Joe R. Monroe, MPAS, PA

A 12-year-old girl is referred by her pediatrician for evaluation and treatment of facial lesions. She’s had them for almost five years, and several treatment attempts have been unsuccessful. Most recently, she tried topical adapalene gel for presumed acne, but this only irritated the area and had no beneficial effect on the “bumps.” Oral antibiotics did not help, either.

The presenting complaint is complicated somewhat by the fact that the same area of her skin is often dark—a problem thought to be related. The patient admits to licking her lips frequently (something her parents have also observed).

The patient’s history is significant for Hodgkin’s lymphoma, diagnosed and successfully treated five years ago. It was around that time that the bumps first appeared, while she was undergoing chemotherapy.

EXAMINATION
There is a ring of sharply demarcated, modest hyperpigmentation around the entire perioral area, extending outward about 2 cm. Closer questioning reveals that this aspect of the problem “comes and goes.” 

The main concern is the collection of planar, pinkish brown papules around the mouth. These are mostly located inferior to the lips, although a few tiny papules are on the maxilla. All papules are uniform in size (≤ 1 mm) and shape. None are inflamed or umbilicated.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
The HPV family has more than 100 distinct DNA types, several of which have particular morphologic characteristics and favored locations. Depending on the affected site, warts can assume many appearances, including planar (flat-topped) papules that generally favor the legs and face of a child or adolescent. Chemotherapy made this patient susceptible, and the lack of a diagnosis in the intervening years compounded the problem.

The perioral hyperpigmentation is, of course, secondary to her lip licking, which dries and irritates the thin facial skin. On a blond or red-haired, fair-skinned patient, it would appear pink or red. But with our patient’s type IV skin, inflammation begets darkening. The two problems are probably unrelated. 

Treatment of flat warts on the face of a young woman is problematic, especially when dark skin is a factor. Treatments such as liquid nitrogen would not only be painful if applied to the face but could also cause permanent pigment changes. Irritants and acids (eg, cantharidin or salicylic acid) would have that same potential, so we tend to treat this area with the least invasive, least irritating modalities, knowing that the perfect treatment has yet to be invented. 

A sinecatechins ointment —a botanical product made from the extract of green tea leaves—was prescribed. The patient was instructed to apply it three times per day for a month, then return to the clinic for re-evaluation. Treatment alternatives at that point will include imiquimod, which stimulates the skin to produce interferon (known to discourage viral growth) and 5-fluorouracil (5FU) cream, which has also been used with some success for warts. (For the record, I have no financial interest in any of these products.)

Chances are good that with time and treatment, the patient’s warts will disappear. It should be noted that the differential included acne, molluscum contagiosum, and perioral dermatitis. A simple shallow shave biopsy could have been performed to confirm the diagnosis, if necessary.

TAKE-HOME LEARNING POINTS
• The HPV family of warts contains more than 100 distinct genomic types, which can present in a wide variety of morphologies.

• Flat warts (verucca planae) are commonly seen on faces and legs but can appear in other locations. Shaving spreads them.

• No perfect treatment for warts exists. All have drawbacks, including potential for irritation, pain, and dyschromia—the latter a particular problem for patients with darker skin.

• For these patients, sinecatechins ointment, imiquimod, and 5-fluorouracil cream are decent choices. 

A 12-year-old girl is referred by her pediatrician for evaluation and treatment of facial lesions. She’s had them for almost five years, and several treatment attempts have been unsuccessful. Most recently, she tried topical adapalene gel for presumed acne, but this only irritated the area and had no beneficial effect on the “bumps.” Oral antibiotics did not help, either.

The presenting complaint is complicated somewhat by the fact that the same area of her skin is often dark—a problem thought to be related. The patient admits to licking her lips frequently (something her parents have also observed).

The patient’s history is significant for Hodgkin’s lymphoma, diagnosed and successfully treated five years ago. It was around that time that the bumps first appeared, while she was undergoing chemotherapy.

EXAMINATION
There is a ring of sharply demarcated, modest hyperpigmentation around the entire perioral area, extending outward about 2 cm. Closer questioning reveals that this aspect of the problem “comes and goes.” 

The main concern is the collection of planar, pinkish brown papules around the mouth. These are mostly located inferior to the lips, although a few tiny papules are on the maxilla. All papules are uniform in size (≤ 1 mm) and shape. None are inflamed or umbilicated.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
The HPV family has more than 100 distinct DNA types, several of which have particular morphologic characteristics and favored locations. Depending on the affected site, warts can assume many appearances, including planar (flat-topped) papules that generally favor the legs and face of a child or adolescent. Chemotherapy made this patient susceptible, and the lack of a diagnosis in the intervening years compounded the problem.

The perioral hyperpigmentation is, of course, secondary to her lip licking, which dries and irritates the thin facial skin. On a blond or red-haired, fair-skinned patient, it would appear pink or red. But with our patient’s type IV skin, inflammation begets darkening. The two problems are probably unrelated. 

Treatment of flat warts on the face of a young woman is problematic, especially when dark skin is a factor. Treatments such as liquid nitrogen would not only be painful if applied to the face but could also cause permanent pigment changes. Irritants and acids (eg, cantharidin or salicylic acid) would have that same potential, so we tend to treat this area with the least invasive, least irritating modalities, knowing that the perfect treatment has yet to be invented. 

A sinecatechins ointment —a botanical product made from the extract of green tea leaves—was prescribed. The patient was instructed to apply it three times per day for a month, then return to the clinic for re-evaluation. Treatment alternatives at that point will include imiquimod, which stimulates the skin to produce interferon (known to discourage viral growth) and 5-fluorouracil (5FU) cream, which has also been used with some success for warts. (For the record, I have no financial interest in any of these products.)

Chances are good that with time and treatment, the patient’s warts will disappear. It should be noted that the differential included acne, molluscum contagiosum, and perioral dermatitis. A simple shallow shave biopsy could have been performed to confirm the diagnosis, if necessary.

TAKE-HOME LEARNING POINTS
• The HPV family of warts contains more than 100 distinct genomic types, which can present in a wide variety of morphologies.

• Flat warts (verucca planae) are commonly seen on faces and legs but can appear in other locations. Shaving spreads them.

• No perfect treatment for warts exists. All have drawbacks, including potential for irritation, pain, and dyschromia—the latter a particular problem for patients with darker skin.

• For these patients, sinecatechins ointment, imiquimod, and 5-fluorouracil cream are decent choices. 

A 12-year-old girl is referred by her pediatrician for evaluation and treatment of facial lesions. She’s had them for almost five years, and several treatment attempts have been unsuccessful. Most recently, she tried topical adapalene gel for presumed acne, but this only irritated the area and had no beneficial effect on the “bumps.” Oral antibiotics did not help, either.

The presenting complaint is complicated somewhat by the fact that the same area of her skin is often dark—a problem thought to be related. The patient admits to licking her lips frequently (something her parents have also observed).

The patient’s history is significant for Hodgkin’s lymphoma, diagnosed and successfully treated five years ago. It was around that time that the bumps first appeared, while she was undergoing chemotherapy.

EXAMINATION
There is a ring of sharply demarcated, modest hyperpigmentation around the entire perioral area, extending outward about 2 cm. Closer questioning reveals that this aspect of the problem “comes and goes.” 

The main concern is the collection of planar, pinkish brown papules around the mouth. These are mostly located inferior to the lips, although a few tiny papules are on the maxilla. All papules are uniform in size (≤ 1 mm) and shape. None are inflamed or umbilicated.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
The HPV family has more than 100 distinct DNA types, several of which have particular morphologic characteristics and favored locations. Depending on the affected site, warts can assume many appearances, including planar (flat-topped) papules that generally favor the legs and face of a child or adolescent. Chemotherapy made this patient susceptible, and the lack of a diagnosis in the intervening years compounded the problem.

The perioral hyperpigmentation is, of course, secondary to her lip licking, which dries and irritates the thin facial skin. On a blond or red-haired, fair-skinned patient, it would appear pink or red. But with our patient’s type IV skin, inflammation begets darkening. The two problems are probably unrelated. 

Treatment of flat warts on the face of a young woman is problematic, especially when dark skin is a factor. Treatments such as liquid nitrogen would not only be painful if applied to the face but could also cause permanent pigment changes. Irritants and acids (eg, cantharidin or salicylic acid) would have that same potential, so we tend to treat this area with the least invasive, least irritating modalities, knowing that the perfect treatment has yet to be invented. 

A sinecatechins ointment —a botanical product made from the extract of green tea leaves—was prescribed. The patient was instructed to apply it three times per day for a month, then return to the clinic for re-evaluation. Treatment alternatives at that point will include imiquimod, which stimulates the skin to produce interferon (known to discourage viral growth) and 5-fluorouracil (5FU) cream, which has also been used with some success for warts. (For the record, I have no financial interest in any of these products.)

Chances are good that with time and treatment, the patient’s warts will disappear. It should be noted that the differential included acne, molluscum contagiosum, and perioral dermatitis. A simple shallow shave biopsy could have been performed to confirm the diagnosis, if necessary.

TAKE-HOME LEARNING POINTS
• The HPV family of warts contains more than 100 distinct genomic types, which can present in a wide variety of morphologies.

• Flat warts (verucca planae) are commonly seen on faces and legs but can appear in other locations. Shaving spreads them.

• No perfect treatment for warts exists. All have drawbacks, including potential for irritation, pain, and dyschromia—the latter a particular problem for patients with darker skin.

• For these patients, sinecatechins ointment, imiquimod, and 5-fluorouracil cream are decent choices. 

Six month ago, this 36-year-old man’s left fourth finger began to bother him. He’s tried topical antibiotics (triple-antibiotic cream and mupirocin), hot soaks in solutions of Epsom salts, application of colloidal silver solution, and courses of two different oral antibiotics (cephalexin and ciprofloxacin). None have provided any relief from the pain.

The patient admits removing a hangnail from the nail in question, causing a little bleeding. Then followed the slow onset of chronic pain and swelling, which has never been severe but is painful enough to interfere with normal activities—particularly his job, which requires extensive computer time.

EXAMINATION
The medial perionychial area of his left fourth finger is modestly swollen and red and markedly tender to touch. No pus can be expressed from the area, and there are no palpable lymph nodes in either the epitrochlear or axillary locations of this arm. No lymphangiitic streaking is seen on the hand or arm. The affected area is a small section of the nail fold, where glistening, friable tissue is seen in the proximal invaginated area.

After a brief discussion of treatment alternatives, the decision is made to anesthetize the digit by means of a digital block, using 2 cc of 2% plain lidocaine. Once anesthesia is achieved, the hand is elevated above the chest and a tourniquet applied to minimize bleeding. The back of the patient’s hand is placed on his chest, then the swollen nail fold is pulled back. A 3-mm remnant of hangnail, still attached proximally, is revealed. It is removed and the area curetted. The site is cleaned and dressed, then the tourniquet is released. 

Within 2 weeks, the finger is no longer swollen or painful. 

Continue for Joe Monroe's discussion and take-home learning points >> 

DISCUSSION
“Infection” is only one potential cause of redness, swelling, increased warmth, and localized pain. Classically termed rubor, tumor, calor, and dolor, these are indicators of inflammation, which can occur in many conditions besides “infection.” One tragic example is inflammatory breast cancer, which is all too often mistreated as mastitis until the lack of response to treatment finally forces—often belatedly—consideration of other items in the differential.

A far less dramatic example is the case described, in which a simple hangnail is incompletely removed, leaving a shard of nail that then digs into the perionychial skin as it grows out. This sets into motion a healing process that cannot proceed to resolution, because the tissue is re-injured every time the finger strikes the computer keyboard. This not only causes the wound to get stuck in a certain phase of healing (angioneogenesis) but also prevents completion of the process. The tissue’s response is what we see with this patient, invariably (and erroneously) called “infection.”

This is basically the identical process we see with ingrown toenails, except for the unfortunate fact that we stand upright, compress the toe with a shoe, and walk on it—all of which greatly magnify the pain, redness, and swelling. With toes more than fingers, we also tend to see the production of a button of granulated tissue at the site. This results from ongoing, inappropriate angioneogenesis. Sometimes termed pyogenic granuloma (or sclerosing hemangioma), this tissue is quite friable and bleeds copiously with any amount of trauma.

Ironically, acute bacterial paronychia of the fingers, usually caused by ordinary staph, can start in much the same way (without, of course, the retained nail shard). However, it presents with more focal concentration of redness and swelling, a collection of thick, green pus, and exquisite tenderness, all of which is relieved by simple incision and drainage.

With this patient, and those with ingrown toenails, it’s quite compelling to prescribe oral antibiotics. But these never help, and for good reason: The problem is intolerance of the “foreign body,” not infection. The solution is to “reboot” the healing process by removing the offending nail shard.

TAKE-HOME LEARNING POINTS
• While “ingrown fingernails” are far less common than ingrown toenails, both are caused by nail fragments slicing into live tissue. 

• The cure is to remove the offending fragment, which allows the wound to heal.

• For ingrown toenails, an extra step is often necessary: destroying the offending segment of nail matrix with curettement and/or application of phenol.

• Anesthesia for digits should never be accomplished by local infiltration of the affected area for these kinds of procedures. Instead, employ a digital block technique, which is far less painful and provides complete anesthesia when done properly.

• Resist the urge to reflexively diagnose “infection” when confronted with redness, swelling, etc. Instead, consider other potential causes for inflammation first.

Six month ago, this 36-year-old man’s left fourth finger began to bother him. He’s tried topical antibiotics (triple-antibiotic cream and mupirocin), hot soaks in solutions of Epsom salts, application of colloidal silver solution, and courses of two different oral antibiotics (cephalexin and ciprofloxacin). None have provided any relief from the pain.

The patient admits removing a hangnail from the nail in question, causing a little bleeding. Then followed the slow onset of chronic pain and swelling, which has never been severe but is painful enough to interfere with normal activities—particularly his job, which requires extensive computer time.

EXAMINATION
The medial perionychial area of his left fourth finger is modestly swollen and red and markedly tender to touch. No pus can be expressed from the area, and there are no palpable lymph nodes in either the epitrochlear or axillary locations of this arm. No lymphangiitic streaking is seen on the hand or arm. The affected area is a small section of the nail fold, where glistening, friable tissue is seen in the proximal invaginated area.

After a brief discussion of treatment alternatives, the decision is made to anesthetize the digit by means of a digital block, using 2 cc of 2% plain lidocaine. Once anesthesia is achieved, the hand is elevated above the chest and a tourniquet applied to minimize bleeding. The back of the patient’s hand is placed on his chest, then the swollen nail fold is pulled back. A 3-mm remnant of hangnail, still attached proximally, is revealed. It is removed and the area curetted. The site is cleaned and dressed, then the tourniquet is released. 

Within 2 weeks, the finger is no longer swollen or painful. 

Continue for Joe Monroe's discussion and take-home learning points >> 

DISCUSSION
“Infection” is only one potential cause of redness, swelling, increased warmth, and localized pain. Classically termed rubor, tumor, calor, and dolor, these are indicators of inflammation, which can occur in many conditions besides “infection.” One tragic example is inflammatory breast cancer, which is all too often mistreated as mastitis until the lack of response to treatment finally forces—often belatedly—consideration of other items in the differential.

A far less dramatic example is the case described, in which a simple hangnail is incompletely removed, leaving a shard of nail that then digs into the perionychial skin as it grows out. This sets into motion a healing process that cannot proceed to resolution, because the tissue is re-injured every time the finger strikes the computer keyboard. This not only causes the wound to get stuck in a certain phase of healing (angioneogenesis) but also prevents completion of the process. The tissue’s response is what we see with this patient, invariably (and erroneously) called “infection.”

This is basically the identical process we see with ingrown toenails, except for the unfortunate fact that we stand upright, compress the toe with a shoe, and walk on it—all of which greatly magnify the pain, redness, and swelling. With toes more than fingers, we also tend to see the production of a button of granulated tissue at the site. This results from ongoing, inappropriate angioneogenesis. Sometimes termed pyogenic granuloma (or sclerosing hemangioma), this tissue is quite friable and bleeds copiously with any amount of trauma.

Ironically, acute bacterial paronychia of the fingers, usually caused by ordinary staph, can start in much the same way (without, of course, the retained nail shard). However, it presents with more focal concentration of redness and swelling, a collection of thick, green pus, and exquisite tenderness, all of which is relieved by simple incision and drainage.

With this patient, and those with ingrown toenails, it’s quite compelling to prescribe oral antibiotics. But these never help, and for good reason: The problem is intolerance of the “foreign body,” not infection. The solution is to “reboot” the healing process by removing the offending nail shard.

TAKE-HOME LEARNING POINTS
• While “ingrown fingernails” are far less common than ingrown toenails, both are caused by nail fragments slicing into live tissue. 

• The cure is to remove the offending fragment, which allows the wound to heal.

• For ingrown toenails, an extra step is often necessary: destroying the offending segment of nail matrix with curettement and/or application of phenol.

• Anesthesia for digits should never be accomplished by local infiltration of the affected area for these kinds of procedures. Instead, employ a digital block technique, which is far less painful and provides complete anesthesia when done properly.

• Resist the urge to reflexively diagnose “infection” when confronted with redness, swelling, etc. Instead, consider other potential causes for inflammation first.

Six month ago, this 36-year-old man’s left fourth finger began to bother him. He’s tried topical antibiotics (triple-antibiotic cream and mupirocin), hot soaks in solutions of Epsom salts, application of colloidal silver solution, and courses of two different oral antibiotics (cephalexin and ciprofloxacin). None have provided any relief from the pain.

The patient admits removing a hangnail from the nail in question, causing a little bleeding. Then followed the slow onset of chronic pain and swelling, which has never been severe but is painful enough to interfere with normal activities—particularly his job, which requires extensive computer time.

EXAMINATION
The medial perionychial area of his left fourth finger is modestly swollen and red and markedly tender to touch. No pus can be expressed from the area, and there are no palpable lymph nodes in either the epitrochlear or axillary locations of this arm. No lymphangiitic streaking is seen on the hand or arm. The affected area is a small section of the nail fold, where glistening, friable tissue is seen in the proximal invaginated area.

After a brief discussion of treatment alternatives, the decision is made to anesthetize the digit by means of a digital block, using 2 cc of 2% plain lidocaine. Once anesthesia is achieved, the hand is elevated above the chest and a tourniquet applied to minimize bleeding. The back of the patient’s hand is placed on his chest, then the swollen nail fold is pulled back. A 3-mm remnant of hangnail, still attached proximally, is revealed. It is removed and the area curetted. The site is cleaned and dressed, then the tourniquet is released. 

Within 2 weeks, the finger is no longer swollen or painful. 

Continue for Joe Monroe's discussion and take-home learning points >> 

DISCUSSION
“Infection” is only one potential cause of redness, swelling, increased warmth, and localized pain. Classically termed rubor, tumor, calor, and dolor, these are indicators of inflammation, which can occur in many conditions besides “infection.” One tragic example is inflammatory breast cancer, which is all too often mistreated as mastitis until the lack of response to treatment finally forces—often belatedly—consideration of other items in the differential.

A far less dramatic example is the case described, in which a simple hangnail is incompletely removed, leaving a shard of nail that then digs into the perionychial skin as it grows out. This sets into motion a healing process that cannot proceed to resolution, because the tissue is re-injured every time the finger strikes the computer keyboard. This not only causes the wound to get stuck in a certain phase of healing (angioneogenesis) but also prevents completion of the process. The tissue’s response is what we see with this patient, invariably (and erroneously) called “infection.”

This is basically the identical process we see with ingrown toenails, except for the unfortunate fact that we stand upright, compress the toe with a shoe, and walk on it—all of which greatly magnify the pain, redness, and swelling. With toes more than fingers, we also tend to see the production of a button of granulated tissue at the site. This results from ongoing, inappropriate angioneogenesis. Sometimes termed pyogenic granuloma (or sclerosing hemangioma), this tissue is quite friable and bleeds copiously with any amount of trauma.

Ironically, acute bacterial paronychia of the fingers, usually caused by ordinary staph, can start in much the same way (without, of course, the retained nail shard). However, it presents with more focal concentration of redness and swelling, a collection of thick, green pus, and exquisite tenderness, all of which is relieved by simple incision and drainage.

With this patient, and those with ingrown toenails, it’s quite compelling to prescribe oral antibiotics. But these never help, and for good reason: The problem is intolerance of the “foreign body,” not infection. The solution is to “reboot” the healing process by removing the offending nail shard.

TAKE-HOME LEARNING POINTS
• While “ingrown fingernails” are far less common than ingrown toenails, both are caused by nail fragments slicing into live tissue. 

• The cure is to remove the offending fragment, which allows the wound to heal.

• For ingrown toenails, an extra step is often necessary: destroying the offending segment of nail matrix with curettement and/or application of phenol.

• Anesthesia for digits should never be accomplished by local infiltration of the affected area for these kinds of procedures. Instead, employ a digital block technique, which is far less painful and provides complete anesthesia when done properly.

• Resist the urge to reflexively diagnose “infection” when confronted with redness, swelling, etc. Instead, consider other potential causes for inflammation first.

An 18-year-old boy is brought by his parents for evaluation of several relatively minor skin problems, including warts, moles, and skin tags. The patient’s history is notable for multiple as-yet-unexplained bony fractures that have occurred with minimal trauma since he was born. He has a brother who was diagnosed with osteogenesis imperfecta, yet, despite an extensive workup, the patient’s constellation of findings has thus far failed to corroborate that or any other definitive diagnosis.

As an afterthought, the parents also ask about changes they have noted on the patient's gums.

There is no history of seizures, and the patient takes no medication regularly.

EXAMINATION
The potential connection to a heritable syndrome draws attention to the patient’s teeth and gums. The latter appear to be overgrown and, as such, far more prominent than normal. They also appear a bit inflamed, especially the portion of the gingiva bordering the teeth. Advanced gingival recession is noted in some of these locations. Closer examination reveals extensive plaque formation on the adjacent teeth. 

During the exam, the patient is observed to be a mouth-breather. His parents corroborate this fact.

Continue for Joe Monroe's discussion and learning points >>

DISCUSSION
The most common cause of gingival overgrowth (GO) is thought to be gingivitis, itself a result of inflammation caused by dental plaque and plaque-associated bacteria. The obvious gingivitis, gingival recession, and extensive dental plaque seen in this patient are more common in younger, mouth-breathing persons. Higher levels of growth hormone might account for the gingival growth, while the dehydration of teeth and gums promoted by mouth-breathing appears to exacerbate gingivitis.

Formerly called gingival hyperplasia, the term gingival overgrowth has been posited as more inclusive of all forms of such findings. Advocates of this change in terminology point out that confirmation of the diagnosis of gingival hypertrophy (an increase in the size of individual cells) or gingival hyperplasia (an increase in the number of cells) would require biopsy and microscopic examination.

Three major categories of potential causes of GO are commonly described in the literature. They include (in descending order of frequency):

1. Inflammation: such as that described, with apparent connection with gingivitis

2. Drugs: A number of medications have been associated with GO, including anticonvulsants such as phenytoin (approximately 50% of cases), calcium channel blockers such as nifedipine (20%), and immunosuppressants such as cyclosporine (30%).

3. Systemic causes: These include pregnancy, puberty, vitamin C deficiency, leukemia, and granulomatous diseases such as Wegener granulomatosis. It can also manifest as a perineoplastic sign (associated with known or occult cancers).

Treatment, of course, depends on the cause. Even when drugs are to blame, however, co-existing gingivitis can be a contributing factor; it can be addressed with plaque scaling, better dental care, or even gingivectomy. Drugs can be changed or eliminated or doses can be reduced. Other, less common systemic conditions associated with GO can be sought through additional history, laboratory work, and more extensive examination.

TAKE-HOME LEARNING POINTS
• The term gingival hypertrophy is being replaced by the more inclusive gingival overgrowth (GO).

• The most common cause of GO is chronic gingivitis.

• Drug classes associated with GO include anticonvulsants, calcium channel blockers, and immunosuppressants.

• Systemic diseases can trigger GO; these include pregnancy, puberty, and cancer (eg, leukemia).

• Addressing oral hygiene is a good place to start treatment of GO, regardless of the trigger, since it often co-exists with other causation. 

An 18-year-old boy is brought by his parents for evaluation of several relatively minor skin problems, including warts, moles, and skin tags. The patient’s history is notable for multiple as-yet-unexplained bony fractures that have occurred with minimal trauma since he was born. He has a brother who was diagnosed with osteogenesis imperfecta, yet, despite an extensive workup, the patient’s constellation of findings has thus far failed to corroborate that or any other definitive diagnosis.

As an afterthought, the parents also ask about changes they have noted on the patient's gums.

There is no history of seizures, and the patient takes no medication regularly.

EXAMINATION
The potential connection to a heritable syndrome draws attention to the patient’s teeth and gums. The latter appear to be overgrown and, as such, far more prominent than normal. They also appear a bit inflamed, especially the portion of the gingiva bordering the teeth. Advanced gingival recession is noted in some of these locations. Closer examination reveals extensive plaque formation on the adjacent teeth. 

During the exam, the patient is observed to be a mouth-breather. His parents corroborate this fact.

Continue for Joe Monroe's discussion and learning points >>

DISCUSSION
The most common cause of gingival overgrowth (GO) is thought to be gingivitis, itself a result of inflammation caused by dental plaque and plaque-associated bacteria. The obvious gingivitis, gingival recession, and extensive dental plaque seen in this patient are more common in younger, mouth-breathing persons. Higher levels of growth hormone might account for the gingival growth, while the dehydration of teeth and gums promoted by mouth-breathing appears to exacerbate gingivitis.

Formerly called gingival hyperplasia, the term gingival overgrowth has been posited as more inclusive of all forms of such findings. Advocates of this change in terminology point out that confirmation of the diagnosis of gingival hypertrophy (an increase in the size of individual cells) or gingival hyperplasia (an increase in the number of cells) would require biopsy and microscopic examination.

Three major categories of potential causes of GO are commonly described in the literature. They include (in descending order of frequency):

1. Inflammation: such as that described, with apparent connection with gingivitis

2. Drugs: A number of medications have been associated with GO, including anticonvulsants such as phenytoin (approximately 50% of cases), calcium channel blockers such as nifedipine (20%), and immunosuppressants such as cyclosporine (30%).

3. Systemic causes: These include pregnancy, puberty, vitamin C deficiency, leukemia, and granulomatous diseases such as Wegener granulomatosis. It can also manifest as a perineoplastic sign (associated with known or occult cancers).

Treatment, of course, depends on the cause. Even when drugs are to blame, however, co-existing gingivitis can be a contributing factor; it can be addressed with plaque scaling, better dental care, or even gingivectomy. Drugs can be changed or eliminated or doses can be reduced. Other, less common systemic conditions associated with GO can be sought through additional history, laboratory work, and more extensive examination.

TAKE-HOME LEARNING POINTS
• The term gingival hypertrophy is being replaced by the more inclusive gingival overgrowth (GO).

• The most common cause of GO is chronic gingivitis.

• Drug classes associated with GO include anticonvulsants, calcium channel blockers, and immunosuppressants.

• Systemic diseases can trigger GO; these include pregnancy, puberty, and cancer (eg, leukemia).

• Addressing oral hygiene is a good place to start treatment of GO, regardless of the trigger, since it often co-exists with other causation. 

An 18-year-old boy is brought by his parents for evaluation of several relatively minor skin problems, including warts, moles, and skin tags. The patient’s history is notable for multiple as-yet-unexplained bony fractures that have occurred with minimal trauma since he was born. He has a brother who was diagnosed with osteogenesis imperfecta, yet, despite an extensive workup, the patient’s constellation of findings has thus far failed to corroborate that or any other definitive diagnosis.

As an afterthought, the parents also ask about changes they have noted on the patient's gums.

There is no history of seizures, and the patient takes no medication regularly.

EXAMINATION
The potential connection to a heritable syndrome draws attention to the patient’s teeth and gums. The latter appear to be overgrown and, as such, far more prominent than normal. They also appear a bit inflamed, especially the portion of the gingiva bordering the teeth. Advanced gingival recession is noted in some of these locations. Closer examination reveals extensive plaque formation on the adjacent teeth. 

During the exam, the patient is observed to be a mouth-breather. His parents corroborate this fact.

Continue for Joe Monroe's discussion and learning points >>

DISCUSSION
The most common cause of gingival overgrowth (GO) is thought to be gingivitis, itself a result of inflammation caused by dental plaque and plaque-associated bacteria. The obvious gingivitis, gingival recession, and extensive dental plaque seen in this patient are more common in younger, mouth-breathing persons. Higher levels of growth hormone might account for the gingival growth, while the dehydration of teeth and gums promoted by mouth-breathing appears to exacerbate gingivitis.

Formerly called gingival hyperplasia, the term gingival overgrowth has been posited as more inclusive of all forms of such findings. Advocates of this change in terminology point out that confirmation of the diagnosis of gingival hypertrophy (an increase in the size of individual cells) or gingival hyperplasia (an increase in the number of cells) would require biopsy and microscopic examination.

Three major categories of potential causes of GO are commonly described in the literature. They include (in descending order of frequency):

1. Inflammation: such as that described, with apparent connection with gingivitis

2. Drugs: A number of medications have been associated with GO, including anticonvulsants such as phenytoin (approximately 50% of cases), calcium channel blockers such as nifedipine (20%), and immunosuppressants such as cyclosporine (30%).

3. Systemic causes: These include pregnancy, puberty, vitamin C deficiency, leukemia, and granulomatous diseases such as Wegener granulomatosis. It can also manifest as a perineoplastic sign (associated with known or occult cancers).

Treatment, of course, depends on the cause. Even when drugs are to blame, however, co-existing gingivitis can be a contributing factor; it can be addressed with plaque scaling, better dental care, or even gingivectomy. Drugs can be changed or eliminated or doses can be reduced. Other, less common systemic conditions associated with GO can be sought through additional history, laboratory work, and more extensive examination.

TAKE-HOME LEARNING POINTS
• The term gingival hypertrophy is being replaced by the more inclusive gingival overgrowth (GO).

• The most common cause of GO is chronic gingivitis.

• Drug classes associated with GO include anticonvulsants, calcium channel blockers, and immunosuppressants.

• Systemic diseases can trigger GO; these include pregnancy, puberty, and cancer (eg, leukemia).

• Addressing oral hygiene is a good place to start treatment of GO, regardless of the trigger, since it often co-exists with other causation. 

A 41-year-old man complains of “red lines” that appear on his skin soon after minor scratching trauma. They manifest rapidly but disappear within minutes (occasionally as long as an hour), leaving no trace. They cause no symptoms but are nonetheless disturbing to the patient.

In terms of his overall health, the patient has few problems beyond mild seasonal allergies. However, he reports experiencing a great deal of stress recently. He denies taking any prescription medications regularly, though in the spring, he often takes OTC antihistamines to ward off sneezing and itchy eyes.

EXAMINATION
A linear wheal appears after the skin is scratched with the dull edge of a fingernail. The initial reaction to the scratch is a macular red flare, followed within seconds by a broadening band of erythema. Seconds later, the frank wheal appears. The lesion is warmer than the surrounding skin but not at all tender. As expected, it clears completely within a few minutes, leaving no sign of its ever having been there.

On the next page: Diagnosis and Joe Monroe's Discussion >>

DISCUSSION
This form of urticaria is called dermatographism (literally, “skin writing”) and is of unknown origin. It affects 2% to 5% of the population. Most affected patients are asymptomatic, although perhaps 10% of them will report itching and burning. This condition exhibits neither gender nor race bias.

Dermatographism is the most common form of the physical urticarias, which can also be caused by pressure, cold, and vibration. The speed with which the wheal forms is remarkable and unique to histamine-mediated conditions, though the exact mechanism is debatable. (Its three-stage formation is collectively referred to as the triple response of Lewis.) One theory holds that the trauma of scratching provokes an antigen to interact with mast cell bound IgE, triggering the release of inflammatory mediators (eg, histamine, bradykinins, or leukotrienes). Bolstering this theory is the observation that 75% of patients with hypereosinophilic syndrome have dermatographism.

Dermatographism effectively confirms the presence of traditional urticaria, itself more common in atopic patients. The rapidity of the appearance and disappearance of urticaria, a phenomenon termed evanescence, often presents a challenge to diagnosis until it is confirmed.

Most patients with dermatographism first note it in their second to third decade of life. When it’s congenital, symptomatic dermatographism suggests the possibility of a mast cell disorder, such as urticaria pigmentosa or systemic mastocytosis. These can be confirmed by biopsy and/or measurement of histamine in a 24-hour urine sample. 

TAKE-HOME LEARNING POINTS
• Dermatographism is an extremely common form of physical urticaria.

• It is asymptomatic in the majority of cases and disappears on its own in minutes to hours.

• It can herald the presence of more serious chronic symptomatic urticaria.

• The rapid appearance of the linear wheal and its subsequent rapid disappearance, termed evanescence, are unique to urticarial disorders.

• The phenomena by which the initial red linear flare widens quickly before forming the evanescent linear wheal are collectively known as the “triple response of Lewis.”

A 41-year-old man complains of “red lines” that appear on his skin soon after minor scratching trauma. They manifest rapidly but disappear within minutes (occasionally as long as an hour), leaving no trace. They cause no symptoms but are nonetheless disturbing to the patient.

In terms of his overall health, the patient has few problems beyond mild seasonal allergies. However, he reports experiencing a great deal of stress recently. He denies taking any prescription medications regularly, though in the spring, he often takes OTC antihistamines to ward off sneezing and itchy eyes.

EXAMINATION
A linear wheal appears after the skin is scratched with the dull edge of a fingernail. The initial reaction to the scratch is a macular red flare, followed within seconds by a broadening band of erythema. Seconds later, the frank wheal appears. The lesion is warmer than the surrounding skin but not at all tender. As expected, it clears completely within a few minutes, leaving no sign of its ever having been there.

On the next page: Diagnosis and Joe Monroe's Discussion >>

DISCUSSION
This form of urticaria is called dermatographism (literally, “skin writing”) and is of unknown origin. It affects 2% to 5% of the population. Most affected patients are asymptomatic, although perhaps 10% of them will report itching and burning. This condition exhibits neither gender nor race bias.

Dermatographism is the most common form of the physical urticarias, which can also be caused by pressure, cold, and vibration. The speed with which the wheal forms is remarkable and unique to histamine-mediated conditions, though the exact mechanism is debatable. (Its three-stage formation is collectively referred to as the triple response of Lewis.) One theory holds that the trauma of scratching provokes an antigen to interact with mast cell bound IgE, triggering the release of inflammatory mediators (eg, histamine, bradykinins, or leukotrienes). Bolstering this theory is the observation that 75% of patients with hypereosinophilic syndrome have dermatographism.

Dermatographism effectively confirms the presence of traditional urticaria, itself more common in atopic patients. The rapidity of the appearance and disappearance of urticaria, a phenomenon termed evanescence, often presents a challenge to diagnosis until it is confirmed.

Most patients with dermatographism first note it in their second to third decade of life. When it’s congenital, symptomatic dermatographism suggests the possibility of a mast cell disorder, such as urticaria pigmentosa or systemic mastocytosis. These can be confirmed by biopsy and/or measurement of histamine in a 24-hour urine sample. 

TAKE-HOME LEARNING POINTS
• Dermatographism is an extremely common form of physical urticaria.

• It is asymptomatic in the majority of cases and disappears on its own in minutes to hours.

• It can herald the presence of more serious chronic symptomatic urticaria.

• The rapid appearance of the linear wheal and its subsequent rapid disappearance, termed evanescence, are unique to urticarial disorders.

• The phenomena by which the initial red linear flare widens quickly before forming the evanescent linear wheal are collectively known as the “triple response of Lewis.”

A 41-year-old man complains of “red lines” that appear on his skin soon after minor scratching trauma. They manifest rapidly but disappear within minutes (occasionally as long as an hour), leaving no trace. They cause no symptoms but are nonetheless disturbing to the patient.

In terms of his overall health, the patient has few problems beyond mild seasonal allergies. However, he reports experiencing a great deal of stress recently. He denies taking any prescription medications regularly, though in the spring, he often takes OTC antihistamines to ward off sneezing and itchy eyes.

EXAMINATION
A linear wheal appears after the skin is scratched with the dull edge of a fingernail. The initial reaction to the scratch is a macular red flare, followed within seconds by a broadening band of erythema. Seconds later, the frank wheal appears. The lesion is warmer than the surrounding skin but not at all tender. As expected, it clears completely within a few minutes, leaving no sign of its ever having been there.

On the next page: Diagnosis and Joe Monroe's Discussion >>

DISCUSSION
This form of urticaria is called dermatographism (literally, “skin writing”) and is of unknown origin. It affects 2% to 5% of the population. Most affected patients are asymptomatic, although perhaps 10% of them will report itching and burning. This condition exhibits neither gender nor race bias.

Dermatographism is the most common form of the physical urticarias, which can also be caused by pressure, cold, and vibration. The speed with which the wheal forms is remarkable and unique to histamine-mediated conditions, though the exact mechanism is debatable. (Its three-stage formation is collectively referred to as the triple response of Lewis.) One theory holds that the trauma of scratching provokes an antigen to interact with mast cell bound IgE, triggering the release of inflammatory mediators (eg, histamine, bradykinins, or leukotrienes). Bolstering this theory is the observation that 75% of patients with hypereosinophilic syndrome have dermatographism.

Dermatographism effectively confirms the presence of traditional urticaria, itself more common in atopic patients. The rapidity of the appearance and disappearance of urticaria, a phenomenon termed evanescence, often presents a challenge to diagnosis until it is confirmed.

Most patients with dermatographism first note it in their second to third decade of life. When it’s congenital, symptomatic dermatographism suggests the possibility of a mast cell disorder, such as urticaria pigmentosa or systemic mastocytosis. These can be confirmed by biopsy and/or measurement of histamine in a 24-hour urine sample. 

TAKE-HOME LEARNING POINTS
• Dermatographism is an extremely common form of physical urticaria.

• It is asymptomatic in the majority of cases and disappears on its own in minutes to hours.

• It can herald the presence of more serious chronic symptomatic urticaria.

• The rapid appearance of the linear wheal and its subsequent rapid disappearance, termed evanescence, are unique to urticarial disorders.

• The phenomena by which the initial red linear flare widens quickly before forming the evanescent linear wheal are collectively known as the “triple response of Lewis.”

An 84-year-old man is seeing an audiologist for hearing problems when the medical assistant notices a lesion on the patient’s right ear. When asked about it, the patient acknowledges that it has been bothering him. It itches and won't heal, no matter how much "medicine" the patient applies. Fortunately, it is not painful. But the patient is greatly annoyed that the lesion sometimes bleeds, leaving spots on his pillowcase and clothing.

The audiologist requests a consultation by the dermatology PA at her clinic.

EXAMINATION
The patient is an elderly white man in a wheelchair who is able to communicate readily. He is adamant that the lesion has only been present for about two weeks. However, his wife, who is with him, is sure it has been there for more than a year.

The lesion is a 1.6-cm ulcer with a telangiectatic, rolled pearly border. It is located between the tragus and antitragus on the outer floor of the patient’s external auditory meatus. It is seen in the context of the patient’s very fair and sun-damaged skin, which is also marked by numerous actinic keratoses on his face.

Under local anesthesia, shave biopsy is performed. A 5-mm slice is removed from the periphery of the lesion.

Continue for the outcome and discussion >>

DISCUSSION
The lesion proved to be the expected basal cell carcinoma (BCC), probably caused by sun exposure when the patient was younger. Patients are often incredulous about this connection, but the nuclei of skin cells have a long memory, often taking decades for cancers to actually develop. In a way, it doesn’t matter, since the damage is long since done even if the patient gets almost no sun at the present time.

But it does matter that this lesion is large and located in a difficult spot, one that does not lend itself to an easy fix. Primary closure would not be possible, given the complete lack of slack in the skin. A Mohs surgeon will need to remove the lesion, to ensure complete excision as well as perform the special procedures required to graft the site for closure.

Even though the lesion proved to be “just" a BCC (ie, not a melanoma), it still had to be dealt with lest it continue to spread. More than a few patients have had to have their entire external ear removed for this reason. Although it’s unusual, BCCs can metastasize to local lymph nodes and even to the brain and lung. More than a century ago, these were known as “rodent ulcers” that caused serious problems. If they could be caught in time, local cautery was the only chance at a cure.

The differential in this case included squamous cell carcinoma, which might have presented a more serious problem, given the location (near an orifice). Another diagnostic possibility was sebaceous carcinoma, a merkel cell cancer. Benign lesions, such as chondrodermatitis nodularis chronica helicis, occasionally present as ulcerated lesions on the ear.

BCCs are, far and away, the most common type of skin cancer, with more than a million new cases diagnosed each year in United States. They occur more commonly on fair-skinned patients and on prominently sun-exposed area (eg, ears, noses, and cheeks) but can also appear in areas where the sun seldom shines.

Several types of BCC have been described, but the nonhealing erosive papule (so-called noduloulcerative type) is the most common presentation. BCCs can also resemble scars or rashes. Though they are typically very slow to grow, not all BCCs are indolent. Some are quite aggressive both in terms of morphologic appearance and internal growth. And, as noted above, there is a differential for new, growing lesions in sun-exposed skin, making biopsy of such lesions mandatory.

Continue for Joe Monroe's take home learning points >>

TAKE-HOME LEARNING POINTS
• Nonhealing lesions on sun-exposed skin are considered to be skin cancers until proven otherwise by biopsy.

• Basal cell carcinomas (BCCs) are the most common skin cancer.

• BCCs typically grow very slowly.

• BCCs, if allowed to remain in place, can become extensive, invasive, destructive, and—in exceptional circumstances—can even metastasize.

• The differential for BCC includes squamous cell carcinoma, which has considerably more potential for metastasis than BCC, especially when it’s near an orifice.

• Quite frequently, it’s next to impossible to differentiate visually between BCC and SCC. 

• BCCs and SCCs can take on several different morphologies, so any changing lesion needs to be biopsied to establish its identity, particularly since both are so common. 

An 84-year-old man is seeing an audiologist for hearing problems when the medical assistant notices a lesion on the patient’s right ear. When asked about it, the patient acknowledges that it has been bothering him. It itches and won't heal, no matter how much "medicine" the patient applies. Fortunately, it is not painful. But the patient is greatly annoyed that the lesion sometimes bleeds, leaving spots on his pillowcase and clothing.

The audiologist requests a consultation by the dermatology PA at her clinic.

EXAMINATION
The patient is an elderly white man in a wheelchair who is able to communicate readily. He is adamant that the lesion has only been present for about two weeks. However, his wife, who is with him, is sure it has been there for more than a year.

The lesion is a 1.6-cm ulcer with a telangiectatic, rolled pearly border. It is located between the tragus and antitragus on the outer floor of the patient’s external auditory meatus. It is seen in the context of the patient’s very fair and sun-damaged skin, which is also marked by numerous actinic keratoses on his face.

Under local anesthesia, shave biopsy is performed. A 5-mm slice is removed from the periphery of the lesion.

Continue for the outcome and discussion >>

DISCUSSION
The lesion proved to be the expected basal cell carcinoma (BCC), probably caused by sun exposure when the patient was younger. Patients are often incredulous about this connection, but the nuclei of skin cells have a long memory, often taking decades for cancers to actually develop. In a way, it doesn’t matter, since the damage is long since done even if the patient gets almost no sun at the present time.

But it does matter that this lesion is large and located in a difficult spot, one that does not lend itself to an easy fix. Primary closure would not be possible, given the complete lack of slack in the skin. A Mohs surgeon will need to remove the lesion, to ensure complete excision as well as perform the special procedures required to graft the site for closure.

Even though the lesion proved to be “just" a BCC (ie, not a melanoma), it still had to be dealt with lest it continue to spread. More than a few patients have had to have their entire external ear removed for this reason. Although it’s unusual, BCCs can metastasize to local lymph nodes and even to the brain and lung. More than a century ago, these were known as “rodent ulcers” that caused serious problems. If they could be caught in time, local cautery was the only chance at a cure.

The differential in this case included squamous cell carcinoma, which might have presented a more serious problem, given the location (near an orifice). Another diagnostic possibility was sebaceous carcinoma, a merkel cell cancer. Benign lesions, such as chondrodermatitis nodularis chronica helicis, occasionally present as ulcerated lesions on the ear.

BCCs are, far and away, the most common type of skin cancer, with more than a million new cases diagnosed each year in United States. They occur more commonly on fair-skinned patients and on prominently sun-exposed area (eg, ears, noses, and cheeks) but can also appear in areas where the sun seldom shines.

Several types of BCC have been described, but the nonhealing erosive papule (so-called noduloulcerative type) is the most common presentation. BCCs can also resemble scars or rashes. Though they are typically very slow to grow, not all BCCs are indolent. Some are quite aggressive both in terms of morphologic appearance and internal growth. And, as noted above, there is a differential for new, growing lesions in sun-exposed skin, making biopsy of such lesions mandatory.

Continue for Joe Monroe's take home learning points >>

TAKE-HOME LEARNING POINTS
• Nonhealing lesions on sun-exposed skin are considered to be skin cancers until proven otherwise by biopsy.

• Basal cell carcinomas (BCCs) are the most common skin cancer.

• BCCs typically grow very slowly.

• BCCs, if allowed to remain in place, can become extensive, invasive, destructive, and—in exceptional circumstances—can even metastasize.

• The differential for BCC includes squamous cell carcinoma, which has considerably more potential for metastasis than BCC, especially when it’s near an orifice.

• Quite frequently, it’s next to impossible to differentiate visually between BCC and SCC. 

• BCCs and SCCs can take on several different morphologies, so any changing lesion needs to be biopsied to establish its identity, particularly since both are so common. 

An 84-year-old man is seeing an audiologist for hearing problems when the medical assistant notices a lesion on the patient’s right ear. When asked about it, the patient acknowledges that it has been bothering him. It itches and won't heal, no matter how much "medicine" the patient applies. Fortunately, it is not painful. But the patient is greatly annoyed that the lesion sometimes bleeds, leaving spots on his pillowcase and clothing.

The audiologist requests a consultation by the dermatology PA at her clinic.

EXAMINATION
The patient is an elderly white man in a wheelchair who is able to communicate readily. He is adamant that the lesion has only been present for about two weeks. However, his wife, who is with him, is sure it has been there for more than a year.

The lesion is a 1.6-cm ulcer with a telangiectatic, rolled pearly border. It is located between the tragus and antitragus on the outer floor of the patient’s external auditory meatus. It is seen in the context of the patient’s very fair and sun-damaged skin, which is also marked by numerous actinic keratoses on his face.

Under local anesthesia, shave biopsy is performed. A 5-mm slice is removed from the periphery of the lesion.

Continue for the outcome and discussion >>

DISCUSSION
The lesion proved to be the expected basal cell carcinoma (BCC), probably caused by sun exposure when the patient was younger. Patients are often incredulous about this connection, but the nuclei of skin cells have a long memory, often taking decades for cancers to actually develop. In a way, it doesn’t matter, since the damage is long since done even if the patient gets almost no sun at the present time.

But it does matter that this lesion is large and located in a difficult spot, one that does not lend itself to an easy fix. Primary closure would not be possible, given the complete lack of slack in the skin. A Mohs surgeon will need to remove the lesion, to ensure complete excision as well as perform the special procedures required to graft the site for closure.

Even though the lesion proved to be “just" a BCC (ie, not a melanoma), it still had to be dealt with lest it continue to spread. More than a few patients have had to have their entire external ear removed for this reason. Although it’s unusual, BCCs can metastasize to local lymph nodes and even to the brain and lung. More than a century ago, these were known as “rodent ulcers” that caused serious problems. If they could be caught in time, local cautery was the only chance at a cure.

The differential in this case included squamous cell carcinoma, which might have presented a more serious problem, given the location (near an orifice). Another diagnostic possibility was sebaceous carcinoma, a merkel cell cancer. Benign lesions, such as chondrodermatitis nodularis chronica helicis, occasionally present as ulcerated lesions on the ear.

BCCs are, far and away, the most common type of skin cancer, with more than a million new cases diagnosed each year in United States. They occur more commonly on fair-skinned patients and on prominently sun-exposed area (eg, ears, noses, and cheeks) but can also appear in areas where the sun seldom shines.

Several types of BCC have been described, but the nonhealing erosive papule (so-called noduloulcerative type) is the most common presentation. BCCs can also resemble scars or rashes. Though they are typically very slow to grow, not all BCCs are indolent. Some are quite aggressive both in terms of morphologic appearance and internal growth. And, as noted above, there is a differential for new, growing lesions in sun-exposed skin, making biopsy of such lesions mandatory.

Continue for Joe Monroe's take home learning points >>

TAKE-HOME LEARNING POINTS
• Nonhealing lesions on sun-exposed skin are considered to be skin cancers until proven otherwise by biopsy.

• Basal cell carcinomas (BCCs) are the most common skin cancer.

• BCCs typically grow very slowly.

• BCCs, if allowed to remain in place, can become extensive, invasive, destructive, and—in exceptional circumstances—can even metastasize.

• The differential for BCC includes squamous cell carcinoma, which has considerably more potential for metastasis than BCC, especially when it’s near an orifice.

• Quite frequently, it’s next to impossible to differentiate visually between BCC and SCC. 

• BCCs and SCCs can take on several different morphologies, so any changing lesion needs to be biopsied to establish its identity, particularly since both are so common. 

It’s somewhat unusual to see a patient with an eight-year history of the same problem, but this is what happens when a 51-year-old man presents to dermatology. Specifically, the problem is a very itchy foot rash, for which the patient has tried many OTC products without success. He has also used halobetasol cream, prescribed by a dermatologist he saw several years ago.

The patient denies having a rash anywhere else. He does, however, have a markedly atopic history, significant for seasonal allergies, asthma, and very sensitive skin.

For the past several years, when the rash has been particularly unbearable, he admits to pouring rubbing alcohol on his feet. This burned terribly, but his feet felt better afterward.

Asked what else happened eight years ago, the patient recalls starting his current job as a lineman for a power company—an occupation that requires him to wear steel-toed leather boots for hours at a time.

EXAMINATION
A dense, red, papulovesicular rash covers both feet in a stocking pattern. The rash stops abruptly at the same place on both lower legs, completely sparing the soles and interdigital skin. Focal areas of scaling and broken skin are seen on the tops and sides of both feet.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
In the ’90s, a commercial for sneakers utilized the catchphrase, "It's the shoes!" And so it is occasionally with rashes on the feet. In this case, the patient was allergic to the leather on the inside of his work boots.

A true allergy such as this would be expected to itch and to manifest as a papulovesicular rash limited to areas touched by the leather on the upper portions of his shoes. And it would persist, despite the quantity of topical medications tried, because the patient wore the shoes for eight to 12 hours a day, five or six days per week, continually re-exposing his skin to the offending material. He had never taken any significant time off work and therefore hadn’t refrained from wearing the shoes long enough to allow the rash to abate.

Often, frustrated and uncomfortable patients take matters into their own hands, which can ultimately compound the problem. This patient didn't do his skin any favors with the rubbing alcohol and other products he'd tried (the most common offender being triple-antibiotic ointment, although this patient used it only on rare occasions). Another strategy these patients often employ is to soak their feet in watered-down bleach. Fortunately, this patient had considered this option but thought better of it. A more benign, but just as ineffective, attempt at self-treatment had been to change laundry detergents, which of course did nothing to resolve the rash. (His first clue should have been that laundry detergent would not affect the tops of his feet while sparing the rest of his body.)

The insides of leather shoes are usually tanned with potassium dichromate, a chemical known to provoke this kind of reaction. Even after the source of the rash was identified, however, getting some distance between the patient and his shoes wasn’t easy. I had to write him a note for work, requesting that he be allowed to refrain from wearing his boots for about two weeks.

During that time, he started a week-long course of cephalexin 500 mg tid and applied clobetasol foam twice a day. In dermatology, we assume that any longstanding wet rash on the feet will become secondarily infected or at least colonized with gram-positive bacteria. Of course, giving him the steroid foam meant we were utilizing a class 1 corticosteroid in a very drying vehicle.

Within a week, he was a new man, with almost totally clear foot skin. This still left him with the problem of the work boots and the job—but one problem at a time.

TAKE-HOME LEARNING POINTS
• The areas spared by a rash are often just as important as those that are affected.

• Laundry detergents, often blamed for rashes, are seldom the culprit.

• Fungal infections rarely affect the dorsum of the foot while sparing interdigital and plantar surfaces.

• The patient’s atopic state will likely render him/her more susceptible to allergens.

• The vehicle (cream, gel, ointment, solution, foam) and strength of topical steroids both matter.

• Patients can become sensitized to the preservatives or other chemicals in OTC or prescription corticosteroid creams.

It’s somewhat unusual to see a patient with an eight-year history of the same problem, but this is what happens when a 51-year-old man presents to dermatology. Specifically, the problem is a very itchy foot rash, for which the patient has tried many OTC products without success. He has also used halobetasol cream, prescribed by a dermatologist he saw several years ago.

The patient denies having a rash anywhere else. He does, however, have a markedly atopic history, significant for seasonal allergies, asthma, and very sensitive skin.

For the past several years, when the rash has been particularly unbearable, he admits to pouring rubbing alcohol on his feet. This burned terribly, but his feet felt better afterward.

Asked what else happened eight years ago, the patient recalls starting his current job as a lineman for a power company—an occupation that requires him to wear steel-toed leather boots for hours at a time.

EXAMINATION
A dense, red, papulovesicular rash covers both feet in a stocking pattern. The rash stops abruptly at the same place on both lower legs, completely sparing the soles and interdigital skin. Focal areas of scaling and broken skin are seen on the tops and sides of both feet.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
In the ’90s, a commercial for sneakers utilized the catchphrase, "It's the shoes!" And so it is occasionally with rashes on the feet. In this case, the patient was allergic to the leather on the inside of his work boots.

A true allergy such as this would be expected to itch and to manifest as a papulovesicular rash limited to areas touched by the leather on the upper portions of his shoes. And it would persist, despite the quantity of topical medications tried, because the patient wore the shoes for eight to 12 hours a day, five or six days per week, continually re-exposing his skin to the offending material. He had never taken any significant time off work and therefore hadn’t refrained from wearing the shoes long enough to allow the rash to abate.

Often, frustrated and uncomfortable patients take matters into their own hands, which can ultimately compound the problem. This patient didn't do his skin any favors with the rubbing alcohol and other products he'd tried (the most common offender being triple-antibiotic ointment, although this patient used it only on rare occasions). Another strategy these patients often employ is to soak their feet in watered-down bleach. Fortunately, this patient had considered this option but thought better of it. A more benign, but just as ineffective, attempt at self-treatment had been to change laundry detergents, which of course did nothing to resolve the rash. (His first clue should have been that laundry detergent would not affect the tops of his feet while sparing the rest of his body.)

The insides of leather shoes are usually tanned with potassium dichromate, a chemical known to provoke this kind of reaction. Even after the source of the rash was identified, however, getting some distance between the patient and his shoes wasn’t easy. I had to write him a note for work, requesting that he be allowed to refrain from wearing his boots for about two weeks.

During that time, he started a week-long course of cephalexin 500 mg tid and applied clobetasol foam twice a day. In dermatology, we assume that any longstanding wet rash on the feet will become secondarily infected or at least colonized with gram-positive bacteria. Of course, giving him the steroid foam meant we were utilizing a class 1 corticosteroid in a very drying vehicle.

Within a week, he was a new man, with almost totally clear foot skin. This still left him with the problem of the work boots and the job—but one problem at a time.

TAKE-HOME LEARNING POINTS
• The areas spared by a rash are often just as important as those that are affected.

• Laundry detergents, often blamed for rashes, are seldom the culprit.

• Fungal infections rarely affect the dorsum of the foot while sparing interdigital and plantar surfaces.

• The patient’s atopic state will likely render him/her more susceptible to allergens.

• The vehicle (cream, gel, ointment, solution, foam) and strength of topical steroids both matter.

• Patients can become sensitized to the preservatives or other chemicals in OTC or prescription corticosteroid creams.

It’s somewhat unusual to see a patient with an eight-year history of the same problem, but this is what happens when a 51-year-old man presents to dermatology. Specifically, the problem is a very itchy foot rash, for which the patient has tried many OTC products without success. He has also used halobetasol cream, prescribed by a dermatologist he saw several years ago.

The patient denies having a rash anywhere else. He does, however, have a markedly atopic history, significant for seasonal allergies, asthma, and very sensitive skin.

For the past several years, when the rash has been particularly unbearable, he admits to pouring rubbing alcohol on his feet. This burned terribly, but his feet felt better afterward.

Asked what else happened eight years ago, the patient recalls starting his current job as a lineman for a power company—an occupation that requires him to wear steel-toed leather boots for hours at a time.

EXAMINATION
A dense, red, papulovesicular rash covers both feet in a stocking pattern. The rash stops abruptly at the same place on both lower legs, completely sparing the soles and interdigital skin. Focal areas of scaling and broken skin are seen on the tops and sides of both feet.

Continue for Joe Monroe's diagnosis and discussion >>

DISCUSSION
In the ’90s, a commercial for sneakers utilized the catchphrase, "It's the shoes!" And so it is occasionally with rashes on the feet. In this case, the patient was allergic to the leather on the inside of his work boots.

A true allergy such as this would be expected to itch and to manifest as a papulovesicular rash limited to areas touched by the leather on the upper portions of his shoes. And it would persist, despite the quantity of topical medications tried, because the patient wore the shoes for eight to 12 hours a day, five or six days per week, continually re-exposing his skin to the offending material. He had never taken any significant time off work and therefore hadn’t refrained from wearing the shoes long enough to allow the rash to abate.

Often, frustrated and uncomfortable patients take matters into their own hands, which can ultimately compound the problem. This patient didn't do his skin any favors with the rubbing alcohol and other products he'd tried (the most common offender being triple-antibiotic ointment, although this patient used it only on rare occasions). Another strategy these patients often employ is to soak their feet in watered-down bleach. Fortunately, this patient had considered this option but thought better of it. A more benign, but just as ineffective, attempt at self-treatment had been to change laundry detergents, which of course did nothing to resolve the rash. (His first clue should have been that laundry detergent would not affect the tops of his feet while sparing the rest of his body.)

The insides of leather shoes are usually tanned with potassium dichromate, a chemical known to provoke this kind of reaction. Even after the source of the rash was identified, however, getting some distance between the patient and his shoes wasn’t easy. I had to write him a note for work, requesting that he be allowed to refrain from wearing his boots for about two weeks.

During that time, he started a week-long course of cephalexin 500 mg tid and applied clobetasol foam twice a day. In dermatology, we assume that any longstanding wet rash on the feet will become secondarily infected or at least colonized with gram-positive bacteria. Of course, giving him the steroid foam meant we were utilizing a class 1 corticosteroid in a very drying vehicle.

Within a week, he was a new man, with almost totally clear foot skin. This still left him with the problem of the work boots and the job—but one problem at a time.

TAKE-HOME LEARNING POINTS
• The areas spared by a rash are often just as important as those that are affected.

• Laundry detergents, often blamed for rashes, are seldom the culprit.

• Fungal infections rarely affect the dorsum of the foot while sparing interdigital and plantar surfaces.

• The patient’s atopic state will likely render him/her more susceptible to allergens.

• The vehicle (cream, gel, ointment, solution, foam) and strength of topical steroids both matter.

• Patients can become sensitized to the preservatives or other chemicals in OTC or prescription corticosteroid creams.

A 73-year-old woman is urgently referred to dermatology for evaluation of a facial lesion. It is unclear how long the lesion has been present, but it has caused great alarm to the patient's visiting relatives. The patient herself is not at all worried, saying that she doubts “a little thing like that could cause too much trouble.”

She denies any symptoms associated with the lesion and claims to be in good health. There is no history of weight loss, cough, or changes in mentation or gastrointestinal/genitourinary function. She admits to some sun exposure as a young adult but claims she has never been sunburned; she reports tanning easily and holding  a tan well.

EXAMINATION
The lesion is a 1.4-cm round epidermal plaque with a rough, warty surface. It is located in the left lower medial epicanthal area, verging on the upper nasal sidewall. Its dark brown color is uniform, as is its surface texture. It appears in the context of the patient’s relatively dark type III skin, which is largely free of signs of sun damage.

PROCEDURE
After potential treatments are discussed with the patient, she opts to have cryosurgery. During the procedure, it is noted that the lesion remained white for several seconds after it was frozen.

Two months later, the site is rechecked. The lesion is virtually gone, except for a faint shadow of hyperpigmentation in the treated area.

Continue for Joe Monroe's discussion >>

DISCUSSION
The top three problems for which patients are seen in dermatology are acne, warts, and seborrheic keratoses (SK). The last are, hands down, the most common problem I see. With their dark color and raised surface, they epitomize what patients imagine skin cancer to look like.

Very likely, given the lesion’s size and location, it had been there for quite some time. But to the visiting relatives who hadn’t seen the patient in a while, it was new and alarming. (“Are you sure?” one of them asked when the patient shrugged off any concerns. “It looks so ugly!”)

I understand why SKs are worrisome to patients and their families. But, as a matter of fact, I was sure this lesion was safe. Why? Here are some reasons:

1. The lesion was epidermal in nature—that is, “stuck on” the surface of the skin, as opposed to being in, or part of, it. Epidermal lesions are almost always safe; intradermal ones, while not necessarily "bad," tend to require more attention.

2. Warty and rough are both good signs, dermatologically speaking. 

3. Uniformity in color, texture, and borders is also usually positive; the "bad stuff" tends to be somewhat irregular in all three respects.

4. Cryo-white is our term for “stays white after treatment with liquid nitrogen." By contrast, things like skin cancer thaw almost instantly. Why? The blood supply to a cancerous lesion is far better than that to an epidermal SK, which has little if any vascularization. Warm blood dissipates the cold quickly.

5. Liquid nitrogen also highlights another diagnostic feature of SKs: pseudocysts. Peculiar to SKs, these porelike surface features are usually seen as minute follicular orifices.

6. Other diagnostic features of SKs: Most affected patients have several similar lesions. Usually, the history of SK is that it’s "been there forever,” although this case illustrates an exception. SKs are typically seen in older people, but I’ve seen them on teenagers, too.

The introduction of the liquid nitrogen gun 35 years ago made SK treatment much easier and provided a potential diagnostic tool. We often use cryotherapy as a kind of final test of whether a lesion is benign or malignant. If the lesion responds to routine cryotherapy by resolving, chances are quite good it was benign. If it doesn’t, you may need to reconsider your diagnosis.

TAKE-HOME LEARNING POINTS
• SKs are extremely common, often numerous, and favor older patients.

• SKs are usually rough, epidermal, round to oval, and tan to dark brown.

• SKs, treated with liquid nitrogen, turn white and stay that way for a few seconds at least, while the dangerous lookalikes (eg, melanoma) thaw much more quickly.

• Liquid nitrogen treatment can help with diagnosis: If the treated lesion fails to disappear as intended, it might not be an SK after all. (Note, however, that this process can take up to two weeks.)

• Liquid nitrogen also highlights surface pseudocysts, which are pathognomic for SKs.

• When cryotherapy fails to elicit the desired changes, the lesion needs to be biopsied.

A 73-year-old woman is urgently referred to dermatology for evaluation of a facial lesion. It is unclear how long the lesion has been present, but it has caused great alarm to the patient's visiting relatives. The patient herself is not at all worried, saying that she doubts “a little thing like that could cause too much trouble.”

She denies any symptoms associated with the lesion and claims to be in good health. There is no history of weight loss, cough, or changes in mentation or gastrointestinal/genitourinary function. She admits to some sun exposure as a young adult but claims she has never been sunburned; she reports tanning easily and holding  a tan well.

EXAMINATION
The lesion is a 1.4-cm round epidermal plaque with a rough, warty surface. It is located in the left lower medial epicanthal area, verging on the upper nasal sidewall. Its dark brown color is uniform, as is its surface texture. It appears in the context of the patient’s relatively dark type III skin, which is largely free of signs of sun damage.

PROCEDURE
After potential treatments are discussed with the patient, she opts to have cryosurgery. During the procedure, it is noted that the lesion remained white for several seconds after it was frozen.

Two months later, the site is rechecked. The lesion is virtually gone, except for a faint shadow of hyperpigmentation in the treated area.

Continue for Joe Monroe's discussion >>

DISCUSSION
The top three problems for which patients are seen in dermatology are acne, warts, and seborrheic keratoses (SK). The last are, hands down, the most common problem I see. With their dark color and raised surface, they epitomize what patients imagine skin cancer to look like.

Very likely, given the lesion’s size and location, it had been there for quite some time. But to the visiting relatives who hadn’t seen the patient in a while, it was new and alarming. (“Are you sure?” one of them asked when the patient shrugged off any concerns. “It looks so ugly!”)

I understand why SKs are worrisome to patients and their families. But, as a matter of fact, I was sure this lesion was safe. Why? Here are some reasons:

1. The lesion was epidermal in nature—that is, “stuck on” the surface of the skin, as opposed to being in, or part of, it. Epidermal lesions are almost always safe; intradermal ones, while not necessarily "bad," tend to require more attention.

2. Warty and rough are both good signs, dermatologically speaking. 

3. Uniformity in color, texture, and borders is also usually positive; the "bad stuff" tends to be somewhat irregular in all three respects.

4. Cryo-white is our term for “stays white after treatment with liquid nitrogen." By contrast, things like skin cancer thaw almost instantly. Why? The blood supply to a cancerous lesion is far better than that to an epidermal SK, which has little if any vascularization. Warm blood dissipates the cold quickly.

5. Liquid nitrogen also highlights another diagnostic feature of SKs: pseudocysts. Peculiar to SKs, these porelike surface features are usually seen as minute follicular orifices.

6. Other diagnostic features of SKs: Most affected patients have several similar lesions. Usually, the history of SK is that it’s "been there forever,” although this case illustrates an exception. SKs are typically seen in older people, but I’ve seen them on teenagers, too.

The introduction of the liquid nitrogen gun 35 years ago made SK treatment much easier and provided a potential diagnostic tool. We often use cryotherapy as a kind of final test of whether a lesion is benign or malignant. If the lesion responds to routine cryotherapy by resolving, chances are quite good it was benign. If it doesn’t, you may need to reconsider your diagnosis.

TAKE-HOME LEARNING POINTS
• SKs are extremely common, often numerous, and favor older patients.

• SKs are usually rough, epidermal, round to oval, and tan to dark brown.

• SKs, treated with liquid nitrogen, turn white and stay that way for a few seconds at least, while the dangerous lookalikes (eg, melanoma) thaw much more quickly.

• Liquid nitrogen treatment can help with diagnosis: If the treated lesion fails to disappear as intended, it might not be an SK after all. (Note, however, that this process can take up to two weeks.)

• Liquid nitrogen also highlights surface pseudocysts, which are pathognomic for SKs.

• When cryotherapy fails to elicit the desired changes, the lesion needs to be biopsied.

A 73-year-old woman is urgently referred to dermatology for evaluation of a facial lesion. It is unclear how long the lesion has been present, but it has caused great alarm to the patient's visiting relatives. The patient herself is not at all worried, saying that she doubts “a little thing like that could cause too much trouble.”

She denies any symptoms associated with the lesion and claims to be in good health. There is no history of weight loss, cough, or changes in mentation or gastrointestinal/genitourinary function. She admits to some sun exposure as a young adult but claims she has never been sunburned; she reports tanning easily and holding  a tan well.

EXAMINATION
The lesion is a 1.4-cm round epidermal plaque with a rough, warty surface. It is located in the left lower medial epicanthal area, verging on the upper nasal sidewall. Its dark brown color is uniform, as is its surface texture. It appears in the context of the patient’s relatively dark type III skin, which is largely free of signs of sun damage.

PROCEDURE
After potential treatments are discussed with the patient, she opts to have cryosurgery. During the procedure, it is noted that the lesion remained white for several seconds after it was frozen.

Two months later, the site is rechecked. The lesion is virtually gone, except for a faint shadow of hyperpigmentation in the treated area.

Continue for Joe Monroe's discussion >>

DISCUSSION
The top three problems for which patients are seen in dermatology are acne, warts, and seborrheic keratoses (SK). The last are, hands down, the most common problem I see. With their dark color and raised surface, they epitomize what patients imagine skin cancer to look like.

Very likely, given the lesion’s size and location, it had been there for quite some time. But to the visiting relatives who hadn’t seen the patient in a while, it was new and alarming. (“Are you sure?” one of them asked when the patient shrugged off any concerns. “It looks so ugly!”)

I understand why SKs are worrisome to patients and their families. But, as a matter of fact, I was sure this lesion was safe. Why? Here are some reasons:

1. The lesion was epidermal in nature—that is, “stuck on” the surface of the skin, as opposed to being in, or part of, it. Epidermal lesions are almost always safe; intradermal ones, while not necessarily "bad," tend to require more attention.

2. Warty and rough are both good signs, dermatologically speaking. 

3. Uniformity in color, texture, and borders is also usually positive; the "bad stuff" tends to be somewhat irregular in all three respects.

4. Cryo-white is our term for “stays white after treatment with liquid nitrogen." By contrast, things like skin cancer thaw almost instantly. Why? The blood supply to a cancerous lesion is far better than that to an epidermal SK, which has little if any vascularization. Warm blood dissipates the cold quickly.

5. Liquid nitrogen also highlights another diagnostic feature of SKs: pseudocysts. Peculiar to SKs, these porelike surface features are usually seen as minute follicular orifices.

6. Other diagnostic features of SKs: Most affected patients have several similar lesions. Usually, the history of SK is that it’s "been there forever,” although this case illustrates an exception. SKs are typically seen in older people, but I’ve seen them on teenagers, too.

The introduction of the liquid nitrogen gun 35 years ago made SK treatment much easier and provided a potential diagnostic tool. We often use cryotherapy as a kind of final test of whether a lesion is benign or malignant. If the lesion responds to routine cryotherapy by resolving, chances are quite good it was benign. If it doesn’t, you may need to reconsider your diagnosis.

TAKE-HOME LEARNING POINTS
• SKs are extremely common, often numerous, and favor older patients.

• SKs are usually rough, epidermal, round to oval, and tan to dark brown.

• SKs, treated with liquid nitrogen, turn white and stay that way for a few seconds at least, while the dangerous lookalikes (eg, melanoma) thaw much more quickly.

• Liquid nitrogen treatment can help with diagnosis: If the treated lesion fails to disappear as intended, it might not be an SK after all. (Note, however, that this process can take up to two weeks.)

• Liquid nitrogen also highlights surface pseudocysts, which are pathognomic for SKs.

• When cryotherapy fails to elicit the desired changes, the lesion needs to be biopsied.