sex, some studies suggest that hypopigmented MF has a female predominance.^6,10

Classical MF is characterized by an epidermotropic infiltrate of CD4⁺ T helper cells,¹⁰ whereas CD8⁺ epidermotropism is considered hallmark in hypopigmented MF.^10-12 The other typical histopathologic features of hypopigmented MF generally are identical to those of classical MF, with solitary or small groups of atypical haloed lymphocytes within the basal layer, exocytosis of lymphocytes out of proportion to spongiosis, and papillary dermal fibrosis. Immunohistochemistry generally is helpful in distinguishing between classical MF and hypopigmented MF.

The clinical differential diagnosis for hypopigmented MF includes the early (inflammatory) stage of vitiligo, postinflammatory hypopigmentation, lichen sclerosus, pityriasis alba, and leprosy.

First-line treatment for hypopigmented MF consists of phototherapy/photochemotherapy and topical steroids.^9,13 Narrowband UVB phototherapy has been used with good success in pediatric patients.¹⁴ However, narrowband UVB may not be as effective in darker-skinned individuals; it has been hypothesized that this lack of efficacy could be due to the protective effects of increased melanin in the skin.¹ Other topical therapies may include topical carmustine and topical nitrogen mustard.

The Diagnosis: Hypopigmented Mycosis Fungoides

The patient was started on clobetasol dipropionate cream 0.05% twice daily, which she did not tolerate due to a burning sensation on application. She then was started on narrowband UVB phototherapy 2 to 3 times weekly, and the hypopigmented areas began to improve. Narrowband UVB phototherapy was discontinued after 7 weeks due to the high cost to the patient, but the hypopigmented patches on the left thigh appeared to remit, and the patient did not return to the clinic for 6 months. She returned when the areas on the left thigh reappeared, along with new areas on the right buttock and right medial upper arm. Serial biopsies of the new patches also revealed a CD8⁺ atypical lymphocytic infiltrate consistent with hypopigmented patch-stage mycosis fungoides (MF). She was started on halobetasol ointment 0.05% twice daily to affected areas, which she tolerated well. Complete blood count and peripheral blood smear were unremarkable, and the patient continued to deny systemic symptoms. Over the next year, the patient's cutaneous findings continued to wax and wane with topical treatment, and she was referred to a regional cancer treatment center for a second opinion from a hematopathologist. Hematopathologic and dermatopathologic review of the case, including hematoxylin and eosin and immunohistochemical staining, was highly consistent with hypopigmented MF (Figures 1-3).

Mycosis fungoides is an uncommon disease characterized by atypical clonal T cells exhibiting epidermotropism. Most commonly, MF is characterized by a CD4⁺ lymphocytic infiltrate. Mycosis fungoides can be difficult to diagnose in its early stages, as it may resemble benign inflammatory conditions (eg, chronic atopic dermatitis, nummular eczema) and often requires biopsy and additional studies, such as immunohistochemistry, to secure a diagnosis. Hypopigmented MF is regarded as a subtype of MF, as it can exhibit different clinical and pathologic characteristics from classical MF. In particular, the lymphocytic phenotype in hypopigmented MF is more likely to be CD8⁺. 

In general, the progression of MF is characterized as stage IA (patches or plaques involving less than 10% body surface area [BSA]), IB (patches or plaques involving ≥10% BSA without lymph node or visceral involvement), IIA (patches or plaques of any percentage of BSA with lymph node involvement), IIB (cutaneous tumors with or without lymph node involvement), III (erythroderma with low blood tumor burden), or IV (erythroderma with high blood tumor burden with or without visceral involvement). Hypopigmented MF generally presents in early patch stage and rarely progresses past stage IB, and thus generally has a favorable prognosis.^1,2 Kim et al³ demonstrated that evolution from patch to plaque stage MF is accompanied by a shift in lymphocytes from the T helper 1 (Th1) to T helper 2 phenotype; therefore the Th1 phenotype, CD8⁺ T cells are associated with lower risk for disease progression. Other investigators also have hypothesized that predominance of Th1 phenotype, CD8⁺ T cells may have an immunoregulatory effect, thus preventing evolution of disease from patch to plaque stage and explaining why hypopigmented MF, with a predominantly CD8⁺ phenotype, confers better prognosis with less chance for disease progression than classical MF.^4,5 The patch- or plaque-stage lesions of classical MF have a predilection for non-sun exposed areas (eg, buttocks, medial thighs, breasts),² whereas hypopigmented MF tends to present with hypopigmented or depigmented lesions mainly distributed on the trunk, arms, and legs. These lesions may become more visible following sun exposure.¹ The size of the hypopigmented lesions can vary, and patients may complain of pruritus with variable intensity.

Hypopigmented MF presents more commonly in younger populations, in contrast to classical MF.^6-8 However, like classical MF, hypopigmented MF appears to more frequently affect individuals with darker Fitzpatrick skin types.^1,9,10 Although it generally is accepted that hypopigmented MF does not favor either sex, some studies suggest that hypopigmented MF has a female predominance.^6,10

Classical MF is characterized by an epidermotropic infiltrate of CD4⁺ T helper cells,¹⁰ whereas CD8⁺ epidermotropism is considered hallmark in hypopigmented MF.^10-12 The other typical histopathologic features of hypopigmented MF generally are identical to those of classical MF, with solitary or small groups of atypical haloed lymphocytes within the basal layer, exocytosis of lymphocytes out of proportion to spongiosis, and papillary dermal fibrosis. Immunohistochemistry generally is helpful in distinguishing between classical MF and hypopigmented MF.

The clinical differential diagnosis for hypopigmented MF includes the early (inflammatory) stage of vitiligo, postinflammatory hypopigmentation, lichen sclerosus, pityriasis alba, and leprosy.

First-line treatment for hypopigmented MF consists of phototherapy/photochemotherapy and topical steroids.^9,13 Narrowband UVB phototherapy has been used with good success in pediatric patients.¹⁴ However, narrowband UVB may not be as effective in darker-skinned individuals; it has been hypothesized that this lack of efficacy could be due to the protective effects of increased melanin in the skin.¹ Other topical therapies may include topical carmustine and topical nitrogen mustard.