Joe R. Monroe, MPAS, PA

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

Several weeks ago, this 14-year-old boy developed an itchy spot on his neck. Concerned that the problem was “ringworm,” the boy’s grandfather took him to the primary care provider, who prescribed nystatin cream. This produced modest improvement in the appearance of the lesion but had no effect on the associated itching. At that point, they were referred to dermatology for further evaluation.

The patient denies any other skin problems. The only animal he has been exposed to is his own dog, who has been part of the household for years. The boy is not involved in contact sports (eg, football, wrestling), and he reports that none of his siblings or friends have any skin complaints.

He is otherwise healthy and does not take any prescription medications.

EXAMINATION
The “rash” consists of a single, 2-cm lesion on the patient’s anterolateral neck. It is perfectly round and slightly erythematous, with a cleared center and scaly advancing margin. Palpable adenopathy is evident just above the lesion. There are no other lesions elsewhere, and the patient’s skin is otherwise unremarkable.

What is the diagnosis?

DISCUSSION
A KOH prep revealed abundant fungal elements, confirming the diagnosis of tinea corporis. This conclusion had already been reached empirically by the primary care provider, who chose nystatin cream for treatment. When that drug faltered, diagnostic doubt reared its head. The KOH settled the question once and for all—a crucial step, since nystatin is often prescribed for conditions that have no likelihood of responding to it (eg, eczema, psoriasis, granuloma annulare).

Nystatin, a polyene antifungal, was discovered and brought to market in 1950—that’s nearly 66 years ago! At that time, very few antifungal agents were available, so nystatin gained instant acceptance practically overnight. Since then, although dozens of newer and better antifungals have come on the market, nystatin continues to be prescribed out of sheer habit. A lot of water has gone down the river since 1950!

Nystatin was first isolated and developed by two scientists (Brown and Fuller) who worked in the lab at the New York State Health Department in the ’40s and ’50s. A popular practice at the time was to collect soil samples from local farmers to see what bacteria could be isolated. Brown and Fuller found a unique species of Streptomyces that they named S noursei after the dairy farmer whose soil they sampled.

They noted that this organism exuded a substance that inhibited yeast, mold, and fungi in vitro; when this substance was isolated and purified, it worked topically as well. They named this substance nystatin in honor of their employer, the New York State Health Department.

As charming as this history is, in the intervening 60+ years, better antifungals have been introduced and organisms have become less responsive to nystatin. In my opinion, except for unusual selective instances, there is no reason to prescribe nystatin instead of imidazole and allylamine (eg, miconazole, terbinafine, or naftifine).

For this patient, I prescribed oxiconazole lotion for twice-daily application to this small and limited lesion. With more extensive disease, I might add an oral antifungal, such as terbinafine. The patient’s lesion should resolve in two weeks or less.

One final note: In dermatology, we discourage the use of the term ringworm because it contributes to the “ick” factor associated with “worms”—which are not even involved in tinea corporis.

TAKE-HOME LEARNING POINTS
• Nystatin is a 66-year-old relic that has no place in treating ordinary dermatophytosis.

• “Newer” antifungals are more effective and kill a wider range of organisms, including yeast and fungi.

• In my experience, most nystatin is prescribed for conditions that have no chance of responding to it (eg, eczema, psoriasis, or granuloma annulare), because a differential was not considered.

• Primary care offices that are comfortable doing wet preps for clue cells and trichomonas feel no such need to perform KOHs to confirm fungal infection, and so diagnostic confusion results.

• There is no medical entity called ringworm. This is lay terminology based on the misbelief that worms are somehow involved in tinea.

ANSWER
The correct answer is food (choice “a”), which for many generations has been blamed for worsening acne (along with other nonfactors, such as makeup). All the others are demonstrably involved in the genesis and perpetuation of acne.

DISCUSSION
Teenagers have a hard enough time dealing with acne and other vicissitudes of puberty, and then they get blamed for eating the wrong kinds of food …. Would that it could be that simple! I think it’s important for us as providers to set the record straight by making sure parents and patients know what matters and what doesn’t.

When we’ve done that, the patient (or occasionally a parent) might say, “Well, every time I eat (insert item here), my acne flares.” To which we of course reply, “Well then, don’t do that!” After all, we certainly wouldn’t object to the patient consuming a better diet.

Once the unimportance of pizza, makeup, and soft drinks has been established, there remains the opportunity to enlighten the patient (and family) about the factors that do play a significant role—all but one of which can be addressed. (The exception, of course, is heredity; still, I believe it’s important to recognize its role in acne.) We can reduce the amount of sebum through use of retinoids and cut down on bacteria by using oral or topical antibiotics (though erythromycin is not especially effective). Hormonal therapy can be accomplished with oral contraceptives or oral spironolactone, though neither is perfect.

Treatment
This particular patient was prescribed a six-month course of isotretinoin (40 mg/d), after which her acne was completely and permanently gone. This is the result in about 70% of cases when this medicine is used correctly.

Proper procedure, including pregnancy tests and blood work, was followed before the patient was placed on the medication. The decision to use it was made after a careful discussion of other options, most of which she had already exhausted, and of the risks versus benefits of all available choices.

The biggest obstacle to starting the patient on isotretinoin was the perception that the drug is dangerous. It certainly must be used with caution, in carefully selected patients, and after a full disclosure of the associated risks. But when used appropriately, it is an effective treatment for acne that has failed to respond to other medications.

Summary
Acne is an extremely common complaint and happens to be exceedingly well studied. There are numerous treatment options, although none is perfect. Our job is to guide patients and families through the maze of information to plan a course of action acceptable to all.

ANSWER
The correct answer is food (choice “a”), which for many generations has been blamed for worsening acne (along with other nonfactors, such as makeup). All the others are demonstrably involved in the genesis and perpetuation of acne.

DISCUSSION
Teenagers have a hard enough time dealing with acne and other vicissitudes of puberty, and then they get blamed for eating the wrong kinds of food …. Would that it could be that simple! I think it’s important for us as providers to set the record straight by making sure parents and patients know what matters and what doesn’t.

When we’ve done that, the patient (or occasionally a parent) might say, “Well, every time I eat (insert item here), my acne flares.” To which we of course reply, “Well then, don’t do that!” After all, we certainly wouldn’t object to the patient consuming a better diet.

Once the unimportance of pizza, makeup, and soft drinks has been established, there remains the opportunity to enlighten the patient (and family) about the factors that do play a significant role—all but one of which can be addressed. (The exception, of course, is heredity; still, I believe it’s important to recognize its role in acne.) We can reduce the amount of sebum through use of retinoids and cut down on bacteria by using oral or topical antibiotics (though erythromycin is not especially effective). Hormonal therapy can be accomplished with oral contraceptives or oral spironolactone, though neither is perfect.

Treatment
This particular patient was prescribed a six-month course of isotretinoin (40 mg/d), after which her acne was completely and permanently gone. This is the result in about 70% of cases when this medicine is used correctly.

Proper procedure, including pregnancy tests and blood work, was followed before the patient was placed on the medication. The decision to use it was made after a careful discussion of other options, most of which she had already exhausted, and of the risks versus benefits of all available choices.

The biggest obstacle to starting the patient on isotretinoin was the perception that the drug is dangerous. It certainly must be used with caution, in carefully selected patients, and after a full disclosure of the associated risks. But when used appropriately, it is an effective treatment for acne that has failed to respond to other medications.

Summary
Acne is an extremely common complaint and happens to be exceedingly well studied. There are numerous treatment options, although none is perfect. Our job is to guide patients and families through the maze of information to plan a course of action acceptable to all.

ANSWER
The correct answer is food (choice “a”), which for many generations has been blamed for worsening acne (along with other nonfactors, such as makeup). All the others are demonstrably involved in the genesis and perpetuation of acne.

DISCUSSION
Teenagers have a hard enough time dealing with acne and other vicissitudes of puberty, and then they get blamed for eating the wrong kinds of food …. Would that it could be that simple! I think it’s important for us as providers to set the record straight by making sure parents and patients know what matters and what doesn’t.

When we’ve done that, the patient (or occasionally a parent) might say, “Well, every time I eat (insert item here), my acne flares.” To which we of course reply, “Well then, don’t do that!” After all, we certainly wouldn’t object to the patient consuming a better diet.

Once the unimportance of pizza, makeup, and soft drinks has been established, there remains the opportunity to enlighten the patient (and family) about the factors that do play a significant role—all but one of which can be addressed. (The exception, of course, is heredity; still, I believe it’s important to recognize its role in acne.) We can reduce the amount of sebum through use of retinoids and cut down on bacteria by using oral or topical antibiotics (though erythromycin is not especially effective). Hormonal therapy can be accomplished with oral contraceptives or oral spironolactone, though neither is perfect.

Treatment
This particular patient was prescribed a six-month course of isotretinoin (40 mg/d), after which her acne was completely and permanently gone. This is the result in about 70% of cases when this medicine is used correctly.

Proper procedure, including pregnancy tests and blood work, was followed before the patient was placed on the medication. The decision to use it was made after a careful discussion of other options, most of which she had already exhausted, and of the risks versus benefits of all available choices.

The biggest obstacle to starting the patient on isotretinoin was the perception that the drug is dangerous. It certainly must be used with caution, in carefully selected patients, and after a full disclosure of the associated risks. But when used appropriately, it is an effective treatment for acne that has failed to respond to other medications.

Summary
Acne is an extremely common complaint and happens to be exceedingly well studied. There are numerous treatment options, although none is perfect. Our job is to guide patients and families through the maze of information to plan a course of action acceptable to all.

An 81-year-old man is brought in by his wife for evaluation of a very itchy rash on his bilateral lower tibial areas. He says the problem started about six months ago, after a spate of summer yardwork during which he sustained what he assumed was a bug bite. It was itchy, so he scratched it.

Of course, in the way of most itches, the scratching offered temporary relief, after which the itching resumed. The patient tried any number of OTC products, including rubbing alcohol, hydrogen peroxide, tea tree oil, several different essential oils, and triple-antibiotic cream and ointment. The worse the itching became, the more products he applied—all to no avail.

The patient describes his health as otherwise decent. He does have type 2 diabetes, which he says is in good control.

EXAMINATION
The lower anterior tibial areas of both legs are covered by a scaly red rash. The left leg is more heavily affected, and obvious edema can be seen distal to the rash on that leg. The surface scales of the rash have a polygonal look, resembling a dried lake bed or finely cracked porcelain. The edges of the cracks turn upward, resulting in a rough feel on palpation.

The patient’s skin is quite dry in general but otherwise within normal limits.

What is the diagnosis?

DISCUSSION
Leg skin is unique in many respects. For one thing, it’s down there, where gravity takes and often holds blood and other fluids that might not accumulate elsewhere. It’s also a long trip for blood to get out to the extremities and often a longer return trip.

Leg skin is also remarkable because it has far fewer sebaceous glands than the scalp, face, and chest, which means it tends to be quite dry. This is especially true in older patients already prone to dry skin and in those who seldom moisturize to counteract this problem (in other words, men!).

This is why most patients with asteatotic eczema (AE) are men. Also known as eczema craquele and xerotic eczema, AE is especially common in the dry winter months, when long, hot showers are so appealing, as are wearing warmer clothes and sleeping under heavy covers.

Patients with AE, including this one, often make matters worse by applying a multiplicity of contactants. The edema noted in the exam, although due to the AE, also served to worsen the condition by making the skin tighter and drier still.

At this point, the problem often starts to take on aspects of lichen simplex chronicus, in which more scratching leads to more itching (and then more scratching, and so on). Clearly, what this patient needed (and got) was a definitive diagnosis and a treatment plan dictated by that diagnosis.

AE can be a challenge to treat, but the first step is to help the patient understand the nature of the problem and his role in the solution. The patient also needs to stop applying nonprescribed/recommended contactants, which don’t help and may exacerbate the problem.

To achieve relief, the patient can soak the leg with wet compresses for 10 minutes, remove excess water, and then apply a medium-strength steroid ointment (eg, triamcinolone 0.5%) in a thin but thorough coat. The area can then be covered with an occlusive covering, such as saran wrap, taped in place. This should be left on all night. During the day, the patient should apply only petroleum jelly to the affected area.

This approach will take 90% of patients out of the crisis stage. After a week or two, attention must shift to preventing recurrence, with generous use of emollients such as petroleum jelly. The patient should also be instructed to avoid using harsh (colored, scented, high pH) soaps, switch to shorter, relatively cool showers, and stop using anything but his hand to wash with (ie, no washcloths or loofahs).

For nondiabetic patients with severe AE that persists despite these measures, an intramuscular injection of a glucocorticoid (eg, triamcinolone 40 - 60 mg) can work wonders.

TAKE-HOME LEARNING POINTS
• Asteatotic eczema (AE), also called xerotic eczema or eczema craquele, is quite common, especially on the lower legs of older men.

• The particular rash of AE is said to resemble the cracked surface of a porcelain vessel.

• AE is often accompanied by edema distal to the rash.

• A topical steroid ointment applied to water-soaked skin, held in place overnight with an occlusive dressing, usually takes the patient out of the crisis phase.

• Prevention is then directed at avoiding drying of the affected areas.

An 81-year-old man is brought in by his wife for evaluation of a very itchy rash on his bilateral lower tibial areas. He says the problem started about six months ago, after a spate of summer yardwork during which he sustained what he assumed was a bug bite. It was itchy, so he scratched it.

Of course, in the way of most itches, the scratching offered temporary relief, after which the itching resumed. The patient tried any number of OTC products, including rubbing alcohol, hydrogen peroxide, tea tree oil, several different essential oils, and triple-antibiotic cream and ointment. The worse the itching became, the more products he applied—all to no avail.

The patient describes his health as otherwise decent. He does have type 2 diabetes, which he says is in good control.

EXAMINATION
The lower anterior tibial areas of both legs are covered by a scaly red rash. The left leg is more heavily affected, and obvious edema can be seen distal to the rash on that leg. The surface scales of the rash have a polygonal look, resembling a dried lake bed or finely cracked porcelain. The edges of the cracks turn upward, resulting in a rough feel on palpation.

The patient’s skin is quite dry in general but otherwise within normal limits.

What is the diagnosis?

DISCUSSION
Leg skin is unique in many respects. For one thing, it’s down there, where gravity takes and often holds blood and other fluids that might not accumulate elsewhere. It’s also a long trip for blood to get out to the extremities and often a longer return trip.

Leg skin is also remarkable because it has far fewer sebaceous glands than the scalp, face, and chest, which means it tends to be quite dry. This is especially true in older patients already prone to dry skin and in those who seldom moisturize to counteract this problem (in other words, men!).

This is why most patients with asteatotic eczema (AE) are men. Also known as eczema craquele and xerotic eczema, AE is especially common in the dry winter months, when long, hot showers are so appealing, as are wearing warmer clothes and sleeping under heavy covers.

Patients with AE, including this one, often make matters worse by applying a multiplicity of contactants. The edema noted in the exam, although due to the AE, also served to worsen the condition by making the skin tighter and drier still.

At this point, the problem often starts to take on aspects of lichen simplex chronicus, in which more scratching leads to more itching (and then more scratching, and so on). Clearly, what this patient needed (and got) was a definitive diagnosis and a treatment plan dictated by that diagnosis.

AE can be a challenge to treat, but the first step is to help the patient understand the nature of the problem and his role in the solution. The patient also needs to stop applying nonprescribed/recommended contactants, which don’t help and may exacerbate the problem.

To achieve relief, the patient can soak the leg with wet compresses for 10 minutes, remove excess water, and then apply a medium-strength steroid ointment (eg, triamcinolone 0.5%) in a thin but thorough coat. The area can then be covered with an occlusive covering, such as saran wrap, taped in place. This should be left on all night. During the day, the patient should apply only petroleum jelly to the affected area.

This approach will take 90% of patients out of the crisis stage. After a week or two, attention must shift to preventing recurrence, with generous use of emollients such as petroleum jelly. The patient should also be instructed to avoid using harsh (colored, scented, high pH) soaps, switch to shorter, relatively cool showers, and stop using anything but his hand to wash with (ie, no washcloths or loofahs).

For nondiabetic patients with severe AE that persists despite these measures, an intramuscular injection of a glucocorticoid (eg, triamcinolone 40 - 60 mg) can work wonders.

TAKE-HOME LEARNING POINTS
• Asteatotic eczema (AE), also called xerotic eczema or eczema craquele, is quite common, especially on the lower legs of older men.

• The particular rash of AE is said to resemble the cracked surface of a porcelain vessel.

• AE is often accompanied by edema distal to the rash.

• A topical steroid ointment applied to water-soaked skin, held in place overnight with an occlusive dressing, usually takes the patient out of the crisis phase.

• Prevention is then directed at avoiding drying of the affected areas.

An 81-year-old man is brought in by his wife for evaluation of a very itchy rash on his bilateral lower tibial areas. He says the problem started about six months ago, after a spate of summer yardwork during which he sustained what he assumed was a bug bite. It was itchy, so he scratched it.

Of course, in the way of most itches, the scratching offered temporary relief, after which the itching resumed. The patient tried any number of OTC products, including rubbing alcohol, hydrogen peroxide, tea tree oil, several different essential oils, and triple-antibiotic cream and ointment. The worse the itching became, the more products he applied—all to no avail.

The patient describes his health as otherwise decent. He does have type 2 diabetes, which he says is in good control.

EXAMINATION
The lower anterior tibial areas of both legs are covered by a scaly red rash. The left leg is more heavily affected, and obvious edema can be seen distal to the rash on that leg. The surface scales of the rash have a polygonal look, resembling a dried lake bed or finely cracked porcelain. The edges of the cracks turn upward, resulting in a rough feel on palpation.

The patient’s skin is quite dry in general but otherwise within normal limits.

What is the diagnosis?

DISCUSSION
Leg skin is unique in many respects. For one thing, it’s down there, where gravity takes and often holds blood and other fluids that might not accumulate elsewhere. It’s also a long trip for blood to get out to the extremities and often a longer return trip.

Leg skin is also remarkable because it has far fewer sebaceous glands than the scalp, face, and chest, which means it tends to be quite dry. This is especially true in older patients already prone to dry skin and in those who seldom moisturize to counteract this problem (in other words, men!).

This is why most patients with asteatotic eczema (AE) are men. Also known as eczema craquele and xerotic eczema, AE is especially common in the dry winter months, when long, hot showers are so appealing, as are wearing warmer clothes and sleeping under heavy covers.

Patients with AE, including this one, often make matters worse by applying a multiplicity of contactants. The edema noted in the exam, although due to the AE, also served to worsen the condition by making the skin tighter and drier still.

At this point, the problem often starts to take on aspects of lichen simplex chronicus, in which more scratching leads to more itching (and then more scratching, and so on). Clearly, what this patient needed (and got) was a definitive diagnosis and a treatment plan dictated by that diagnosis.

AE can be a challenge to treat, but the first step is to help the patient understand the nature of the problem and his role in the solution. The patient also needs to stop applying nonprescribed/recommended contactants, which don’t help and may exacerbate the problem.

To achieve relief, the patient can soak the leg with wet compresses for 10 minutes, remove excess water, and then apply a medium-strength steroid ointment (eg, triamcinolone 0.5%) in a thin but thorough coat. The area can then be covered with an occlusive covering, such as saran wrap, taped in place. This should be left on all night. During the day, the patient should apply only petroleum jelly to the affected area.

This approach will take 90% of patients out of the crisis stage. After a week or two, attention must shift to preventing recurrence, with generous use of emollients such as petroleum jelly. The patient should also be instructed to avoid using harsh (colored, scented, high pH) soaps, switch to shorter, relatively cool showers, and stop using anything but his hand to wash with (ie, no washcloths or loofahs).

For nondiabetic patients with severe AE that persists despite these measures, an intramuscular injection of a glucocorticoid (eg, triamcinolone 40 - 60 mg) can work wonders.

TAKE-HOME LEARNING POINTS
• Asteatotic eczema (AE), also called xerotic eczema or eczema craquele, is quite common, especially on the lower legs of older men.

• The particular rash of AE is said to resemble the cracked surface of a porcelain vessel.

• AE is often accompanied by edema distal to the rash.

• A topical steroid ointment applied to water-soaked skin, held in place overnight with an occlusive dressing, usually takes the patient out of the crisis phase.

• Prevention is then directed at avoiding drying of the affected areas.

A 54-year-old woman self-refers to dermatology for evaluation of asymptomatic lesions on her legs. Over the past several years, they have slowly grown larger, redder, and shinier. She denies any other skin problems. Medical history is significant for type 2 diabetes, which, according to the patient, is under good control.

The patient has sought care from a variety of professionals, including her primary care provider, her endocrinologist, and her gynecologist. Various diagnoses, including “fungal infection,” have been posited; treatment with antifungal cream and oral medications produced no effect.

She also consulted the proprietor of her local health food store, who actually examined her before diagnosing “yeast infection” and advising her to change her diet.

EXAMINATION
There are large, oval, reddish brown shiny plaques, measuring about 8 x 4 cm, on both anterior tibial areas. On closer inspection, the affected skin is yellowish pink and appears quite atrophic. This effect is more pronounced toward the centers of the lesions, which also display distinct telangiectasias. The borders of the plaques are slightly raised.

Examination of the rest of the patient’s skin reveals no other abnormalities.

What is the diagnosis?

DISCUSSION
Necrobiosis lipoidica (NL), though uncommon, is far from rare; it is seen somewhat regularly in dermatology practices. As this case demonstrates, it is one of hundreds of dermatologic diagnoses that you either know about or you don’t. Providers in the latter group invariably call it “fungal infection” because of its rounded borders—and because they simply have nothing else to call it.

True fungal infections are usually very superficial, involving only the outer layer of skin. This means they will manifest with scaling, a feature notably absent in this case. But more to the point, what was needed was a specific diagnosis, rather than another blind attempt at empiric treatment. Correct diagnosis dictates correct treatment.

NL was first described by Oppenhein in 1929, when he saw it in a diabetic patient. But it got its modern name in 1932 from Urbach, who thought it was invariably connected to diabetes. Now we know nondiabetic persons can develop it as well.

A number of theories exist as to the origins of this condition. One pinpoints microangiopathy of the same sort seen in the kidneys and eyes of diabetic patients. Another, proposed to account for the fact that NL is not exclusively seen in diabetes, holds that an autoimmune process might be involved—an opinion bolstered by the finding of increased TNF-alpha in the sera and skin of NL patients.

In any case, these atrophic plaques can grow quite large, eventually breaking down and ulcerating focally. Although the condition is usually asymptomatic, 25% of NL patients with advanced disease report pain.

Definitive diagnosis is made by punch biopsy, though visual diagnosis is quite adequate for those who can recognize the condition. NL lesions are most commonly seen on bilateral anterior tibial areas but can occasionally develop on the arm, face, or even genitals. The lesions can also koebnerize (ie, form along lines of trauma), occasionally being seen in surgical scars or even insulin injection sites.

Treatment, though largely unsatisfactory, includes topical and intralesional steroids. Particular care is taken to avoid or at least limit the formation of ulcers. In advanced cases, patients are referred to a wound care specialist. Oddly enough, neither the severity nor the prognosis of NL seem to have anything to do with how well or poorly the patient’s diabetes is controlled.

This patient was started on topical clobetasol cream, to be applied mostly to the actively advancing peripheral margin. Her prognosis, as with all NL patients, is guarded.

TAKE-HOME LEARNING POINTS
• Necrobiosis lipoidica (NL) is a disease of collagen degeneration that induces a granulomatous response that manifests microscopically with microangiopathy.

• NL usually appears on bilateral anterior tibial areas (but can affect the arms, face, or genitalia), as pinkish brown plaques with atrophic centers that tend to be yellow and telangiectatic.

• Though NL is usually associated with diabetes, it can develop in nondiabetic persons as well.

• The most feared complication of NL is eventual ulceration, which is why treatment is directed at taking care to avoid wounds to the plaques. 

A 54-year-old woman self-refers to dermatology for evaluation of asymptomatic lesions on her legs. Over the past several years, they have slowly grown larger, redder, and shinier. She denies any other skin problems. Medical history is significant for type 2 diabetes, which, according to the patient, is under good control.

The patient has sought care from a variety of professionals, including her primary care provider, her endocrinologist, and her gynecologist. Various diagnoses, including “fungal infection,” have been posited; treatment with antifungal cream and oral medications produced no effect.

She also consulted the proprietor of her local health food store, who actually examined her before diagnosing “yeast infection” and advising her to change her diet.

EXAMINATION
There are large, oval, reddish brown shiny plaques, measuring about 8 x 4 cm, on both anterior tibial areas. On closer inspection, the affected skin is yellowish pink and appears quite atrophic. This effect is more pronounced toward the centers of the lesions, which also display distinct telangiectasias. The borders of the plaques are slightly raised.

Examination of the rest of the patient’s skin reveals no other abnormalities.

What is the diagnosis?

DISCUSSION
Necrobiosis lipoidica (NL), though uncommon, is far from rare; it is seen somewhat regularly in dermatology practices. As this case demonstrates, it is one of hundreds of dermatologic diagnoses that you either know about or you don’t. Providers in the latter group invariably call it “fungal infection” because of its rounded borders—and because they simply have nothing else to call it.

True fungal infections are usually very superficial, involving only the outer layer of skin. This means they will manifest with scaling, a feature notably absent in this case. But more to the point, what was needed was a specific diagnosis, rather than another blind attempt at empiric treatment. Correct diagnosis dictates correct treatment.

NL was first described by Oppenhein in 1929, when he saw it in a diabetic patient. But it got its modern name in 1932 from Urbach, who thought it was invariably connected to diabetes. Now we know nondiabetic persons can develop it as well.

A number of theories exist as to the origins of this condition. One pinpoints microangiopathy of the same sort seen in the kidneys and eyes of diabetic patients. Another, proposed to account for the fact that NL is not exclusively seen in diabetes, holds that an autoimmune process might be involved—an opinion bolstered by the finding of increased TNF-alpha in the sera and skin of NL patients.

In any case, these atrophic plaques can grow quite large, eventually breaking down and ulcerating focally. Although the condition is usually asymptomatic, 25% of NL patients with advanced disease report pain.

Definitive diagnosis is made by punch biopsy, though visual diagnosis is quite adequate for those who can recognize the condition. NL lesions are most commonly seen on bilateral anterior tibial areas but can occasionally develop on the arm, face, or even genitals. The lesions can also koebnerize (ie, form along lines of trauma), occasionally being seen in surgical scars or even insulin injection sites.

Treatment, though largely unsatisfactory, includes topical and intralesional steroids. Particular care is taken to avoid or at least limit the formation of ulcers. In advanced cases, patients are referred to a wound care specialist. Oddly enough, neither the severity nor the prognosis of NL seem to have anything to do with how well or poorly the patient’s diabetes is controlled.

This patient was started on topical clobetasol cream, to be applied mostly to the actively advancing peripheral margin. Her prognosis, as with all NL patients, is guarded.

TAKE-HOME LEARNING POINTS
• Necrobiosis lipoidica (NL) is a disease of collagen degeneration that induces a granulomatous response that manifests microscopically with microangiopathy.

• NL usually appears on bilateral anterior tibial areas (but can affect the arms, face, or genitalia), as pinkish brown plaques with atrophic centers that tend to be yellow and telangiectatic.

• Though NL is usually associated with diabetes, it can develop in nondiabetic persons as well.

• The most feared complication of NL is eventual ulceration, which is why treatment is directed at taking care to avoid wounds to the plaques. 

A 54-year-old woman self-refers to dermatology for evaluation of asymptomatic lesions on her legs. Over the past several years, they have slowly grown larger, redder, and shinier. She denies any other skin problems. Medical history is significant for type 2 diabetes, which, according to the patient, is under good control.

The patient has sought care from a variety of professionals, including her primary care provider, her endocrinologist, and her gynecologist. Various diagnoses, including “fungal infection,” have been posited; treatment with antifungal cream and oral medications produced no effect.

She also consulted the proprietor of her local health food store, who actually examined her before diagnosing “yeast infection” and advising her to change her diet.

EXAMINATION
There are large, oval, reddish brown shiny plaques, measuring about 8 x 4 cm, on both anterior tibial areas. On closer inspection, the affected skin is yellowish pink and appears quite atrophic. This effect is more pronounced toward the centers of the lesions, which also display distinct telangiectasias. The borders of the plaques are slightly raised.

Examination of the rest of the patient’s skin reveals no other abnormalities.

What is the diagnosis?

DISCUSSION
Necrobiosis lipoidica (NL), though uncommon, is far from rare; it is seen somewhat regularly in dermatology practices. As this case demonstrates, it is one of hundreds of dermatologic diagnoses that you either know about or you don’t. Providers in the latter group invariably call it “fungal infection” because of its rounded borders—and because they simply have nothing else to call it.

True fungal infections are usually very superficial, involving only the outer layer of skin. This means they will manifest with scaling, a feature notably absent in this case. But more to the point, what was needed was a specific diagnosis, rather than another blind attempt at empiric treatment. Correct diagnosis dictates correct treatment.

NL was first described by Oppenhein in 1929, when he saw it in a diabetic patient. But it got its modern name in 1932 from Urbach, who thought it was invariably connected to diabetes. Now we know nondiabetic persons can develop it as well.

A number of theories exist as to the origins of this condition. One pinpoints microangiopathy of the same sort seen in the kidneys and eyes of diabetic patients. Another, proposed to account for the fact that NL is not exclusively seen in diabetes, holds that an autoimmune process might be involved—an opinion bolstered by the finding of increased TNF-alpha in the sera and skin of NL patients.

In any case, these atrophic plaques can grow quite large, eventually breaking down and ulcerating focally. Although the condition is usually asymptomatic, 25% of NL patients with advanced disease report pain.

Definitive diagnosis is made by punch biopsy, though visual diagnosis is quite adequate for those who can recognize the condition. NL lesions are most commonly seen on bilateral anterior tibial areas but can occasionally develop on the arm, face, or even genitals. The lesions can also koebnerize (ie, form along lines of trauma), occasionally being seen in surgical scars or even insulin injection sites.

Treatment, though largely unsatisfactory, includes topical and intralesional steroids. Particular care is taken to avoid or at least limit the formation of ulcers. In advanced cases, patients are referred to a wound care specialist. Oddly enough, neither the severity nor the prognosis of NL seem to have anything to do with how well or poorly the patient’s diabetes is controlled.

This patient was started on topical clobetasol cream, to be applied mostly to the actively advancing peripheral margin. Her prognosis, as with all NL patients, is guarded.

TAKE-HOME LEARNING POINTS
• Necrobiosis lipoidica (NL) is a disease of collagen degeneration that induces a granulomatous response that manifests microscopically with microangiopathy.

• NL usually appears on bilateral anterior tibial areas (but can affect the arms, face, or genitalia), as pinkish brown plaques with atrophic centers that tend to be yellow and telangiectatic.

• Though NL is usually associated with diabetes, it can develop in nondiabetic persons as well.

• The most feared complication of NL is eventual ulceration, which is why treatment is directed at taking care to avoid wounds to the plaques. 

ANSWER
The correct answer is to obtain a biopsy (choice “d”), the results of which would likely dictate rational and effective treatment. The other choices are largely empirical and not based on available evidence.

DISCUSSION
In this case, the biopsy (with samples from the arm rash as well as from the ears) showed unequivocal evidence of connective tissue disease—almost certainly lupus.

Systemic lupus erythematosus (SLE) has protean manifestations because it can affect so many different organs in so many different ways. Reduced to its simplest elements, lupus is an autoimmune process that results in a form of vasculitis that can affect any perfused tissue.

In terms of the skin, the visible manifestations of lupus are numerous and not always obvious. Sun is a known exacerbating factor, as this case demonstrated quite well: The patient’s rash was pronounced on sun-exposed skin but spared covered skin. When this was brought to her attention, the patient recalled a baby-sitting job earlier in the year (summer) that had required her to spend time outdoors. She also acknowledged that her smoking habit often took her into the backyard, where she would stand in the sun.

That being said, neither the arm rash nor the ear changes are “typical” of lupus (although the latter did include patulous follicular orifices, enlarged pores often seen focally with lupus). The effect is simply the result of the patient’s normal dark skin color; on a white person, the discoloration would have been pink or red.

Although these changes were suspicious for lupus, it was necessary to establish the diagnosis by biopsy—especially since the patient was already being treated for the disease. With that accomplished, the patient was sent back to her rheumatologist, who indicated he would probably treat her with a biologic, plus or minus methotrexate.

ANSWER
The correct answer is to obtain a biopsy (choice “d”), the results of which would likely dictate rational and effective treatment. The other choices are largely empirical and not based on available evidence.

DISCUSSION
In this case, the biopsy (with samples from the arm rash as well as from the ears) showed unequivocal evidence of connective tissue disease—almost certainly lupus.

Systemic lupus erythematosus (SLE) has protean manifestations because it can affect so many different organs in so many different ways. Reduced to its simplest elements, lupus is an autoimmune process that results in a form of vasculitis that can affect any perfused tissue.

In terms of the skin, the visible manifestations of lupus are numerous and not always obvious. Sun is a known exacerbating factor, as this case demonstrated quite well: The patient’s rash was pronounced on sun-exposed skin but spared covered skin. When this was brought to her attention, the patient recalled a baby-sitting job earlier in the year (summer) that had required her to spend time outdoors. She also acknowledged that her smoking habit often took her into the backyard, where she would stand in the sun.

That being said, neither the arm rash nor the ear changes are “typical” of lupus (although the latter did include patulous follicular orifices, enlarged pores often seen focally with lupus). The effect is simply the result of the patient’s normal dark skin color; on a white person, the discoloration would have been pink or red.

Although these changes were suspicious for lupus, it was necessary to establish the diagnosis by biopsy—especially since the patient was already being treated for the disease. With that accomplished, the patient was sent back to her rheumatologist, who indicated he would probably treat her with a biologic, plus or minus methotrexate.

ANSWER
The correct answer is to obtain a biopsy (choice “d”), the results of which would likely dictate rational and effective treatment. The other choices are largely empirical and not based on available evidence.

DISCUSSION
In this case, the biopsy (with samples from the arm rash as well as from the ears) showed unequivocal evidence of connective tissue disease—almost certainly lupus.

Systemic lupus erythematosus (SLE) has protean manifestations because it can affect so many different organs in so many different ways. Reduced to its simplest elements, lupus is an autoimmune process that results in a form of vasculitis that can affect any perfused tissue.

In terms of the skin, the visible manifestations of lupus are numerous and not always obvious. Sun is a known exacerbating factor, as this case demonstrated quite well: The patient’s rash was pronounced on sun-exposed skin but spared covered skin. When this was brought to her attention, the patient recalled a baby-sitting job earlier in the year (summer) that had required her to spend time outdoors. She also acknowledged that her smoking habit often took her into the backyard, where she would stand in the sun.

That being said, neither the arm rash nor the ear changes are “typical” of lupus (although the latter did include patulous follicular orifices, enlarged pores often seen focally with lupus). The effect is simply the result of the patient’s normal dark skin color; on a white person, the discoloration would have been pink or red.

Although these changes were suspicious for lupus, it was necessary to establish the diagnosis by biopsy—especially since the patient was already being treated for the disease. With that accomplished, the patient was sent back to her rheumatologist, who indicated he would probably treat her with a biologic, plus or minus methotrexate.

A 70-year-old woman presents to dermatology with asymptomatic lesions on her legs that, she reports, have been there for decades but are now becoming larger and more unsightly. She’s tried several courses of antifungal creams and pills with no success.

In all this time, she hasn’t seen a dermatology provider, because “no one ever felt the need” to refer her since her diagnosis was so “obvious.” When the changes began, however, her children finally convinced her to consult a specialist.

Her medical history is otherwise unremarkable, with no problems directly related to her skin issues. She denies both personal and family history of diabetes.

EXAMINATION
There are numerous impressive, reddish brown, annular plaques with slightly raised borders and clearing centers on the patient’s legs. There are also a few on her arms and one or two on her trunk. There is no epidermal component (scale or other surface disruption) on any of the lesions, which range in size from 2 cm to 15 cm.

What is the diagnosis?

DISCUSSION
It’s hard to believe that any patient could go this long with such a florid condition and never be seen by dermatology. Patients have an obligation to speak up—to complain, as it were—but some are too compliant. This woman’s primary care providers should have attached some significance to the nonresponse to treatment, one explanation for which might have been erroneous diagnosis.

Everybody knows that big round things are fungal, except when they aren’t. That’s where dermatology providers shine. Our training is all about development of differentials, as in: What are the various potential explanations for big round lesions? What would those things look like, and how could we distinguish them from fungal infection?

Here’s one huge clue: Fungal infection commonly refers to a relatively trivial, superficial infection of the outermost layer of the skin, the stratum corneum. By its very nature, it almost always involves scaling; if those scales are examined microscopically, the fungal elements can be seen, thus confirming the diagnosis.

When there is no scale, and the condition fails to respond to antifungal medications, alternative diagnoses must be considered. One major item that fits the bill is granuloma annulare (GA), an asymptomatic condition that presents with reddish brown, distinctly annular papules and plaques with raised (papular) borders and cleared centers. Though GA is extremely common, it is almost always misdiagnosed initially as fungal infection.

Besides the lack of scaling, GA lesions have some other characteristics that aid diagnosis. They’re commonly seen on extremities, especially the dorsa of feet and hands, and are far more common on women (especially young ones) than on men.

Although usually reddish brown, the lesions will be darker on patients with darker skin. It should be mentioned that this patient’s lesions were unusually large and extensive. Most cases are far more modest in size and distribution.

When necessary, punch biopsy shows what is called a palisaded granuloma. This, taken in context with the clinical picture, nails down the diagnosis.

One other piece of information is good to know: GA is quite common. You will see it, regularly.

Since the cause of GA is unknown, treatment can be problematic. Fortunately, the problem almost always resolves, with or without treatment. A few of this patient’s lesions were treated (for cosmetic reasons) with intralesional steroid injection.

TAKE-HOME LEARNING POINTS
• Granuloma annulare (GA) is a benign asymptomatic condition that presents with annular, reddish brown intradermal lesions.

• GA is commonly seen on the dorsa of feet, hands, and arms, especially of young women.

• GA lesions are intradermal, not epidermal, so there is no scaling or other disturbance of the skin surface.

• GA treatment is problematic, but the problem usually resolves on its own. 

A 70-year-old woman presents to dermatology with asymptomatic lesions on her legs that, she reports, have been there for decades but are now becoming larger and more unsightly. She’s tried several courses of antifungal creams and pills with no success.

In all this time, she hasn’t seen a dermatology provider, because “no one ever felt the need” to refer her since her diagnosis was so “obvious.” When the changes began, however, her children finally convinced her to consult a specialist.

Her medical history is otherwise unremarkable, with no problems directly related to her skin issues. She denies both personal and family history of diabetes.

EXAMINATION
There are numerous impressive, reddish brown, annular plaques with slightly raised borders and clearing centers on the patient’s legs. There are also a few on her arms and one or two on her trunk. There is no epidermal component (scale or other surface disruption) on any of the lesions, which range in size from 2 cm to 15 cm.

What is the diagnosis?

DISCUSSION
It’s hard to believe that any patient could go this long with such a florid condition and never be seen by dermatology. Patients have an obligation to speak up—to complain, as it were—but some are too compliant. This woman’s primary care providers should have attached some significance to the nonresponse to treatment, one explanation for which might have been erroneous diagnosis.

Everybody knows that big round things are fungal, except when they aren’t. That’s where dermatology providers shine. Our training is all about development of differentials, as in: What are the various potential explanations for big round lesions? What would those things look like, and how could we distinguish them from fungal infection?

Here’s one huge clue: Fungal infection commonly refers to a relatively trivial, superficial infection of the outermost layer of the skin, the stratum corneum. By its very nature, it almost always involves scaling; if those scales are examined microscopically, the fungal elements can be seen, thus confirming the diagnosis.

When there is no scale, and the condition fails to respond to antifungal medications, alternative diagnoses must be considered. One major item that fits the bill is granuloma annulare (GA), an asymptomatic condition that presents with reddish brown, distinctly annular papules and plaques with raised (papular) borders and cleared centers. Though GA is extremely common, it is almost always misdiagnosed initially as fungal infection.

Besides the lack of scaling, GA lesions have some other characteristics that aid diagnosis. They’re commonly seen on extremities, especially the dorsa of feet and hands, and are far more common on women (especially young ones) than on men.

Although usually reddish brown, the lesions will be darker on patients with darker skin. It should be mentioned that this patient’s lesions were unusually large and extensive. Most cases are far more modest in size and distribution.

When necessary, punch biopsy shows what is called a palisaded granuloma. This, taken in context with the clinical picture, nails down the diagnosis.

One other piece of information is good to know: GA is quite common. You will see it, regularly.

Since the cause of GA is unknown, treatment can be problematic. Fortunately, the problem almost always resolves, with or without treatment. A few of this patient’s lesions were treated (for cosmetic reasons) with intralesional steroid injection.

TAKE-HOME LEARNING POINTS
• Granuloma annulare (GA) is a benign asymptomatic condition that presents with annular, reddish brown intradermal lesions.

• GA is commonly seen on the dorsa of feet, hands, and arms, especially of young women.

• GA lesions are intradermal, not epidermal, so there is no scaling or other disturbance of the skin surface.

• GA treatment is problematic, but the problem usually resolves on its own. 

A 70-year-old woman presents to dermatology with asymptomatic lesions on her legs that, she reports, have been there for decades but are now becoming larger and more unsightly. She’s tried several courses of antifungal creams and pills with no success.

In all this time, she hasn’t seen a dermatology provider, because “no one ever felt the need” to refer her since her diagnosis was so “obvious.” When the changes began, however, her children finally convinced her to consult a specialist.

Her medical history is otherwise unremarkable, with no problems directly related to her skin issues. She denies both personal and family history of diabetes.

EXAMINATION
There are numerous impressive, reddish brown, annular plaques with slightly raised borders and clearing centers on the patient’s legs. There are also a few on her arms and one or two on her trunk. There is no epidermal component (scale or other surface disruption) on any of the lesions, which range in size from 2 cm to 15 cm.

What is the diagnosis?

DISCUSSION
It’s hard to believe that any patient could go this long with such a florid condition and never be seen by dermatology. Patients have an obligation to speak up—to complain, as it were—but some are too compliant. This woman’s primary care providers should have attached some significance to the nonresponse to treatment, one explanation for which might have been erroneous diagnosis.

Everybody knows that big round things are fungal, except when they aren’t. That’s where dermatology providers shine. Our training is all about development of differentials, as in: What are the various potential explanations for big round lesions? What would those things look like, and how could we distinguish them from fungal infection?

Here’s one huge clue: Fungal infection commonly refers to a relatively trivial, superficial infection of the outermost layer of the skin, the stratum corneum. By its very nature, it almost always involves scaling; if those scales are examined microscopically, the fungal elements can be seen, thus confirming the diagnosis.

When there is no scale, and the condition fails to respond to antifungal medications, alternative diagnoses must be considered. One major item that fits the bill is granuloma annulare (GA), an asymptomatic condition that presents with reddish brown, distinctly annular papules and plaques with raised (papular) borders and cleared centers. Though GA is extremely common, it is almost always misdiagnosed initially as fungal infection.

Besides the lack of scaling, GA lesions have some other characteristics that aid diagnosis. They’re commonly seen on extremities, especially the dorsa of feet and hands, and are far more common on women (especially young ones) than on men.

Although usually reddish brown, the lesions will be darker on patients with darker skin. It should be mentioned that this patient’s lesions were unusually large and extensive. Most cases are far more modest in size and distribution.

When necessary, punch biopsy shows what is called a palisaded granuloma. This, taken in context with the clinical picture, nails down the diagnosis.

One other piece of information is good to know: GA is quite common. You will see it, regularly.

Since the cause of GA is unknown, treatment can be problematic. Fortunately, the problem almost always resolves, with or without treatment. A few of this patient’s lesions were treated (for cosmetic reasons) with intralesional steroid injection.

TAKE-HOME LEARNING POINTS
• Granuloma annulare (GA) is a benign asymptomatic condition that presents with annular, reddish brown intradermal lesions.

• GA is commonly seen on the dorsa of feet, hands, and arms, especially of young women.

• GA lesions are intradermal, not epidermal, so there is no scaling or other disturbance of the skin surface.

• GA treatment is problematic, but the problem usually resolves on its own. 

ANSWER
The correct answer is all of the above (choice “e”). This particular form of tinea capitis is called black dot tinea capitis (BDTC), a somewhat unusual dermatophytosis (superficial fungal infection) that mostly affects children. The causative organisms are anthropophilic—that is, acquired from human sources, such as other children, during activities that involve skin-to-skin contact (eg, sports).

The vast majority of these organisms are from the Trichophyton family, such as T tonsurans or T violaceum. They invade the hair shaft itself, leaving the hard covering (the cuticle) intact. The black dots represent the tips of broken-off hairs, themselves full of fungal elements, seen in the photomicrograph. The term endothrix is given to this kind of fungal infection, in which the organisms are contained within the hair shaft, which, as a result, becomes brittle and breaks off. This is a relatively common type of infection.

A more unusual form of tinea capitis is caused by zoophilic organisms, such as Microsporum canis (from dogs and cats), Microsporum gypseum (pigs or cows), or T equinum (horses). These infect the external surface of the hair shaft, breaking down the cuticle. This allows for identification of the infection by Wood’s lamp, which causes the affected area to turn a yellowish color. These infections also tend to provoke a more brisk inflammatory response in the victim and are more difficult to treat.

Diagnosis can be made from a combination of clinical findings, KOH prep (as in this patient), and/or fungal culture.

Treatment can entail griseofulvin or terbinafine; the case patient was treated with a two-month course of the latter (125 mg/d). Topical treatment is of limited usefulness.

ANSWER
The correct answer is all of the above (choice “e”). This particular form of tinea capitis is called black dot tinea capitis (BDTC), a somewhat unusual dermatophytosis (superficial fungal infection) that mostly affects children. The causative organisms are anthropophilic—that is, acquired from human sources, such as other children, during activities that involve skin-to-skin contact (eg, sports).

The vast majority of these organisms are from the Trichophyton family, such as T tonsurans or T violaceum. They invade the hair shaft itself, leaving the hard covering (the cuticle) intact. The black dots represent the tips of broken-off hairs, themselves full of fungal elements, seen in the photomicrograph. The term endothrix is given to this kind of fungal infection, in which the organisms are contained within the hair shaft, which, as a result, becomes brittle and breaks off. This is a relatively common type of infection.

A more unusual form of tinea capitis is caused by zoophilic organisms, such as Microsporum canis (from dogs and cats), Microsporum gypseum (pigs or cows), or T equinum (horses). These infect the external surface of the hair shaft, breaking down the cuticle. This allows for identification of the infection by Wood’s lamp, which causes the affected area to turn a yellowish color. These infections also tend to provoke a more brisk inflammatory response in the victim and are more difficult to treat.

Diagnosis can be made from a combination of clinical findings, KOH prep (as in this patient), and/or fungal culture.

Treatment can entail griseofulvin or terbinafine; the case patient was treated with a two-month course of the latter (125 mg/d). Topical treatment is of limited usefulness.

ANSWER
The correct answer is all of the above (choice “e”). This particular form of tinea capitis is called black dot tinea capitis (BDTC), a somewhat unusual dermatophytosis (superficial fungal infection) that mostly affects children. The causative organisms are anthropophilic—that is, acquired from human sources, such as other children, during activities that involve skin-to-skin contact (eg, sports).

The vast majority of these organisms are from the Trichophyton family, such as T tonsurans or T violaceum. They invade the hair shaft itself, leaving the hard covering (the cuticle) intact. The black dots represent the tips of broken-off hairs, themselves full of fungal elements, seen in the photomicrograph. The term endothrix is given to this kind of fungal infection, in which the organisms are contained within the hair shaft, which, as a result, becomes brittle and breaks off. This is a relatively common type of infection.

A more unusual form of tinea capitis is caused by zoophilic organisms, such as Microsporum canis (from dogs and cats), Microsporum gypseum (pigs or cows), or T equinum (horses). These infect the external surface of the hair shaft, breaking down the cuticle. This allows for identification of the infection by Wood’s lamp, which causes the affected area to turn a yellowish color. These infections also tend to provoke a more brisk inflammatory response in the victim and are more difficult to treat.

Diagnosis can be made from a combination of clinical findings, KOH prep (as in this patient), and/or fungal culture.

Treatment can entail griseofulvin or terbinafine; the case patient was treated with a two-month course of the latter (125 mg/d). Topical treatment is of limited usefulness.

A 49-year-old woman presents to dermatology with a lesion on her back. It’s been there for at least 20 years, slowly growing to its present size; it is now so prominent that it shows through her clothes and is subject to traumatization. The visibility of the lesion, particularly when the patient wears a swimsuit, is a source of considerable embarrassment.

Notable medical history includes polycystic ovarian syndrome and related diabetes and dyslipidemia. Family history reveals that the patient’s mother died of heart disease in her 40s.

EXAMINATION
The lesion, which measures 3 cm x 3 cm, is an impressive, pedunculated, doughy, rubbery, skin-colored mass protruding from her left mid back. No redness or edema is seen on or around the lesion. On palpation, the lesion is found to be uniformly soft and rubbery.

The patient is quite obese and has numerous skin tags in skin folds, under the arms, and around the neck.

What is the diagnosis?

DISCUSSION
The lesion was excised with deep margins and submitted to pathology. The report showed benign histology, consistent with a fibroepitheliomatous polyp.

In one sense, it’s hard to believe this huge lesion was a “skin tag,” and there are other things it might have been. But the microscopic examination of the tissue proved it was simply a large version of the same skin tags we see around necks and in axillae. These lesions are known by various names, including fibroepitheliomatous polyps (FEP) and acrochordons. A more typical FEP would be the size of a grain of rice, but they can take on various forms and sizes.

There is a differential for lesions that look like FEPs; it includes seborrheic  keratoses, warts, molluscum contagiosum, neurofibromas, and fibrolipomas. Even melanoma and squamous cell carcinoma can assume a tag-like morphology. So it pays to take a close look at these lesions, checking to see if they’re soft and pliable, as well as skin colored. With any odd feature, including increased size, they need to be removed and sent for pathologic examination.

Heredity appears to play a role in the development of FEPs, as do age and obesity. There are studies showing an association between FEPs and insulin resistance and others identifying FEPs as a marker for increased risk for atherosclerotic vessel disease. In any case, 59% of the population has them by age 70, with men and women affected equally. Of the general population, 46% has some sort of skin tag somewhere.

Treatment may entail cryotherapy, excision, or electrodessication. With lesions as large as the case patient’s, excision is the only reasonable option. Deep margins are required, since a “shave” would leave a gaping, open wound. For the case patient, there was no postoperative sequelae aside from some scarring.

TAKE-HOME LEARNING POINTS
• Skin tags, also known as fibroepitheliomas, fibroepitheliomatous polyps, or acrochordons, are typically the size of a grain of rice, and tend to appear in skin folds (eg, axillae, neck, groin).

• Studies have shown that there may be an association between having skin tags and developing CAD or insulin resistance.

• Obesity, age, and heredity also appear to be factors in developing skin tags.

• Large or odd tags need to be captured and sent for pathologic examination.

• Skin tags are extremely common, affecting 59% of the population older than 70. 

A 49-year-old woman presents to dermatology with a lesion on her back. It’s been there for at least 20 years, slowly growing to its present size; it is now so prominent that it shows through her clothes and is subject to traumatization. The visibility of the lesion, particularly when the patient wears a swimsuit, is a source of considerable embarrassment.

Notable medical history includes polycystic ovarian syndrome and related diabetes and dyslipidemia. Family history reveals that the patient’s mother died of heart disease in her 40s.

EXAMINATION
The lesion, which measures 3 cm x 3 cm, is an impressive, pedunculated, doughy, rubbery, skin-colored mass protruding from her left mid back. No redness or edema is seen on or around the lesion. On palpation, the lesion is found to be uniformly soft and rubbery.

The patient is quite obese and has numerous skin tags in skin folds, under the arms, and around the neck.

What is the diagnosis?

DISCUSSION
The lesion was excised with deep margins and submitted to pathology. The report showed benign histology, consistent with a fibroepitheliomatous polyp.

In one sense, it’s hard to believe this huge lesion was a “skin tag,” and there are other things it might have been. But the microscopic examination of the tissue proved it was simply a large version of the same skin tags we see around necks and in axillae. These lesions are known by various names, including fibroepitheliomatous polyps (FEP) and acrochordons. A more typical FEP would be the size of a grain of rice, but they can take on various forms and sizes.

There is a differential for lesions that look like FEPs; it includes seborrheic  keratoses, warts, molluscum contagiosum, neurofibromas, and fibrolipomas. Even melanoma and squamous cell carcinoma can assume a tag-like morphology. So it pays to take a close look at these lesions, checking to see if they’re soft and pliable, as well as skin colored. With any odd feature, including increased size, they need to be removed and sent for pathologic examination.

Heredity appears to play a role in the development of FEPs, as do age and obesity. There are studies showing an association between FEPs and insulin resistance and others identifying FEPs as a marker for increased risk for atherosclerotic vessel disease. In any case, 59% of the population has them by age 70, with men and women affected equally. Of the general population, 46% has some sort of skin tag somewhere.

Treatment may entail cryotherapy, excision, or electrodessication. With lesions as large as the case patient’s, excision is the only reasonable option. Deep margins are required, since a “shave” would leave a gaping, open wound. For the case patient, there was no postoperative sequelae aside from some scarring.

TAKE-HOME LEARNING POINTS
• Skin tags, also known as fibroepitheliomas, fibroepitheliomatous polyps, or acrochordons, are typically the size of a grain of rice, and tend to appear in skin folds (eg, axillae, neck, groin).

• Studies have shown that there may be an association between having skin tags and developing CAD or insulin resistance.

• Obesity, age, and heredity also appear to be factors in developing skin tags.

• Large or odd tags need to be captured and sent for pathologic examination.

• Skin tags are extremely common, affecting 59% of the population older than 70. 

A 49-year-old woman presents to dermatology with a lesion on her back. It’s been there for at least 20 years, slowly growing to its present size; it is now so prominent that it shows through her clothes and is subject to traumatization. The visibility of the lesion, particularly when the patient wears a swimsuit, is a source of considerable embarrassment.

Notable medical history includes polycystic ovarian syndrome and related diabetes and dyslipidemia. Family history reveals that the patient’s mother died of heart disease in her 40s.

EXAMINATION
The lesion, which measures 3 cm x 3 cm, is an impressive, pedunculated, doughy, rubbery, skin-colored mass protruding from her left mid back. No redness or edema is seen on or around the lesion. On palpation, the lesion is found to be uniformly soft and rubbery.

The patient is quite obese and has numerous skin tags in skin folds, under the arms, and around the neck.

What is the diagnosis?

DISCUSSION
The lesion was excised with deep margins and submitted to pathology. The report showed benign histology, consistent with a fibroepitheliomatous polyp.

In one sense, it’s hard to believe this huge lesion was a “skin tag,” and there are other things it might have been. But the microscopic examination of the tissue proved it was simply a large version of the same skin tags we see around necks and in axillae. These lesions are known by various names, including fibroepitheliomatous polyps (FEP) and acrochordons. A more typical FEP would be the size of a grain of rice, but they can take on various forms and sizes.

There is a differential for lesions that look like FEPs; it includes seborrheic  keratoses, warts, molluscum contagiosum, neurofibromas, and fibrolipomas. Even melanoma and squamous cell carcinoma can assume a tag-like morphology. So it pays to take a close look at these lesions, checking to see if they’re soft and pliable, as well as skin colored. With any odd feature, including increased size, they need to be removed and sent for pathologic examination.

Heredity appears to play a role in the development of FEPs, as do age and obesity. There are studies showing an association between FEPs and insulin resistance and others identifying FEPs as a marker for increased risk for atherosclerotic vessel disease. In any case, 59% of the population has them by age 70, with men and women affected equally. Of the general population, 46% has some sort of skin tag somewhere.

Treatment may entail cryotherapy, excision, or electrodessication. With lesions as large as the case patient’s, excision is the only reasonable option. Deep margins are required, since a “shave” would leave a gaping, open wound. For the case patient, there was no postoperative sequelae aside from some scarring.

TAKE-HOME LEARNING POINTS
• Skin tags, also known as fibroepitheliomas, fibroepitheliomatous polyps, or acrochordons, are typically the size of a grain of rice, and tend to appear in skin folds (eg, axillae, neck, groin).

• Studies have shown that there may be an association between having skin tags and developing CAD or insulin resistance.

• Obesity, age, and heredity also appear to be factors in developing skin tags.

• Large or odd tags need to be captured and sent for pathologic examination.

• Skin tags are extremely common, affecting 59% of the population older than 70. 

A 14-year-old girl is brought to dermatology by her mother, following referral from her pediatrician for evaluation of fingernail changes. Initially, a faint brown streak was observed in the nail of her left fourth finger. Over time, the spot darkened and widened, and the adjacent nail plate flattened.

A few weeks before presentation to dermatology, the adjacent cuticle darkened. The patient denies any sensitivity in the area. Her mother denies any significant or relevant medical history.

EXAMINATION
The dark brown streak measures 4.5 mm in width and runs longitudinally the entire length of the nail plate. The discolored area coincides exactly with flattening of the nail plate, which, when viewed on edge, also exhibits darkening. Significantly, the adjacent cuticle is similarly affected.

No changes are observed on other digits. The child is of Native American ancestry, with type IV skin.

What is the diagnosis?

DISCUSSION
Generically, this problem is termed melanonychia; this case represents the most common type, longitudinal melanonychia (LM). Typically, it originates in the nail matrix with increased melanin production; this causes darkening of the onchocytes, which migrate distally as the nail plate grows.

This benign version is an extremely common problem, especially in darker-skinned patients. Almost 100% of African-Americans older than 50 have it, often in several nails, as do 77% of African Americans older than 20 and 10% to 20% of Japanese persons. Comparatively, only 1% to 2% of white individuals are affected.

The main significance of LM, of course, is the fact that it can represent melanoma, which, for a variety of reasons, is often belatedly identified in subungual areas and is therefore associated with relatively poor survival. Five-year survival rates for subungual melanoma are around 30%, while 10-year survival is only 13%—much lower than for melanomas elsewhere on the body. For example, patients with melanomas removed from other areas of the hand demonstrate 100% five-year survival rates. 

Subungual melanoma presenting in this manner is considered one of the so-called acrolentiginous melanomas, which present in peripheral “acral” locations (eg, scalp, soles, mucosal surfaces). While these are not inherently more dangerous in terms of biologic behavior, they tend to escape detection because of their location and (often) atypical appearance, thus having more time in which to become invasive.

Perhaps the most useful and puzzling conundrum associated with acrolentiginous melanomas is this: Darker-skinned patients are, in general, at low risk for melanoma compared to fair-skinned redheads and blondes. However, when dark-skinned patients do develop melanoma, it tends to manifest in an acral area (one reason why melanoma in these patients has a relatively poor prognosis).

Darkening under or in the nails can have other causes; it has been associated with Cushing disease, Addison disease, and alkaptonuria, to name just a few. It can also be associated with skin diseases, including psoriasis, Darier disease, lichen planus, and lichen striatus. A number of drugs, among them minocycline, can produce focal discoloration in or under the nails.

This subungual lesion was biopsied at its proximal origin, under digital block and using a tourniquet. The 3-mm punch specimen was sent for pathologic examination, which showed benign nevoid tissue—effectively ruling out melanoma. Even if the nail is permanently deformed, this was considered a small price to pay for the patient’s peace of mind.

TAKE-HOME LEARNING POINTS
• Dark streaks under fingernails are common in those with darker skin, in whom they often appear in multiple fingers. In the absence of change, these are usually safe.

• The related conundrum is that when those with darker skin develop melanoma, the subungual areas, or other light-skinned areas (sole, mouth, palms), are often where it manifests.

• New and/or changing areas of subungual pigmentation need to be referred to dermatology for evaluation and possible biopsy.

• When this discoloration also involves the adjacent cuticle or other perionychial skin, even more urgency is added to the referral. 

A 14-year-old girl is brought to dermatology by her mother, following referral from her pediatrician for evaluation of fingernail changes. Initially, a faint brown streak was observed in the nail of her left fourth finger. Over time, the spot darkened and widened, and the adjacent nail plate flattened.

A few weeks before presentation to dermatology, the adjacent cuticle darkened. The patient denies any sensitivity in the area. Her mother denies any significant or relevant medical history.

EXAMINATION
The dark brown streak measures 4.5 mm in width and runs longitudinally the entire length of the nail plate. The discolored area coincides exactly with flattening of the nail plate, which, when viewed on edge, also exhibits darkening. Significantly, the adjacent cuticle is similarly affected.

No changes are observed on other digits. The child is of Native American ancestry, with type IV skin.

What is the diagnosis?

DISCUSSION
Generically, this problem is termed melanonychia; this case represents the most common type, longitudinal melanonychia (LM). Typically, it originates in the nail matrix with increased melanin production; this causes darkening of the onchocytes, which migrate distally as the nail plate grows.

This benign version is an extremely common problem, especially in darker-skinned patients. Almost 100% of African-Americans older than 50 have it, often in several nails, as do 77% of African Americans older than 20 and 10% to 20% of Japanese persons. Comparatively, only 1% to 2% of white individuals are affected.

The main significance of LM, of course, is the fact that it can represent melanoma, which, for a variety of reasons, is often belatedly identified in subungual areas and is therefore associated with relatively poor survival. Five-year survival rates for subungual melanoma are around 30%, while 10-year survival is only 13%—much lower than for melanomas elsewhere on the body. For example, patients with melanomas removed from other areas of the hand demonstrate 100% five-year survival rates. 

Subungual melanoma presenting in this manner is considered one of the so-called acrolentiginous melanomas, which present in peripheral “acral” locations (eg, scalp, soles, mucosal surfaces). While these are not inherently more dangerous in terms of biologic behavior, they tend to escape detection because of their location and (often) atypical appearance, thus having more time in which to become invasive.

Perhaps the most useful and puzzling conundrum associated with acrolentiginous melanomas is this: Darker-skinned patients are, in general, at low risk for melanoma compared to fair-skinned redheads and blondes. However, when dark-skinned patients do develop melanoma, it tends to manifest in an acral area (one reason why melanoma in these patients has a relatively poor prognosis).

Darkening under or in the nails can have other causes; it has been associated with Cushing disease, Addison disease, and alkaptonuria, to name just a few. It can also be associated with skin diseases, including psoriasis, Darier disease, lichen planus, and lichen striatus. A number of drugs, among them minocycline, can produce focal discoloration in or under the nails.

This subungual lesion was biopsied at its proximal origin, under digital block and using a tourniquet. The 3-mm punch specimen was sent for pathologic examination, which showed benign nevoid tissue—effectively ruling out melanoma. Even if the nail is permanently deformed, this was considered a small price to pay for the patient’s peace of mind.

TAKE-HOME LEARNING POINTS
• Dark streaks under fingernails are common in those with darker skin, in whom they often appear in multiple fingers. In the absence of change, these are usually safe.

• The related conundrum is that when those with darker skin develop melanoma, the subungual areas, or other light-skinned areas (sole, mouth, palms), are often where it manifests.

• New and/or changing areas of subungual pigmentation need to be referred to dermatology for evaluation and possible biopsy.

• When this discoloration also involves the adjacent cuticle or other perionychial skin, even more urgency is added to the referral. 

A 14-year-old girl is brought to dermatology by her mother, following referral from her pediatrician for evaluation of fingernail changes. Initially, a faint brown streak was observed in the nail of her left fourth finger. Over time, the spot darkened and widened, and the adjacent nail plate flattened.

A few weeks before presentation to dermatology, the adjacent cuticle darkened. The patient denies any sensitivity in the area. Her mother denies any significant or relevant medical history.

EXAMINATION
The dark brown streak measures 4.5 mm in width and runs longitudinally the entire length of the nail plate. The discolored area coincides exactly with flattening of the nail plate, which, when viewed on edge, also exhibits darkening. Significantly, the adjacent cuticle is similarly affected.

No changes are observed on other digits. The child is of Native American ancestry, with type IV skin.

What is the diagnosis?

DISCUSSION
Generically, this problem is termed melanonychia; this case represents the most common type, longitudinal melanonychia (LM). Typically, it originates in the nail matrix with increased melanin production; this causes darkening of the onchocytes, which migrate distally as the nail plate grows.

This benign version is an extremely common problem, especially in darker-skinned patients. Almost 100% of African-Americans older than 50 have it, often in several nails, as do 77% of African Americans older than 20 and 10% to 20% of Japanese persons. Comparatively, only 1% to 2% of white individuals are affected.

The main significance of LM, of course, is the fact that it can represent melanoma, which, for a variety of reasons, is often belatedly identified in subungual areas and is therefore associated with relatively poor survival. Five-year survival rates for subungual melanoma are around 30%, while 10-year survival is only 13%—much lower than for melanomas elsewhere on the body. For example, patients with melanomas removed from other areas of the hand demonstrate 100% five-year survival rates. 

Subungual melanoma presenting in this manner is considered one of the so-called acrolentiginous melanomas, which present in peripheral “acral” locations (eg, scalp, soles, mucosal surfaces). While these are not inherently more dangerous in terms of biologic behavior, they tend to escape detection because of their location and (often) atypical appearance, thus having more time in which to become invasive.

Perhaps the most useful and puzzling conundrum associated with acrolentiginous melanomas is this: Darker-skinned patients are, in general, at low risk for melanoma compared to fair-skinned redheads and blondes. However, when dark-skinned patients do develop melanoma, it tends to manifest in an acral area (one reason why melanoma in these patients has a relatively poor prognosis).

Darkening under or in the nails can have other causes; it has been associated with Cushing disease, Addison disease, and alkaptonuria, to name just a few. It can also be associated with skin diseases, including psoriasis, Darier disease, lichen planus, and lichen striatus. A number of drugs, among them minocycline, can produce focal discoloration in or under the nails.

This subungual lesion was biopsied at its proximal origin, under digital block and using a tourniquet. The 3-mm punch specimen was sent for pathologic examination, which showed benign nevoid tissue—effectively ruling out melanoma. Even if the nail is permanently deformed, this was considered a small price to pay for the patient’s peace of mind.

TAKE-HOME LEARNING POINTS
• Dark streaks under fingernails are common in those with darker skin, in whom they often appear in multiple fingers. In the absence of change, these are usually safe.

• The related conundrum is that when those with darker skin develop melanoma, the subungual areas, or other light-skinned areas (sole, mouth, palms), are often where it manifests.

• New and/or changing areas of subungual pigmentation need to be referred to dermatology for evaluation and possible biopsy.

• When this discoloration also involves the adjacent cuticle or other perionychial skin, even more urgency is added to the referral. 

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.

ANSWER
The correct answer is erythema nodosum (EN; choice “c”), a reactive form of septal panniculitis with many potential triggers.

Erythema induratum (choice “a”) is a manifestation of lobular panniculitis, which affects the fat lobules but not the septae. It too has numerous triggers, but it tends to manifest with more discrete nodules, which eventually open and drain. It is far less common than EN.

Urticaria (choice “b”), also known as hives, presents as itchy, stingy wheals that are typically evanescent (eg, they appear suddenly, within seconds, and disappear within hours). Despite the itching and stinging, urticaria rarely hurts when it presents on the skin.

Erysipelas (choice “d”) is a superficial form of skin infection. More superficial than cellulitis, it usually is caused by a member of the Streptococcus family. It has a bright red appearance and sharply demarcated margins, with a peau d’orange (dimpled, like an orange peel) effect on its surface. It is acute in origin and responds readily to most common anti­biotics.

DISCUSSION
Erythema nodosum, a reactive process involving fibrous septae that support and separate subcutaneous adipocytes, is notable for the complete lack of epidermal change (eg, scaling, broken skin, pointing, draining). The incidence is about 2 in 10,000 population, with women outnumbering men at a rate of 4:1 and the 18-to-34 age-group most affected. The anterior leg is involved in the vast majority of cases.

EN often starts with flulike symptoms, followed by the appearance of discrete, bright red nodules, measuring 2 to 4 cm, on the anterior legs; these darken and coalesce over a period of seven to 10 weeks. New lesions can continue to appear for up to six weeks. As they progress, the lesions often become ecchymotic. Idiopathic cases (at least 20%) can last months.

Notable triggers include Crohn disease flares and use of drugs such as sulfa, gold salts, and oral contraceptives. Several infections have been identified as triggers, including strep, mycoplasma, and campylobacter, as well as deep fungal infections (histoplasmosis, blastomycosis, coccidioidomycosis, and sporotrichosis). More unusual causes include pregnancy and diseases such as sarcoidosis, tuberculosis, Behçet disease, and leukemia/lymphoma.

The diagnostic workup for EN includes punch biopsy of deep adipose tissue and throat culture, and when indicated, ASO titer (if strep is suspected) and chest films (to rule out tuberculosis and sarcoid). In most cases, the diagnosis can be made on clinical grounds alone, although the triggering entity may be difficult to identify. The identification and elimination of the underlying trigger is nonetheless crucial for diagnosis and treatment.

That issue aside, most cases of EN resolve with minimal treatment; this can include the use of NSAIDs and elevation of the limbs when possible. In this particular case, the intense pain the patient was experiencing called for stronger therapy (ibuprofen 800 mg tid, plus a two-week taper of prednisone 40 mg). She responded quite well, and the problem was almost totally resolved at a follow-up visit several weeks later.

In the absence of findings to the contrary, it is likely that the trigger for this patient’s EN was strep, given the timing of its manifestation after a sore throat.