The Journal of Family Practice

There is now an additional option for the prevention of respiratory syncytial virus (RSV), the most common cause of hospitalization among infants and children in the United States. In July, the US Food and Drug Administration (FDA) approved nirsevimab, an RSV preventive monoclonal antibody, for use in neonates and infants born during or entering their first RSV season and in children up to 24 months of age who remain vulnerable to RSV during their second season.¹ The Advisory Committee on Immunization Practices (ACIP) subsequently made 2 recommendations regarding use of nirsevimab, which I’ll detail in a moment.²

First, a word about RSV. The Centers for Disease Control and Prevention estimates that each year in children younger than 5 years, RSV is responsible for 1.5 million outpatient clinic visits, 520,000 emergency department visits, 58,000 to 80,000 hospitalizations, and 100 to 200 deaths.² The risk for hospitalization from RSV is highest in the second and third months of life and decreases with increasing age.

There are some racial disparities in RSV severity, likely reflecting social drivers of health: ICU admission rates are 1.2 to 1.6 times higher among non-Hispanic Black infants younger than 6 months than among non-Hispanic White infants, and hospitalization rates are up to 5 times higher in American Indian and Alaska Native populations.²

What nirsevimab adds to the toolbox. Until recently, there was only 1 RSV preventive agent available: palivizumab, also a monoclonal antibody. The American Academy of Pediatrics has recommended palivizumab be used only for infants at high risk for RSV infection, due to its high cost and the need for monthly injections for the duration of an RSV season. In addition, the Academy has noted that palivizumab has limited effect on RSV hospitalizations on a population basis and does not appear to affect mortality.³

Nirsevimab has a longer half-life than palivizumab, and only 1 injection is needed for the RSV season. Early studies on nirsevimab demonstrate 79% effectiveness in preventing medical-attended lower respiratory tract infection, 80.6% effectiveness in preventing hospitalization, and 90% effectiveness in preventing ICU admission. The number needed to immunize with nirsevimab to prevent an outpatient visit is estimated to be 17; to prevent an ED visit, 48; and to prevent an inpatient admission, 128. Due to the low RSV death rate, the studies were not able to demonstrate reduced mortality.²

What the ACIP recommends. At a special meeting in July, the ACIP recommended 1 dose of nirsevimab for²:

• all infants younger than 8 months who are born during or entering their first RSV season
• children ages 8 to 19 months who are at increased risk for severe RSV disease and entering their second RSV season.

Those at risk include children with chronic lung disease of prematurity who required medical support any time during the 6-month period before the start of their second RSV season; those with severe immunocompromise; those with cystic fibrosis who have manifestations of severe lung disease or weight-for-length < 10th percentile; and American Indian and Alaska Native children.²

How to administer nirsevimab. The dose of nirsevimab is 50 mg IM for those weighing < 5 kg, 100 mg for those weighing ≥ 5 kg, and 200 mg for high-risk children entering their second RSV season.² Nirsevimab can be co-administered with other recommended vaccines; however, both nirsevimab and palivizumab should not be used in the same child in the same RSV season.

Nirsevimab should be administered in the first week of life for infants born shortly before or during RSV season, and shortly before the season for infants younger than 8 months and those ages 8 to 19 months who are at high risk.⁴ The months of highest RSV transmission in most locations are December through February, but this can vary. Local epidemiology and advice from state and local health departments are the best source of information about when RSV season starts and ends in your area.

On the horizon. Nirsevimab will be included in the Vaccines for Children program and covered by commercial health plans with no cost sharing.⁵ A maternal vaccine to prevent RSV in newborns is likely to be approved by the FDA in the near future.

There is now an additional option for the prevention of respiratory syncytial virus (RSV), the most common cause of hospitalization among infants and children in the United States. In July, the US Food and Drug Administration (FDA) approved nirsevimab, an RSV preventive monoclonal antibody, for use in neonates and infants born during or entering their first RSV season and in children up to 24 months of age who remain vulnerable to RSV during their second season.¹ The Advisory Committee on Immunization Practices (ACIP) subsequently made 2 recommendations regarding use of nirsevimab, which I’ll detail in a moment.²

First, a word about RSV. The Centers for Disease Control and Prevention estimates that each year in children younger than 5 years, RSV is responsible for 1.5 million outpatient clinic visits, 520,000 emergency department visits, 58,000 to 80,000 hospitalizations, and 100 to 200 deaths.² The risk for hospitalization from RSV is highest in the second and third months of life and decreases with increasing age.

There are some racial disparities in RSV severity, likely reflecting social drivers of health: ICU admission rates are 1.2 to 1.6 times higher among non-Hispanic Black infants younger than 6 months than among non-Hispanic White infants, and hospitalization rates are up to 5 times higher in American Indian and Alaska Native populations.²

What nirsevimab adds to the toolbox. Until recently, there was only 1 RSV preventive agent available: palivizumab, also a monoclonal antibody. The American Academy of Pediatrics has recommended palivizumab be used only for infants at high risk for RSV infection, due to its high cost and the need for monthly injections for the duration of an RSV season. In addition, the Academy has noted that palivizumab has limited effect on RSV hospitalizations on a population basis and does not appear to affect mortality.³

Nirsevimab has a longer half-life than palivizumab, and only 1 injection is needed for the RSV season. Early studies on nirsevimab demonstrate 79% effectiveness in preventing medical-attended lower respiratory tract infection, 80.6% effectiveness in preventing hospitalization, and 90% effectiveness in preventing ICU admission. The number needed to immunize with nirsevimab to prevent an outpatient visit is estimated to be 17; to prevent an ED visit, 48; and to prevent an inpatient admission, 128. Due to the low RSV death rate, the studies were not able to demonstrate reduced mortality.²

What the ACIP recommends. At a special meeting in July, the ACIP recommended 1 dose of nirsevimab for²:

• all infants younger than 8 months who are born during or entering their first RSV season
• children ages 8 to 19 months who are at increased risk for severe RSV disease and entering their second RSV season.

Those at risk include children with chronic lung disease of prematurity who required medical support any time during the 6-month period before the start of their second RSV season; those with severe immunocompromise; those with cystic fibrosis who have manifestations of severe lung disease or weight-for-length < 10th percentile; and American Indian and Alaska Native children.²

How to administer nirsevimab. The dose of nirsevimab is 50 mg IM for those weighing < 5 kg, 100 mg for those weighing ≥ 5 kg, and 200 mg for high-risk children entering their second RSV season.² Nirsevimab can be co-administered with other recommended vaccines; however, both nirsevimab and palivizumab should not be used in the same child in the same RSV season.

Nirsevimab should be administered in the first week of life for infants born shortly before or during RSV season, and shortly before the season for infants younger than 8 months and those ages 8 to 19 months who are at high risk.⁴ The months of highest RSV transmission in most locations are December through February, but this can vary. Local epidemiology and advice from state and local health departments are the best source of information about when RSV season starts and ends in your area.

On the horizon. Nirsevimab will be included in the Vaccines for Children program and covered by commercial health plans with no cost sharing.⁵ A maternal vaccine to prevent RSV in newborns is likely to be approved by the FDA in the near future.

There is now an additional option for the prevention of respiratory syncytial virus (RSV), the most common cause of hospitalization among infants and children in the United States. In July, the US Food and Drug Administration (FDA) approved nirsevimab, an RSV preventive monoclonal antibody, for use in neonates and infants born during or entering their first RSV season and in children up to 24 months of age who remain vulnerable to RSV during their second season.¹ The Advisory Committee on Immunization Practices (ACIP) subsequently made 2 recommendations regarding use of nirsevimab, which I’ll detail in a moment.²

First, a word about RSV. The Centers for Disease Control and Prevention estimates that each year in children younger than 5 years, RSV is responsible for 1.5 million outpatient clinic visits, 520,000 emergency department visits, 58,000 to 80,000 hospitalizations, and 100 to 200 deaths.² The risk for hospitalization from RSV is highest in the second and third months of life and decreases with increasing age.

There are some racial disparities in RSV severity, likely reflecting social drivers of health: ICU admission rates are 1.2 to 1.6 times higher among non-Hispanic Black infants younger than 6 months than among non-Hispanic White infants, and hospitalization rates are up to 5 times higher in American Indian and Alaska Native populations.²

What nirsevimab adds to the toolbox. Until recently, there was only 1 RSV preventive agent available: palivizumab, also a monoclonal antibody. The American Academy of Pediatrics has recommended palivizumab be used only for infants at high risk for RSV infection, due to its high cost and the need for monthly injections for the duration of an RSV season. In addition, the Academy has noted that palivizumab has limited effect on RSV hospitalizations on a population basis and does not appear to affect mortality.³

Nirsevimab has a longer half-life than palivizumab, and only 1 injection is needed for the RSV season. Early studies on nirsevimab demonstrate 79% effectiveness in preventing medical-attended lower respiratory tract infection, 80.6% effectiveness in preventing hospitalization, and 90% effectiveness in preventing ICU admission. The number needed to immunize with nirsevimab to prevent an outpatient visit is estimated to be 17; to prevent an ED visit, 48; and to prevent an inpatient admission, 128. Due to the low RSV death rate, the studies were not able to demonstrate reduced mortality.²

What the ACIP recommends. At a special meeting in July, the ACIP recommended 1 dose of nirsevimab for²:

• all infants younger than 8 months who are born during or entering their first RSV season
• children ages 8 to 19 months who are at increased risk for severe RSV disease and entering their second RSV season.

Those at risk include children with chronic lung disease of prematurity who required medical support any time during the 6-month period before the start of their second RSV season; those with severe immunocompromise; those with cystic fibrosis who have manifestations of severe lung disease or weight-for-length < 10th percentile; and American Indian and Alaska Native children.²

How to administer nirsevimab. The dose of nirsevimab is 50 mg IM for those weighing < 5 kg, 100 mg for those weighing ≥ 5 kg, and 200 mg for high-risk children entering their second RSV season.² Nirsevimab can be co-administered with other recommended vaccines; however, both nirsevimab and palivizumab should not be used in the same child in the same RSV season.

Nirsevimab should be administered in the first week of life for infants born shortly before or during RSV season, and shortly before the season for infants younger than 8 months and those ages 8 to 19 months who are at high risk.⁴ The months of highest RSV transmission in most locations are December through February, but this can vary. Local epidemiology and advice from state and local health departments are the best source of information about when RSV season starts and ends in your area.

On the horizon. Nirsevimab will be included in the Vaccines for Children program and covered by commercial health plans with no cost sharing.⁵ A maternal vaccine to prevent RSV in newborns is likely to be approved by the FDA in the near future.

A leg ulcer may have many causes, including venous stasis, trauma, vasculitis, infection, or (as in this case) squamous cell carcinoma in situ (SCCis), aka Bowen’s Disease.

SCC and SCCis are common skin cancers that occur less frequently than basal cell carcinomas (BCCs).¹ SCCis is normally scaly and hyperkeratotic, but it can manifest in rare cases as a chronic ulcer. Fair skin, long history of sun damage, and immunosuppression are significant risk factors for both SCCis and SCC.

While history and other clinical features may help narrow the diagnosis, a wound that does not heal despite treatments should be biopsied. Shave and punch biopsies are both excellent ways to diagnose an SCCis that has a classic appearance. However, ulcers and blisters can be caused by inflammatory processes (as in pyoderma gangrenosum or a fixed drug eruption) with characteristic findings deeper in the dermis; these lesions are better assessed with a punch biopsy.

In this case, a 4-mm punch biopsy was performed at the tissue edge and showed atypical keratinocytes limited to the epidermis. These atypical keratinocytes are associated with vesicle formation and ulcer, consistent with SCCis.

SCCis transforms into invasive disease in 3% to 5% of cases.² Surgical treatment includes fusiform excision and electrodessication and curettage, both with cure rates that often exceed 90%.^2,3 Nonsurgical options include topical 5-fluorouracil (67%-92% effective), topical imiquimod (75%-93%), and photodynamic therapy (52%-98%).⁴

Treatment choices depend on patient preference and provider capabilities. With surgical options there is the risk of bleeding and the need to care for a healing wound. Nonsurgical treatments can last longer and require topical treatment regimens and medications.

This patient opted for a fusiform excision and linear closure. She will continue to undergo serial skin evaluations twice a year for at least 2 years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

A leg ulcer may have many causes, including venous stasis, trauma, vasculitis, infection, or (as in this case) squamous cell carcinoma in situ (SCCis), aka Bowen’s Disease.

SCC and SCCis are common skin cancers that occur less frequently than basal cell carcinomas (BCCs).¹ SCCis is normally scaly and hyperkeratotic, but it can manifest in rare cases as a chronic ulcer. Fair skin, long history of sun damage, and immunosuppression are significant risk factors for both SCCis and SCC.

While history and other clinical features may help narrow the diagnosis, a wound that does not heal despite treatments should be biopsied. Shave and punch biopsies are both excellent ways to diagnose an SCCis that has a classic appearance. However, ulcers and blisters can be caused by inflammatory processes (as in pyoderma gangrenosum or a fixed drug eruption) with characteristic findings deeper in the dermis; these lesions are better assessed with a punch biopsy.

In this case, a 4-mm punch biopsy was performed at the tissue edge and showed atypical keratinocytes limited to the epidermis. These atypical keratinocytes are associated with vesicle formation and ulcer, consistent with SCCis.

SCCis transforms into invasive disease in 3% to 5% of cases.² Surgical treatment includes fusiform excision and electrodessication and curettage, both with cure rates that often exceed 90%.^2,3 Nonsurgical options include topical 5-fluorouracil (67%-92% effective), topical imiquimod (75%-93%), and photodynamic therapy (52%-98%).⁴

Treatment choices depend on patient preference and provider capabilities. With surgical options there is the risk of bleeding and the need to care for a healing wound. Nonsurgical treatments can last longer and require topical treatment regimens and medications.

This patient opted for a fusiform excision and linear closure. She will continue to undergo serial skin evaluations twice a year for at least 2 years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

A leg ulcer may have many causes, including venous stasis, trauma, vasculitis, infection, or (as in this case) squamous cell carcinoma in situ (SCCis), aka Bowen’s Disease.

SCC and SCCis are common skin cancers that occur less frequently than basal cell carcinomas (BCCs).¹ SCCis is normally scaly and hyperkeratotic, but it can manifest in rare cases as a chronic ulcer. Fair skin, long history of sun damage, and immunosuppression are significant risk factors for both SCCis and SCC.

While history and other clinical features may help narrow the diagnosis, a wound that does not heal despite treatments should be biopsied. Shave and punch biopsies are both excellent ways to diagnose an SCCis that has a classic appearance. However, ulcers and blisters can be caused by inflammatory processes (as in pyoderma gangrenosum or a fixed drug eruption) with characteristic findings deeper in the dermis; these lesions are better assessed with a punch biopsy.

In this case, a 4-mm punch biopsy was performed at the tissue edge and showed atypical keratinocytes limited to the epidermis. These atypical keratinocytes are associated with vesicle formation and ulcer, consistent with SCCis.

SCCis transforms into invasive disease in 3% to 5% of cases.² Surgical treatment includes fusiform excision and electrodessication and curettage, both with cure rates that often exceed 90%.^2,3 Nonsurgical options include topical 5-fluorouracil (67%-92% effective), topical imiquimod (75%-93%), and photodynamic therapy (52%-98%).⁴

Treatment choices depend on patient preference and provider capabilities. With surgical options there is the risk of bleeding and the need to care for a healing wound. Nonsurgical treatments can last longer and require topical treatment regimens and medications.

This patient opted for a fusiform excision and linear closure. She will continue to undergo serial skin evaluations twice a year for at least 2 years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

The patient was having a flare of pemphigus vulgaris (PV), a rare and sometimes life-threatening acquired autoimmune blistering disease that affects the skin and/or mucosa. Ashkenazi Jewish patients and patients from Mediterranean and Middle Eastern countries are more likely to be affected.

In PV, acquired autoantibodies target the desmosomes that connect epithelial cells together, weakening the intercellular adhesion. It can affect skin, mucosa, or both. Patients present with fragile bullae or ulcers. The connections between the cells are often so damaged that rubbing on the skin creates a new blister called “Nikolsky sign.” In the mouth, bullae erode rapidly. Look for disease affecting the ocular conjunctiva or sclera, as well. PV can also occasionally affect the nasopharynx and esophagus, usually manifesting as hemoptysis, dysphagia, and nosebleeds with ulcer seen on endoscopy or otolaryngoscopy.

Although PV is often severe (and can warrant hospitalization when significant body surface area is involved), some patients may have few active lesions and can be managed safely as outpatients.

The diagnosis requires 2 biopsies and serum for indirect immunofluorescence. One biopsy (either by punch or shave to the upper dermis) is taken from the edge of a bulla or ulcer. Another biopsy (by punch or shave) is taken from nearby normal-looking skin or mucosa for testing the direct immunofluorescence pattern. In the mucosa, a punch biopsy may be left open or closed with absorbable sutures. A serum sample is taken for indirect immunofluorescence to differentiate pemphigus vulgaris from other forms of pemphigus.¹

PV is treated by suppressing the immune system. Focal disease may be treated with super-potent topical steroids, including clobetasol 0.05% ointment. Even in the mouth, topical clobetasol 0.05% may be used off-label twice daily until control is achieved. When topical treatment is used in the mouth, advise patients to apply the clobetasol ointment to a piece of gauze and place the gauze (ointment side down) over affected areas for 20 to 30 minutes twice daily.

Patients with widespread or severe disease should be hospitalized. In severe cases, supportive wound care is provided, and treatment is aimed at immunosuppression. Systemic options include high-dose prednisone 0.5 to 1 mg/kg daily until clear, a steroid-sparing immunosuppressant such as mycophenolate mofetil up to 1000 mg bid, or rituximab in 1 of several regimens.

Three years prior to this patient’s visit, she had been successfully treated for PV with a course of rituximab. To treat the current flare, she was started on prednisone 60 mg/d. In addition, the plan was for her to complete 2 infusions of 1000 mg rituximab 2 weeks apart.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

The patient was having a flare of pemphigus vulgaris (PV), a rare and sometimes life-threatening acquired autoimmune blistering disease that affects the skin and/or mucosa. Ashkenazi Jewish patients and patients from Mediterranean and Middle Eastern countries are more likely to be affected.

In PV, acquired autoantibodies target the desmosomes that connect epithelial cells together, weakening the intercellular adhesion. It can affect skin, mucosa, or both. Patients present with fragile bullae or ulcers. The connections between the cells are often so damaged that rubbing on the skin creates a new blister called “Nikolsky sign.” In the mouth, bullae erode rapidly. Look for disease affecting the ocular conjunctiva or sclera, as well. PV can also occasionally affect the nasopharynx and esophagus, usually manifesting as hemoptysis, dysphagia, and nosebleeds with ulcer seen on endoscopy or otolaryngoscopy.

Although PV is often severe (and can warrant hospitalization when significant body surface area is involved), some patients may have few active lesions and can be managed safely as outpatients.

The diagnosis requires 2 biopsies and serum for indirect immunofluorescence. One biopsy (either by punch or shave to the upper dermis) is taken from the edge of a bulla or ulcer. Another biopsy (by punch or shave) is taken from nearby normal-looking skin or mucosa for testing the direct immunofluorescence pattern. In the mucosa, a punch biopsy may be left open or closed with absorbable sutures. A serum sample is taken for indirect immunofluorescence to differentiate pemphigus vulgaris from other forms of pemphigus.¹

PV is treated by suppressing the immune system. Focal disease may be treated with super-potent topical steroids, including clobetasol 0.05% ointment. Even in the mouth, topical clobetasol 0.05% may be used off-label twice daily until control is achieved. When topical treatment is used in the mouth, advise patients to apply the clobetasol ointment to a piece of gauze and place the gauze (ointment side down) over affected areas for 20 to 30 minutes twice daily.

Patients with widespread or severe disease should be hospitalized. In severe cases, supportive wound care is provided, and treatment is aimed at immunosuppression. Systemic options include high-dose prednisone 0.5 to 1 mg/kg daily until clear, a steroid-sparing immunosuppressant such as mycophenolate mofetil up to 1000 mg bid, or rituximab in 1 of several regimens.

Three years prior to this patient’s visit, she had been successfully treated for PV with a course of rituximab. To treat the current flare, she was started on prednisone 60 mg/d. In addition, the plan was for her to complete 2 infusions of 1000 mg rituximab 2 weeks apart.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

The patient was having a flare of pemphigus vulgaris (PV), a rare and sometimes life-threatening acquired autoimmune blistering disease that affects the skin and/or mucosa. Ashkenazi Jewish patients and patients from Mediterranean and Middle Eastern countries are more likely to be affected.

In PV, acquired autoantibodies target the desmosomes that connect epithelial cells together, weakening the intercellular adhesion. It can affect skin, mucosa, or both. Patients present with fragile bullae or ulcers. The connections between the cells are often so damaged that rubbing on the skin creates a new blister called “Nikolsky sign.” In the mouth, bullae erode rapidly. Look for disease affecting the ocular conjunctiva or sclera, as well. PV can also occasionally affect the nasopharynx and esophagus, usually manifesting as hemoptysis, dysphagia, and nosebleeds with ulcer seen on endoscopy or otolaryngoscopy.

Although PV is often severe (and can warrant hospitalization when significant body surface area is involved), some patients may have few active lesions and can be managed safely as outpatients.

The diagnosis requires 2 biopsies and serum for indirect immunofluorescence. One biopsy (either by punch or shave to the upper dermis) is taken from the edge of a bulla or ulcer. Another biopsy (by punch or shave) is taken from nearby normal-looking skin or mucosa for testing the direct immunofluorescence pattern. In the mucosa, a punch biopsy may be left open or closed with absorbable sutures. A serum sample is taken for indirect immunofluorescence to differentiate pemphigus vulgaris from other forms of pemphigus.¹

PV is treated by suppressing the immune system. Focal disease may be treated with super-potent topical steroids, including clobetasol 0.05% ointment. Even in the mouth, topical clobetasol 0.05% may be used off-label twice daily until control is achieved. When topical treatment is used in the mouth, advise patients to apply the clobetasol ointment to a piece of gauze and place the gauze (ointment side down) over affected areas for 20 to 30 minutes twice daily.

Patients with widespread or severe disease should be hospitalized. In severe cases, supportive wound care is provided, and treatment is aimed at immunosuppression. Systemic options include high-dose prednisone 0.5 to 1 mg/kg daily until clear, a steroid-sparing immunosuppressant such as mycophenolate mofetil up to 1000 mg bid, or rituximab in 1 of several regimens.

Three years prior to this patient’s visit, she had been successfully treated for PV with a course of rituximab. To treat the current flare, she was started on prednisone 60 mg/d. In addition, the plan was for her to complete 2 infusions of 1000 mg rituximab 2 weeks apart.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, Maine.

This patient had more than cystic acne; he had acne conglobata. AC is a severe form of inflammatory acne leading to coalescing lesions with purulent sinus tracts under the skin. It can be seen as part of the follicular tetrad syndrome of cystic acne, hidradenitis suppurativa, dissecting cellulitis, and pilonidal disease. AC is thought to be an elevated tumor necrosis factor (TNF)-alpha response to Propionibacterium acnes (now known as Cutibacterium acnes) that leads to excessive inflammation and sterile abscesses.¹ Acne fulminans (AF) can also manifest as a purulent form of acne, but AF has associated systemic signs and symptoms that include fevers, chills, and malaise.

Due to the depth of the inflammation, AC is treated with systemic medications, most commonly isotretinoin. Isotretinoin can be started at 0.5 mg/kg (divided twice daily to enhance tolerability) and then increased to 1 mg/kg (divided twice daily) for 5 months. There is some variation in dosing regimens in practice; the target goal is 120 to 150 mg/kg over the course of treatment. In AF, the patient is pretreated with systemic steroids, and in AC, some clinicians will even prescribe systemic steroids (prednisone 0.5 mg/kg daily for the first month) along with isotretinoin.

Second-line medications include dapsone (50-150 mg/d).² Case reports describe the successful use of the TNF-alpha antagonist adalimumab, although this is not a usual practice in AC treatment.¹ Note that all of these medications have the potential for severe adverse effects and require laboratory evaluation prior to initiation.

This patient was counseled, prescribed isotretinoin (dose as above), and enrolled in the IPledge prescribing and monitoring system for isotretinoin. At 20 weeks of use, the purulent drainage ceased. The pus-filled sinus tracts and redness had resolved, although he still had thickened tissue and scarring where the tracts had been. In time, the scars will usually get flatter and softer.

If the patient’s AC were to flare, another 20-week course of isotretinoin could be prescribed after a 2-month hiatus or he could be switched to a second-line medication. Referral for any cosmetic therapy is typically delayed for another 6 months in case there is a need to treat a recurrence.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient had more than cystic acne; he had acne conglobata. AC is a severe form of inflammatory acne leading to coalescing lesions with purulent sinus tracts under the skin. It can be seen as part of the follicular tetrad syndrome of cystic acne, hidradenitis suppurativa, dissecting cellulitis, and pilonidal disease. AC is thought to be an elevated tumor necrosis factor (TNF)-alpha response to Propionibacterium acnes (now known as Cutibacterium acnes) that leads to excessive inflammation and sterile abscesses.¹ Acne fulminans (AF) can also manifest as a purulent form of acne, but AF has associated systemic signs and symptoms that include fevers, chills, and malaise.

Due to the depth of the inflammation, AC is treated with systemic medications, most commonly isotretinoin. Isotretinoin can be started at 0.5 mg/kg (divided twice daily to enhance tolerability) and then increased to 1 mg/kg (divided twice daily) for 5 months. There is some variation in dosing regimens in practice; the target goal is 120 to 150 mg/kg over the course of treatment. In AF, the patient is pretreated with systemic steroids, and in AC, some clinicians will even prescribe systemic steroids (prednisone 0.5 mg/kg daily for the first month) along with isotretinoin.

Second-line medications include dapsone (50-150 mg/d).² Case reports describe the successful use of the TNF-alpha antagonist adalimumab, although this is not a usual practice in AC treatment.¹ Note that all of these medications have the potential for severe adverse effects and require laboratory evaluation prior to initiation.

This patient was counseled, prescribed isotretinoin (dose as above), and enrolled in the IPledge prescribing and monitoring system for isotretinoin. At 20 weeks of use, the purulent drainage ceased. The pus-filled sinus tracts and redness had resolved, although he still had thickened tissue and scarring where the tracts had been. In time, the scars will usually get flatter and softer.

If the patient’s AC were to flare, another 20-week course of isotretinoin could be prescribed after a 2-month hiatus or he could be switched to a second-line medication. Referral for any cosmetic therapy is typically delayed for another 6 months in case there is a need to treat a recurrence.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient had more than cystic acne; he had acne conglobata. AC is a severe form of inflammatory acne leading to coalescing lesions with purulent sinus tracts under the skin. It can be seen as part of the follicular tetrad syndrome of cystic acne, hidradenitis suppurativa, dissecting cellulitis, and pilonidal disease. AC is thought to be an elevated tumor necrosis factor (TNF)-alpha response to Propionibacterium acnes (now known as Cutibacterium acnes) that leads to excessive inflammation and sterile abscesses.¹ Acne fulminans (AF) can also manifest as a purulent form of acne, but AF has associated systemic signs and symptoms that include fevers, chills, and malaise.

Due to the depth of the inflammation, AC is treated with systemic medications, most commonly isotretinoin. Isotretinoin can be started at 0.5 mg/kg (divided twice daily to enhance tolerability) and then increased to 1 mg/kg (divided twice daily) for 5 months. There is some variation in dosing regimens in practice; the target goal is 120 to 150 mg/kg over the course of treatment. In AF, the patient is pretreated with systemic steroids, and in AC, some clinicians will even prescribe systemic steroids (prednisone 0.5 mg/kg daily for the first month) along with isotretinoin.

Second-line medications include dapsone (50-150 mg/d).² Case reports describe the successful use of the TNF-alpha antagonist adalimumab, although this is not a usual practice in AC treatment.¹ Note that all of these medications have the potential for severe adverse effects and require laboratory evaluation prior to initiation.

This patient was counseled, prescribed isotretinoin (dose as above), and enrolled in the IPledge prescribing and monitoring system for isotretinoin. At 20 weeks of use, the purulent drainage ceased. The pus-filled sinus tracts and redness had resolved, although he still had thickened tissue and scarring where the tracts had been. In time, the scars will usually get flatter and softer.

If the patient’s AC were to flare, another 20-week course of isotretinoin could be prescribed after a 2-month hiatus or he could be switched to a second-line medication. Referral for any cosmetic therapy is typically delayed for another 6 months in case there is a need to treat a recurrence.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The necrotic eschar on this patient’s thigh is calciphylaxis, also known as calcific uremic arteriolopathy (CUA). Most cases are seen in ESRD and start as painful erythematous, firm lesions that progress to necrotic eschars. Up to 4% of patients with ESRD who are on dialysis develop CUA.¹

The exact pathology of CUA is unknown. Calcification of the arterioles leads to ischemia and necrosis of tissue, which is not limited to the skin and can affect tissue elsewhere (eg, muscles, central nervous system, internal organs).²

Morbidity and mortality of CUA is often due to bacterial infections and sepsis related to the necrotic tissue. CUA can be treated with sodium thiosulfate (25 g in 100 mL of normal saline) infused intravenously during the last 30 minutes of dialysis treatment 3 times per week.³ Sodium thiosulfate (which acts as a calcium binder) and cinacalcet (a calcimimetic that leads to lower parathyroid hormone levels) have been used, but evidence of efficacy is limited. In a multicenter observational study involving 89 patients with chronic kidney disease and CUA, 17% of patients experienced complete wound healing, while 56% died over a median follow-up period of 5.8 months.¹ (No cause of death data were available; sodium thiosulfate and a calcimimetic were the most widely used treatment strategies.) This extrapolated to a mortality rate of 72 patients per 100 individuals over the course of 1 year (the 100 patient-years rate).¹

This patient continued her dialysis regimen and general care. She was seen by the wound care team and treated with topical wound care, including moist dressings for her open lesions. The eschars were not debrided because they showed no sign of active infection. Unfortunately, she was in extremely frail condition and died 1 month after evaluation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The necrotic eschar on this patient’s thigh is calciphylaxis, also known as calcific uremic arteriolopathy (CUA). Most cases are seen in ESRD and start as painful erythematous, firm lesions that progress to necrotic eschars. Up to 4% of patients with ESRD who are on dialysis develop CUA.¹

The exact pathology of CUA is unknown. Calcification of the arterioles leads to ischemia and necrosis of tissue, which is not limited to the skin and can affect tissue elsewhere (eg, muscles, central nervous system, internal organs).²

Morbidity and mortality of CUA is often due to bacterial infections and sepsis related to the necrotic tissue. CUA can be treated with sodium thiosulfate (25 g in 100 mL of normal saline) infused intravenously during the last 30 minutes of dialysis treatment 3 times per week.³ Sodium thiosulfate (which acts as a calcium binder) and cinacalcet (a calcimimetic that leads to lower parathyroid hormone levels) have been used, but evidence of efficacy is limited. In a multicenter observational study involving 89 patients with chronic kidney disease and CUA, 17% of patients experienced complete wound healing, while 56% died over a median follow-up period of 5.8 months.¹ (No cause of death data were available; sodium thiosulfate and a calcimimetic were the most widely used treatment strategies.) This extrapolated to a mortality rate of 72 patients per 100 individuals over the course of 1 year (the 100 patient-years rate).¹

This patient continued her dialysis regimen and general care. She was seen by the wound care team and treated with topical wound care, including moist dressings for her open lesions. The eschars were not debrided because they showed no sign of active infection. Unfortunately, she was in extremely frail condition and died 1 month after evaluation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The necrotic eschar on this patient’s thigh is calciphylaxis, also known as calcific uremic arteriolopathy (CUA). Most cases are seen in ESRD and start as painful erythematous, firm lesions that progress to necrotic eschars. Up to 4% of patients with ESRD who are on dialysis develop CUA.¹

The exact pathology of CUA is unknown. Calcification of the arterioles leads to ischemia and necrosis of tissue, which is not limited to the skin and can affect tissue elsewhere (eg, muscles, central nervous system, internal organs).²

Morbidity and mortality of CUA is often due to bacterial infections and sepsis related to the necrotic tissue. CUA can be treated with sodium thiosulfate (25 g in 100 mL of normal saline) infused intravenously during the last 30 minutes of dialysis treatment 3 times per week.³ Sodium thiosulfate (which acts as a calcium binder) and cinacalcet (a calcimimetic that leads to lower parathyroid hormone levels) have been used, but evidence of efficacy is limited. In a multicenter observational study involving 89 patients with chronic kidney disease and CUA, 17% of patients experienced complete wound healing, while 56% died over a median follow-up period of 5.8 months.¹ (No cause of death data were available; sodium thiosulfate and a calcimimetic were the most widely used treatment strategies.) This extrapolated to a mortality rate of 72 patients per 100 individuals over the course of 1 year (the 100 patient-years rate).¹

This patient continued her dialysis regimen and general care. She was seen by the wound care team and treated with topical wound care, including moist dressings for her open lesions. The eschars were not debrided because they showed no sign of active infection. Unfortunately, she was in extremely frail condition and died 1 month after evaluation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Although it’s easy to jump to the conclusion that facial erythema is rosacea, there are multiple other conditions that can lead to reddening of the face. In this case, excessive sun exposure had resulted in a diffuse actinic change of the malar and lateral aspects of this patient’s face. The palpably rough lesions were actinic keratoses.

Actinic keratoses are caused by exposure to ultraviolet radiation. These lesions are premalignant and common. Areas of the body at greatest risk include those not typically covered by clothing (eg, face, hands, arms, ears, forehead, and top of the scalp—especially in individuals with hair loss). There is a range of estimates regarding the percentage of actinic keratoses that will progress to squamous cell carcinoma in situ, and then invasive squamous cell carcinoma. One study determined that 10% of actinic keratoses progress to squamous cell carcinoma over the course of 2 years.¹

In patients with broad areas of multiple clinically palpable lesions with rough sandpapery texture or visible white scale, there are likely preclinical lesions in the same areas. With so many lesions, field therapy of the entire region is often performed instead of treating the lesions 1 at a time.

There are multiple topical agents for field therapy, including 5-fluorouracil, diclofenac gel, and imiquimod gel.² Since significant erythema and inflammation usually follow application of the topical agent, clinicians may want to have patients treat in segments to make the process more tolerable.

5-fluorouracil has a complete clearance rate (CCR) of 75% to 90% and is usually applied twice daily for 2 weeks, although there are multiple different protocols. Diclofenac has a CCR of 58% over a 60- to 90-day course, and imiquimod has a CCR of 54% after a 120-day course. Photodynamic therapy (PDT) has the advantage of a single treatment but a CCR of 38%. PDT may be advantageous for a patient who has difficulty applying topical medication over a period of weeks.

Niacinamide has been shown to help with skin repair and reduce the risk of additional nonmelanoma skin cancers (NMSC) by 23% and additional actinic keratoses by about 15% in individuals with a history of actinic keratoses or NMSC.³ In contrast to niacin, niacinamide does not cause flushing. Niacinamide is used long term; if discontinued, it no longer confers benefit in helping the skin repair itself.

The patient in this case was prescribed topical 5% fluorouracil cream to be applied twice daily to the malar regions bilaterally for 2 weeks and, if not inflamed by 2 weeks, to extend the treatment until there is robust inflammation (but not to exceed 3 weeks). He was scheduled to follow up in 3 months for reexamination. He was also advised to start taking niacinamide 500 mg twice daily to reduce his risk of additional precancerous and cancerous skin lesions and counseled on the importance of sunscreen, hats, and sun-protective clothing.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The patient’s toenail thickening appeared consistent with possible onychomycosis—but in addition, there was a marked inflammatory and vesicular eruption consistent with an allergic contact dermatitis.

TTO, also known as melaleuca oil, is a popular product used to treat many disorders including alopecia, seborrheic dermatitis, and onychomycosis.¹ Unfortunately, it is a complex compound, and the rate of positive reactions to patch testing ranges from 0.1% to 3.5%.²

There are 2 types of contact dermatitis: irritant and allergic. Irritant contact dermatitis results from an irritating or relatively caustic substance causing direct damage and inflammation to the skin. In allergic contact dermatitis, as occurred here, there is sensitization to a substance that causes a type IV delayed cell-mediated immune response. Although radioallergosorbent blood testing will usually show immunoglobulin E antibodies to the inciting substance, patch testing is more specific and will show a reaction to the imputed substance on direct skin application. This usually is performed as a panel of antigens tested at the same time.

The mainstay of treatment is to identify, stop use of, and then avoid the sensitizing substance. Topical steroids (triamcinolone 0.1% ointment or clobetasol 0.05% ointment twice daily) are helpful in most cases. If the condition is severe or does not respond to initial therapy, systemic steroids (prednisone 40 mg/d for 5 days for most cases or a 2- to 3-week taper for Rhus dermatitis [eg, poison ivy]) are often effective.³

This patient was instructed to stop using TTO and counseled to avoid it in the future. She was told that her nails might fall off due to the inflammation, which might cure her onychomycosis, and that it takes 12 to 18 months to grow new toenails. She was advised to return for evaluation if the new nails developed any abnormalities or if her onychomycosis recurred. Oral terbinafine 250 mg/d for 90 days is usually a safe and effective therapy.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The patient’s toenail thickening appeared consistent with possible onychomycosis—but in addition, there was a marked inflammatory and vesicular eruption consistent with an allergic contact dermatitis.

TTO, also known as melaleuca oil, is a popular product used to treat many disorders including alopecia, seborrheic dermatitis, and onychomycosis.¹ Unfortunately, it is a complex compound, and the rate of positive reactions to patch testing ranges from 0.1% to 3.5%.²

There are 2 types of contact dermatitis: irritant and allergic. Irritant contact dermatitis results from an irritating or relatively caustic substance causing direct damage and inflammation to the skin. In allergic contact dermatitis, as occurred here, there is sensitization to a substance that causes a type IV delayed cell-mediated immune response. Although radioallergosorbent blood testing will usually show immunoglobulin E antibodies to the inciting substance, patch testing is more specific and will show a reaction to the imputed substance on direct skin application. This usually is performed as a panel of antigens tested at the same time.

The mainstay of treatment is to identify, stop use of, and then avoid the sensitizing substance. Topical steroids (triamcinolone 0.1% ointment or clobetasol 0.05% ointment twice daily) are helpful in most cases. If the condition is severe or does not respond to initial therapy, systemic steroids (prednisone 40 mg/d for 5 days for most cases or a 2- to 3-week taper for Rhus dermatitis [eg, poison ivy]) are often effective.³

This patient was instructed to stop using TTO and counseled to avoid it in the future. She was told that her nails might fall off due to the inflammation, which might cure her onychomycosis, and that it takes 12 to 18 months to grow new toenails. She was advised to return for evaluation if the new nails developed any abnormalities or if her onychomycosis recurred. Oral terbinafine 250 mg/d for 90 days is usually a safe and effective therapy.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The patient’s toenail thickening appeared consistent with possible onychomycosis—but in addition, there was a marked inflammatory and vesicular eruption consistent with an allergic contact dermatitis.

TTO, also known as melaleuca oil, is a popular product used to treat many disorders including alopecia, seborrheic dermatitis, and onychomycosis.¹ Unfortunately, it is a complex compound, and the rate of positive reactions to patch testing ranges from 0.1% to 3.5%.²

There are 2 types of contact dermatitis: irritant and allergic. Irritant contact dermatitis results from an irritating or relatively caustic substance causing direct damage and inflammation to the skin. In allergic contact dermatitis, as occurred here, there is sensitization to a substance that causes a type IV delayed cell-mediated immune response. Although radioallergosorbent blood testing will usually show immunoglobulin E antibodies to the inciting substance, patch testing is more specific and will show a reaction to the imputed substance on direct skin application. This usually is performed as a panel of antigens tested at the same time.

The mainstay of treatment is to identify, stop use of, and then avoid the sensitizing substance. Topical steroids (triamcinolone 0.1% ointment or clobetasol 0.05% ointment twice daily) are helpful in most cases. If the condition is severe or does not respond to initial therapy, systemic steroids (prednisone 40 mg/d for 5 days for most cases or a 2- to 3-week taper for Rhus dermatitis [eg, poison ivy]) are often effective.³

This patient was instructed to stop using TTO and counseled to avoid it in the future. She was told that her nails might fall off due to the inflammation, which might cure her onychomycosis, and that it takes 12 to 18 months to grow new toenails. She was advised to return for evaluation if the new nails developed any abnormalities or if her onychomycosis recurred. Oral terbinafine 250 mg/d for 90 days is usually a safe and effective therapy.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The Advisory Committee on Immunization Practices (ACIP) recently issued new recommendations on polio vaccine for adults. The ACIP decided to update its previous recommendations (from 2000) in response to a case in New York that demonstrated the United States is at risk for poliovirus importation as long as the disease has not been eliminated worldwide.¹

What happened in New York? In July 2022, a case of paralytic polio was confirmed in an unvaccinated adult in Rockland County, New York, an area that has low polio vaccine coverage. Subsequent testing of wastewater systems detected poliovirus in a total of 5 New York counties (including 2 in New York City).¹

The Centers for Disease Control and Prevention estimates that this region of the state probably experienced 1000 to 2000 nonparalytic, mostly asymptomatic poliovirus infections. The virus detected in wastewater in New York is genetically linked to polioviruses collected in wastewater in Israel, the United Kingdom, and Canada. No poliovirus has been detected in these wastewater systems since late 2022.^1,2

Why there’s reason for concern. Routine immunization against polio has been part of the immunization schedule for infants and children since the mid-1950s. As a result, endemic polio was eliminated in the United States in 1979 and in the Western Hemisphere in 1994.

However, adult vaccination until now has been recommended only for those at risk for exposure to poliovirus by way of travel or occupation. And while most adults in the United States are immune to polio due to childhood vaccination, unvaccinated adults remain susceptible if exposed to poliovirus—as demonstrated in the New York case.

What does the ACIP now recommend? Two recommendations were adopted by the ACIP this June to address this problem²:

1. Adults who are known or suspected to be unvaccinated or incompletely vaccinated against polio should complete a primary vaccination series with inactivated polio vaccine (IPV).
2. Adults who have received a primary series of oral polio vaccine (OPV) or IPV in any combination and who are at increased risk for poliovirus exposure may receive another dose of IPV. Available data do not indicate a need for > 1 lifetime booster.

A few details: To be considered fully vaccinated, a patient must have received a primary series of ≥ 3 doses of OPV or IPV (in any combination) given at least 4 weeks apart, with the last dose given on or after the 4th birthday and at least 6 months from the previous dose. Most adults who were born and raised in the United States can assume they were vaccinated against polio as children, unless there are specific reasons to suspect otherwise.²

Individuals considered to be at increased risk include: travelers who are going to countries where polio is epidemic or endemic; laboratory and health care workers who handle specimens that might contain polioviruses; and health care workers or other caregivers who have close contact with a person who could be infected with poliovirus.²

Take-home message. Be prepared to discuss and offer IPV (the only form of the vaccine currently in use in the United States) to adults, as either a one-time booster for those at increased risk for exposure to poliovirus or a complete series for those you know or suspect to be unvaccinated or incompletely vaccinated.

The Advisory Committee on Immunization Practices (ACIP) recently issued new recommendations on polio vaccine for adults. The ACIP decided to update its previous recommendations (from 2000) in response to a case in New York that demonstrated the United States is at risk for poliovirus importation as long as the disease has not been eliminated worldwide.¹

What happened in New York? In July 2022, a case of paralytic polio was confirmed in an unvaccinated adult in Rockland County, New York, an area that has low polio vaccine coverage. Subsequent testing of wastewater systems detected poliovirus in a total of 5 New York counties (including 2 in New York City).¹

The Centers for Disease Control and Prevention estimates that this region of the state probably experienced 1000 to 2000 nonparalytic, mostly asymptomatic poliovirus infections. The virus detected in wastewater in New York is genetically linked to polioviruses collected in wastewater in Israel, the United Kingdom, and Canada. No poliovirus has been detected in these wastewater systems since late 2022.^1,2

Why there’s reason for concern. Routine immunization against polio has been part of the immunization schedule for infants and children since the mid-1950s. As a result, endemic polio was eliminated in the United States in 1979 and in the Western Hemisphere in 1994.

However, adult vaccination until now has been recommended only for those at risk for exposure to poliovirus by way of travel or occupation. And while most adults in the United States are immune to polio due to childhood vaccination, unvaccinated adults remain susceptible if exposed to poliovirus—as demonstrated in the New York case.

What does the ACIP now recommend? Two recommendations were adopted by the ACIP this June to address this problem²:

1. Adults who are known or suspected to be unvaccinated or incompletely vaccinated against polio should complete a primary vaccination series with inactivated polio vaccine (IPV).
2. Adults who have received a primary series of oral polio vaccine (OPV) or IPV in any combination and who are at increased risk for poliovirus exposure may receive another dose of IPV. Available data do not indicate a need for > 1 lifetime booster.

A few details: To be considered fully vaccinated, a patient must have received a primary series of ≥ 3 doses of OPV or IPV (in any combination) given at least 4 weeks apart, with the last dose given on or after the 4th birthday and at least 6 months from the previous dose. Most adults who were born and raised in the United States can assume they were vaccinated against polio as children, unless there are specific reasons to suspect otherwise.²

Individuals considered to be at increased risk include: travelers who are going to countries where polio is epidemic or endemic; laboratory and health care workers who handle specimens that might contain polioviruses; and health care workers or other caregivers who have close contact with a person who could be infected with poliovirus.²

Take-home message. Be prepared to discuss and offer IPV (the only form of the vaccine currently in use in the United States) to adults, as either a one-time booster for those at increased risk for exposure to poliovirus or a complete series for those you know or suspect to be unvaccinated or incompletely vaccinated.

The Advisory Committee on Immunization Practices (ACIP) recently issued new recommendations on polio vaccine for adults. The ACIP decided to update its previous recommendations (from 2000) in response to a case in New York that demonstrated the United States is at risk for poliovirus importation as long as the disease has not been eliminated worldwide.¹

What happened in New York? In July 2022, a case of paralytic polio was confirmed in an unvaccinated adult in Rockland County, New York, an area that has low polio vaccine coverage. Subsequent testing of wastewater systems detected poliovirus in a total of 5 New York counties (including 2 in New York City).¹

The Centers for Disease Control and Prevention estimates that this region of the state probably experienced 1000 to 2000 nonparalytic, mostly asymptomatic poliovirus infections. The virus detected in wastewater in New York is genetically linked to polioviruses collected in wastewater in Israel, the United Kingdom, and Canada. No poliovirus has been detected in these wastewater systems since late 2022.^1,2

Why there’s reason for concern. Routine immunization against polio has been part of the immunization schedule for infants and children since the mid-1950s. As a result, endemic polio was eliminated in the United States in 1979 and in the Western Hemisphere in 1994.

However, adult vaccination until now has been recommended only for those at risk for exposure to poliovirus by way of travel or occupation. And while most adults in the United States are immune to polio due to childhood vaccination, unvaccinated adults remain susceptible if exposed to poliovirus—as demonstrated in the New York case.

What does the ACIP now recommend? Two recommendations were adopted by the ACIP this June to address this problem²:

1. Adults who are known or suspected to be unvaccinated or incompletely vaccinated against polio should complete a primary vaccination series with inactivated polio vaccine (IPV).
2. Adults who have received a primary series of oral polio vaccine (OPV) or IPV in any combination and who are at increased risk for poliovirus exposure may receive another dose of IPV. Available data do not indicate a need for > 1 lifetime booster.

A few details: To be considered fully vaccinated, a patient must have received a primary series of ≥ 3 doses of OPV or IPV (in any combination) given at least 4 weeks apart, with the last dose given on or after the 4th birthday and at least 6 months from the previous dose. Most adults who were born and raised in the United States can assume they were vaccinated against polio as children, unless there are specific reasons to suspect otherwise.²

Individuals considered to be at increased risk include: travelers who are going to countries where polio is epidemic or endemic; laboratory and health care workers who handle specimens that might contain polioviruses; and health care workers or other caregivers who have close contact with a person who could be infected with poliovirus.²

Take-home message. Be prepared to discuss and offer IPV (the only form of the vaccine currently in use in the United States) to adults, as either a one-time booster for those at increased risk for exposure to poliovirus or a complete series for those you know or suspect to be unvaccinated or incompletely vaccinated.

Hot Topics in Primary Care 2023 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.

Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
 

• A Patient-Centered Approach to Managing IBS-C and CIC
• Acute Pain in Perspective
• Continuous Glucose Monitoring in Practice
• Early Intervention by Family Physicians to Delay Type 1 Diabetes
• Early Life Nutrition and the Developing Brain
• Insomnia Management: A Review and Update
• New Paradigms for CKD Management in Patients With T2D
• Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D
• Reducing Cardiopulmonary Risk and Exacerbations in COPD
• Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 RAs
• Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future

This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.

Click here to read Hot Topics in Primary Care 2023

This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.

A Patient-Centered Approach to Managing IBS-C and CIC, Brian E. Lacy, MD, PhD, FACG


Acute Pain in Perspective, Bill McCarberg, MD


Continuous Glucose Monitoring in Practice, Eden M. Miller, DO


Early Intervention by Family Physicians to Delay Type 1 Diabetes, Steven Edelman, MD


Early Life Nutrition and the Developing Brain, Danielle Christifano, PhD; Lara Bennett, MS, RD, LD


Insomnia Management: A Review and Update, David P. Shaha, MD


New Paradigms for CKD Management in Patients With T2D, Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP; Stephen A. Brunton, MD, FAAFP, CDCES


Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D, Jay H. Shubrook, DO; Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP


Reducing Cardiopulmonary Risk and Exacerbations in COPD, Barbara Yawn, MD, MSc, FAAFP


Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 Ras, John E. Anderson, MD; Javed Butler, MD, MPH, MBA; Andrei V. Alexandrov, MD


Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future, Neil Skolnik, MD; Marissa Norden, DO; Njira Lugogo, MD: Wendy Wright, DNP, ANP-BC, FNP-BC, FAANP, FAAN, FNAP

Hot Topics in Primary Care 2023 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.

Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
 

• A Patient-Centered Approach to Managing IBS-C and CIC
• Acute Pain in Perspective
• Continuous Glucose Monitoring in Practice
• Early Intervention by Family Physicians to Delay Type 1 Diabetes
• Early Life Nutrition and the Developing Brain
• Insomnia Management: A Review and Update
• New Paradigms for CKD Management in Patients With T2D
• Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D
• Reducing Cardiopulmonary Risk and Exacerbations in COPD
• Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 RAs
• Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future

This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.

Click here to read Hot Topics in Primary Care 2023

This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.

A Patient-Centered Approach to Managing IBS-C and CIC, Brian E. Lacy, MD, PhD, FACG


Acute Pain in Perspective, Bill McCarberg, MD


Continuous Glucose Monitoring in Practice, Eden M. Miller, DO


Early Intervention by Family Physicians to Delay Type 1 Diabetes, Steven Edelman, MD


Early Life Nutrition and the Developing Brain, Danielle Christifano, PhD; Lara Bennett, MS, RD, LD


Insomnia Management: A Review and Update, David P. Shaha, MD


New Paradigms for CKD Management in Patients With T2D, Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP; Stephen A. Brunton, MD, FAAFP, CDCES


Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D, Jay H. Shubrook, DO; Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP


Reducing Cardiopulmonary Risk and Exacerbations in COPD, Barbara Yawn, MD, MSc, FAAFP


Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 Ras, John E. Anderson, MD; Javed Butler, MD, MPH, MBA; Andrei V. Alexandrov, MD


Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future, Neil Skolnik, MD; Marissa Norden, DO; Njira Lugogo, MD: Wendy Wright, DNP, ANP-BC, FNP-BC, FAANP, FAAN, FNAP

Hot Topics in Primary Care 2023 is a resource that explores the newest developments in primary care topics that impact your daily clinical practice.

Click on the link below to access the entire supplement. You can also click on the video panes below to view brief summaries of individual chapters. Titles above the video panes link directly to each article.
 

• A Patient-Centered Approach to Managing IBS-C and CIC
• Acute Pain in Perspective
• Continuous Glucose Monitoring in Practice
• Early Intervention by Family Physicians to Delay Type 1 Diabetes
• Early Life Nutrition and the Developing Brain
• Insomnia Management: A Review and Update
• New Paradigms for CKD Management in Patients With T2D
• Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D
• Reducing Cardiopulmonary Risk and Exacerbations in COPD
• Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 RAs
• Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future

This supplement offers the opportunity to earn a total of 4 continuing medical education (CME) credits. Credit is awarded for successful completion of the evaluation after reading the article. The links can be found within the supplement on the first page of each article where CME credits are offered.

Click here to read Hot Topics in Primary Care 2023

This supplement to The Journal of Family Practice was sponsored by the Primary Care Education Consortium and Primary Care Metabolic Group.
Check out these short video segments, which were prepared by the supplement authors and summarize the individual articles.
The title above each video links to the related article.

A Patient-Centered Approach to Managing IBS-C and CIC, Brian E. Lacy, MD, PhD, FACG


Acute Pain in Perspective, Bill McCarberg, MD


Continuous Glucose Monitoring in Practice, Eden M. Miller, DO


Early Intervention by Family Physicians to Delay Type 1 Diabetes, Steven Edelman, MD


Early Life Nutrition and the Developing Brain, Danielle Christifano, PhD; Lara Bennett, MS, RD, LD


Insomnia Management: A Review and Update, David P. Shaha, MD


New Paradigms for CKD Management in Patients With T2D, Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP; Stephen A. Brunton, MD, FAAFP, CDCES


Optimized Management of Cardio-Renal-Metabolic (CRM) Conditions in Patients with T2D, Jay H. Shubrook, DO; Joshua J. Neumiller, PharmD, CDCES, FADCES, FASCP


Reducing Cardiopulmonary Risk and Exacerbations in COPD, Barbara Yawn, MD, MSc, FAAFP


Reducing Ischemic Stroke in Diabetes: The Role of GLP-1 Ras, John E. Anderson, MD; Javed Butler, MD, MPH, MBA; Andrei V. Alexandrov, MD


Use of ICS and Fast-Acting Bronchodilators in Asthma: Past, Present, and Future, Neil Skolnik, MD; Marissa Norden, DO; Njira Lugogo, MD: Wendy Wright, DNP, ANP-BC, FNP-BC, FAANP, FAAN, FNAP

THE COMPARISON

A A 51-year-old Hispanic man with a squamous cell carcinoma (SCC) of the keratoacanthoma type on the arm.

B A 75-year-old Black man with an SCC of the keratoacanthoma type on the abdomen.

C An African woman with an SCC on the lower lip decades after a large facial burn, which is known as a Marjolin ulcer.

Cutaneous squamous cell carcinoma (SCC) develops from a malignant tumor of the keratinocytes, eccrine glands, or pilosebaceous units that invades the dermis. Risk factors include lighter skin tone, higher cumulative sun exposure, human papillomavirus (HPV) infection, hidradenitis suppurativa (HS), lichen sclerosus, family history of skin cancer,¹ and immunosuppression.² It typically affects sun-exposed areas of the body such as the face, scalp, neck, and extensor surfaces of the arms (FIGURE A).^3,4 However, in those with darker skin tones, the most common anatomic sites are those that are not exposed to the sun (FIGURE B). SCC is diagnosed via skin biopsy. Treatment options include surgical excision, destructive methods such as electrodesiccation and curettage, and Mohs micrographic surgery. Cutaneous SCC has a cure rate of more than 95% and a mortality rate of 1.5% to 2% in the United States.³

Epidemiology

SCC is the most common skin cancer occurring in Black individuals, manifesting primarily in the fifth decade of life.^5-7 It is the second most common skin cancer in White, Hispanic, and Asian individuals and is more common in males.⁸ In a study of organ transplant recipients (N = 413), Pritchett et al⁹ reported that HPV infection was a major risk factor in Hispanic patients because 66.7% of those with SCC had a history of HPV. However, HPV is a risk factor for SCC in all ethnic groups.¹⁰

Key clinical features in people with darker skin tones

Anatomic location

• The lower legs and anogenital areas are the most common sites for SCC in patients with skin of color.^4,11
• In Black women, SCC occurs more often on sun-exposed areas such as the arms and legs compared to Black men.^7,12-14
• The genitalia, perianal area, ocular mucosa, and oral mucosa are the least likely areas to be routinely examined, even in skin cancer clinics that see highrisk patients, despite the SCC risk in the anogenital area.^15,16
• Squamous cell carcinoma of the lips and scalp is more likely to occur in Black women vs Black men.^4,7,17

Clinical appearance

• In those with darker skin tones, SCCs may appear hyperpigmented4 or hyperkeratotic with a lack of erythema and an inconsistent appearance.^6,7,18
• A nonhealing ulceration of the skin should prompt a biopsy to rule out SCC.^3,19

Worth noting

In patients with darker skin tones, the risk for SCC increases in areas with chronic inflammation and scarring of the skin.^{4,6,7,11,18,20-22} In Black patients, 20% to 40% of cases of SCC occur in the setting of chronic inflammation and scarring.^6,7,18 Chronic inflammatory conditions include ulcers, lupus vulgaris, discoid lupus erythematosus, and HPV. In patients with discoid lupus erythematosus, there is an additive effect of sun exposure on the scars, which may play a role in the pathogenesis and metastasis risk for skin cancer in Black patients.⁴ Other scarring conditions include thermal or chemical burn scars, areas of physical trauma, and prior sites of radiation treatment.^14,23 SCC arising in a burn scar is called a Marjolin ulcer or malignant degeneration of a scar (FIGURE C). It is reported more often in lower-income, underresourced countries, which may suggest the need for early detection in populations with skin of color.²⁴

SCC is more aggressive in sites that are not exposed to sun compared to sun-exposed areas.^17,25

Continue to: The risk for SCC...

The risk for SCC is increased in immunocompromised patients,2 especially those with HPV.¹⁰

The prevalence of SCC in those with HS is approximately 4.6%. The chronic inflammation and irritation from HS in association with other risk factors such as tobacco use may contribute to the malignant transformation to SCC.²⁶

Health disparity highlight

• The risk for metastasis from SCC is 20% to 40% in Black patients vs 1% to 4% in White patients.^4,6,27
• Penile SCC was associated with a lower overall survival rate in patients of African descent.^20,21
• The increased morbidity and mortality from SCC in patients with skin of color may be attributed to delays in diagnosis and treatment as well as an incomplete understanding of tumor genetics.^4,6,18

ACKNOWLEDGMENT
The authors thank Elyse Gadra (Philadelphia, Pennsylvania) for assistance in the preparation of this manuscript.