MDedge Dermatology

Pigmented purpuric dermatoses (PPDs) are characterized by petechiae, dusky macules representative of postinflammatory hyperpigmentation and dermal hemosiderin, and purpura generally localized to the lower extremities. They typically represent a spectrum of lymphocytic capillaritis, variable erythrocyte extravasation from papillary dermal blood vessels, and deposition of hemosiderin, yielding the classic red to orange to golden-brown findings on gross examination. Clinical overlap exists, but variants include Schamberg disease (SD), Majocchi purpura, Gougerot-Blum purpura, eczematoid purpura of Doucas and Kapetanakis (DK), and lichen aureus.¹ Other forms are rarer, including linear, granulomatous, quadrantic, transitory, and familial variants. It remains controversial whether PPD may precede or have an association with cutaneous T-cell lymphoma.² Dermoscopy usually shows copper-red pigmentation in the background, oval red dots, linear vessels, brown globules, and follicular openings. Although these findings may be useful in PPD diagnosis, they are not applicable in differentiating among the variants.

Pigmented purpuric dermatoses can easily be mistaken for stasis dermatitis or cellulitis, as these may occur concomitantly or in populations at risk for all 3 conditions, such as women older than 50 years with recent trauma or infection in the affected area. Tissue biopsy and clinical laboratory evaluation may be required to differentiate between PPD from leukocytoclastic vasculitis or the myriad causes of retiform purpura. Importantly, clinicians also should differentiate PPD from the purpuric eruptions of the lower extremities associated with COVID-19 infection.

Pigmented Purpuric Dermatoses

Schamberg Disease—In 1901, Jay Frank Schamberg, a distinguished professor of dermatology in Philadelphia, Pennsylvania, described “a peculiar progressive pigmentary disease of the skin” in a 15-year-old adolescent boy.³ Schamberg disease is the most common PPD, characterized by pruritic spots resembling cayenne pepper (Figure 1) with orange-brown pigmented macules on the legs and feet.⁴ Although platelet dysfunction, coagulation deficiencies, or dermal atrophy may contribute to hemorrhaging that manifests as petechiae or ecchymoses, SD typically is not associated with any laboratory abnormalities, and petechial eruption is not widespread.⁵ Capillary fragility can be assessed by the tourniquet test, in which pressure is applied to the forearm with a blood pressure cuff inflated between systolic and diastolic blood pressure for 5 to 10 minutes. Upon removing the cuff, a positive test is indicated by 15 or more petechiae in an area 5 cm in diameter due to poor platelet function. A positive result may be seen in SD.⁶

Histologically, SD is characterized by patchy parakeratosis, mild spongiosis of the stratum Malpighi, and lymphoid capillaritis (Figure 2).⁷ In addition to CD3⁺, CD4⁺, CD8⁺, CD1a⁺, and CD36⁺ lymphocytes, histology also may contain dendritic cells and cellular adhesion molecules (intercellular adhesion molecule 1, epithelial cell adhesion molecule 1) within the superficial perivascular infiltrate.⁸ There is no definitive therapy, but first-line interventions include emollients, topical steroids, and oral antihistamines. Nonpharmacologic management includes compression or support stockings, elevation of the lower extremities, and avoidance of offending medications (if identifiable).¹

Majocchi Purpura—Domenico Majocchi was a renowned Italian dermatologist who described an entity in 1898 that he called purpura annularis telangiectodes, now also known as Majocchi purpura.⁹ It is more common in females, young adults, and children. Majocchi purpura has rarely been reported in families with a possible autosomal-dominant inheritance.¹⁰ Typically, bluish-red annular macules with central atrophy surrounded by hyperpigmentation may be seen on the lower extremities, potentially extending to the upper extremities.¹ Treatment of Majocchi purpura remains a challenge but may respond to narrowband UVB phototherapy. Emollients and topical steroids also are used as first-line treatments. Biopsy demonstrates telangiectasia, pericapillary infiltration of mononuclear lymphocytes, and papillary dermal hemosiderin.¹¹

Gougerot-Blum Purpura—In 1925, French dermatologists Henri Gougerot and Paul Blum described a pigmented purpuric lichenoid dermatitis known as Gougerot-Blum purpura,¹² a rare PPD characterized by lichenoid papules that eventually coalesce into plaques of various colors, along with red-brown hyperpigmentation.⁴ As with other PPD variants, the legs are most involved, with rare extension to the trunk or thighs. The plaques may resemble and be mistaken for Kaposi sarcoma, cutaneous vasculitis, traumatic purpura, or mycosis fungoides. Dermoscopic examination reveals small, polygonal or round, red dots underlying brown scaly patches.¹³ Gougerot-Blum purpura is found more commonly in adult men and rarely affects children.⁴ Histologically, a lichenoid and superficial perivascular infiltrate composed of lymphocytes and macrophages is seen. Various therapies have been described, including topical steroids, antihistamines, psoralen plus UVA phototherapy, and cyclosporin A.¹⁴

Eczematoid Purpura of Doucas and Kapetanakis—In 1949, Greek dermatologists Christopher Doucas and John Kapetanakis observed several cases of purpuric dermatosis similar in form to the “pigmented purpuric lichenoid dermatitis” of Gougerot-Blum purpura¹² and to the “progressive pigmentary dermatitis” of Schamberg disease.³ After observing a gradual disappearance of the classic yellow color from hemosiderin deposition, Doucas and Kapetanakis described a new bright red eruption with lichenification.¹⁵ Eczematoid purpura of Doucas and Kapetanakis is rare and predominantly seen in middle-aged males. Hyperpigmented or dark brown macules may develop bilaterally on the legs, progressing to the thighs and upper extremities. Unlike the other types of PPD, DK is extensive and severely pruritic.⁴

Although most PPD can be drug induced, DK has shown the greatest tendency for pruritic erythematous plaques following drug usage including but not limited to amlodipine, aspirin, acetaminophen, thiamine, interferon alfa, chlordiazepoxide, and isotretinoin. Additionally, DK has been associated with a contact allergy to clothing dyes and rubber.⁴ On histology, epidermal spongiosis may be seen, correlating with the eczematoid clinical findings. Spontaneous remission also is more common compared to the other PPDs. Treatment consists of topical corticosteroids and antihistamines.¹⁶

Lichen Aureus—Lichen aureus was first observed by the dermatologist R.H. Martin in 1958.¹⁷ It is clinically characterized by closely aggregated purpuric papules with a distinctive golden-brown color more often localized to the lower extremities and sometimes in a dermatomal distribution. Lichen aureus affects males and females equally, and similar to Majocchi purpura can be seen in children.⁴ Histopathologic examination reveals a prominent lichenoid plus superficial and deep perivascular lymphocytic infiltrate, extravasated erythrocytes, papillary dermal edema, hemosiderophages, and an unaffected epidermis. In rare cases, perineural infiltrates may be seen. Topical steroids usually are ineffective in lichen aureus treatment, but responses to psoralen plus UVA therapy also have been noted.¹⁷

Differential Diagnosis

COVID-19–Related Cutaneous Changes—Because COVID-19–related pathology is now a common differential diagnosis for many cutaneous eruptions, one must be mindful of the possibility for patients to have PPD, cutaneous changes from underlying COVID-19, or both.¹⁸ The microvascular changes from COVID-19 infection can be variable.¹⁹ Besides the presence of erythema along a distal digit, manifestations can include reticulated dusky erythema mimicking livedoid vasculopathy or inflammatory purpura.¹⁹

Retiform Purpura—Retiform purpura may occur in the setting of microvascular occlusion and can represent the pattern of underlying dermal vasculature. It is nonblanching and typically stellate or branching.²⁰ The microvascular occlusion may be a result of hypercoagulability or may be secondary to cutaneous vasculitis, resulting in thrombosis and subsequent vascular occlusion.²¹ There are many reasons for hypercoagulability in retiform purpura, including disseminated intravascular coagulation in the setting of COVID-19 infection.²² The treatment of retiform purpura is aimed at alleviating the underlying cause and providing symptomatic relief. Conversely, the PPDs generally are benign and require minimal workup.

Leukocytoclastic Vasculitis—The hallmark of leukocytoclastic vasculitis is palpable purpura, often appearing as nonblanchable papules, typically in a dependent distribution such as the lower extremities (Figure 3). Although it primarily affects children, Henoch-Schönlein purpura is a type of leukocytoclastic vasculitis with lesions potentially similar in appearance to those of PPD.²³ Palpable purpura may be painful and may ulcerate but rarely is pruritic. Leukocytoclastic vasculitis represents perivascular infiltrates composed of neutrophils, lymphocytes, and occasionally eosinophils, along with karyorrhexis, luminal fibrin, and fibrinoid degeneration of blood vessel walls, often resulting from immune complex deposition. Leukocytoclastic vasculitis may affect blood vessels of any size and requires further clinical and laboratory evaluation for infection (including COVID-19), hypercoagulability, autoimmune disease, or medication-related reactions.²⁴

Stasis Dermatitis—Stasis dermatitis, a chronic inflammatory condition stemming from retrograde venous flow due to incompetent venous valves, mimics PPD. Stasis dermatitis initially appears as demarcated erythematous plaques, fissures, and scaling of the lower legs bilaterally, usually involving the medial malleolus.²⁵ With time, the affected region develops overlying brawny hyperpigmentation and fibrosis (Figure 4). Pruritus or pain are common features, while fissures and superficial erosions may heal and recur, leading to lichenification.

Although both commonly appear on the lower extremities, duplex ultrasonography may be helpful to distinguish PPDs from stasis dermatitis since the latter occurs in the context of chronic venous insufficiency, varicose veins, soft tissue edema, and lymphedema.²⁵ Additionally, pruritus, lichenification, and edema often are not seen in most PPD variants, although stasis dermatitis and PPD may occur in tandem. Conservative treatment involves elevation of the extremities, compression, and topical steroids for symptomatic relief.

Cellulitis—The key characteristics of cellulitis are redness, swelling, warmth, tenderness, fever, and leukocytosis. A history of trauma, such as a prior break in the skin, and pain in the affected area suggest cellulitis. Several skin conditions present similarly to cellulitis, including PPD, and thus approximately 30% of cases are misdiagnosed.²⁶ Cellulitis rarely presents in a bilateral or diffusely scattered pattern as seen in PPDs. Rather, it is unilateral with smooth indistinct borders. Variables suggestive of cellulitis include immunosuppression, rapid progression, and previous occurrences. Hyperpigmented plaques or thickening of the skin are more indicative of a chronic process such as stasis dermatitis or lipodermatosclerosis rather than acute cellulitis. Purpura is not a typical finding in most cases of soft tissue cellulitis. Treatment may be case specific depending on severity, presence or absence of sepsis, findings on blood cultures, or other pathologic evaluation. Antibiotics are directed to the causative organism, typically Streptococcus and Staphylococcus species, although coverage against various gram-negative organisms may be indicated.²⁷

Caution With Teledermatology

COVID-19 has established the value of telemedicine in providing access to health care services for at-risk or underserved individuals. The PPDs are benign, often asymptomatic, and potentially identifiable with teledermatology alone; however, they also can easily be mistaken for COVID-19–related eruptions, vasculitis, other types of purpura, stasis dermatitis, or other complications of lower extremity stasis and lymphedema, especially in an aging population. If tissue biopsy is required, as in the workup of vasculitis, the efficacy of telemedicine becomes more questionable. It is important to delineate the potentially confusing PPDs from other potentially dangerous or life-threatening inflammatory dermatoses.²⁸

Pigmented purpuric dermatoses (PPDs) are characterized by petechiae, dusky macules representative of postinflammatory hyperpigmentation and dermal hemosiderin, and purpura generally localized to the lower extremities. They typically represent a spectrum of lymphocytic capillaritis, variable erythrocyte extravasation from papillary dermal blood vessels, and deposition of hemosiderin, yielding the classic red to orange to golden-brown findings on gross examination. Clinical overlap exists, but variants include Schamberg disease (SD), Majocchi purpura, Gougerot-Blum purpura, eczematoid purpura of Doucas and Kapetanakis (DK), and lichen aureus.¹ Other forms are rarer, including linear, granulomatous, quadrantic, transitory, and familial variants. It remains controversial whether PPD may precede or have an association with cutaneous T-cell lymphoma.² Dermoscopy usually shows copper-red pigmentation in the background, oval red dots, linear vessels, brown globules, and follicular openings. Although these findings may be useful in PPD diagnosis, they are not applicable in differentiating among the variants.

Pigmented purpuric dermatoses can easily be mistaken for stasis dermatitis or cellulitis, as these may occur concomitantly or in populations at risk for all 3 conditions, such as women older than 50 years with recent trauma or infection in the affected area. Tissue biopsy and clinical laboratory evaluation may be required to differentiate between PPD from leukocytoclastic vasculitis or the myriad causes of retiform purpura. Importantly, clinicians also should differentiate PPD from the purpuric eruptions of the lower extremities associated with COVID-19 infection.

Pigmented Purpuric Dermatoses

Schamberg Disease—In 1901, Jay Frank Schamberg, a distinguished professor of dermatology in Philadelphia, Pennsylvania, described “a peculiar progressive pigmentary disease of the skin” in a 15-year-old adolescent boy.³ Schamberg disease is the most common PPD, characterized by pruritic spots resembling cayenne pepper (Figure 1) with orange-brown pigmented macules on the legs and feet.⁴ Although platelet dysfunction, coagulation deficiencies, or dermal atrophy may contribute to hemorrhaging that manifests as petechiae or ecchymoses, SD typically is not associated with any laboratory abnormalities, and petechial eruption is not widespread.⁵ Capillary fragility can be assessed by the tourniquet test, in which pressure is applied to the forearm with a blood pressure cuff inflated between systolic and diastolic blood pressure for 5 to 10 minutes. Upon removing the cuff, a positive test is indicated by 15 or more petechiae in an area 5 cm in diameter due to poor platelet function. A positive result may be seen in SD.⁶

Histologically, SD is characterized by patchy parakeratosis, mild spongiosis of the stratum Malpighi, and lymphoid capillaritis (Figure 2).⁷ In addition to CD3⁺, CD4⁺, CD8⁺, CD1a⁺, and CD36⁺ lymphocytes, histology also may contain dendritic cells and cellular adhesion molecules (intercellular adhesion molecule 1, epithelial cell adhesion molecule 1) within the superficial perivascular infiltrate.⁸ There is no definitive therapy, but first-line interventions include emollients, topical steroids, and oral antihistamines. Nonpharmacologic management includes compression or support stockings, elevation of the lower extremities, and avoidance of offending medications (if identifiable).¹

Majocchi Purpura—Domenico Majocchi was a renowned Italian dermatologist who described an entity in 1898 that he called purpura annularis telangiectodes, now also known as Majocchi purpura.⁹ It is more common in females, young adults, and children. Majocchi purpura has rarely been reported in families with a possible autosomal-dominant inheritance.¹⁰ Typically, bluish-red annular macules with central atrophy surrounded by hyperpigmentation may be seen on the lower extremities, potentially extending to the upper extremities.¹ Treatment of Majocchi purpura remains a challenge but may respond to narrowband UVB phototherapy. Emollients and topical steroids also are used as first-line treatments. Biopsy demonstrates telangiectasia, pericapillary infiltration of mononuclear lymphocytes, and papillary dermal hemosiderin.¹¹

Gougerot-Blum Purpura—In 1925, French dermatologists Henri Gougerot and Paul Blum described a pigmented purpuric lichenoid dermatitis known as Gougerot-Blum purpura,¹² a rare PPD characterized by lichenoid papules that eventually coalesce into plaques of various colors, along with red-brown hyperpigmentation.⁴ As with other PPD variants, the legs are most involved, with rare extension to the trunk or thighs. The plaques may resemble and be mistaken for Kaposi sarcoma, cutaneous vasculitis, traumatic purpura, or mycosis fungoides. Dermoscopic examination reveals small, polygonal or round, red dots underlying brown scaly patches.¹³ Gougerot-Blum purpura is found more commonly in adult men and rarely affects children.⁴ Histologically, a lichenoid and superficial perivascular infiltrate composed of lymphocytes and macrophages is seen. Various therapies have been described, including topical steroids, antihistamines, psoralen plus UVA phototherapy, and cyclosporin A.¹⁴

Eczematoid Purpura of Doucas and Kapetanakis—In 1949, Greek dermatologists Christopher Doucas and John Kapetanakis observed several cases of purpuric dermatosis similar in form to the “pigmented purpuric lichenoid dermatitis” of Gougerot-Blum purpura¹² and to the “progressive pigmentary dermatitis” of Schamberg disease.³ After observing a gradual disappearance of the classic yellow color from hemosiderin deposition, Doucas and Kapetanakis described a new bright red eruption with lichenification.¹⁵ Eczematoid purpura of Doucas and Kapetanakis is rare and predominantly seen in middle-aged males. Hyperpigmented or dark brown macules may develop bilaterally on the legs, progressing to the thighs and upper extremities. Unlike the other types of PPD, DK is extensive and severely pruritic.⁴

Although most PPD can be drug induced, DK has shown the greatest tendency for pruritic erythematous plaques following drug usage including but not limited to amlodipine, aspirin, acetaminophen, thiamine, interferon alfa, chlordiazepoxide, and isotretinoin. Additionally, DK has been associated with a contact allergy to clothing dyes and rubber.⁴ On histology, epidermal spongiosis may be seen, correlating with the eczematoid clinical findings. Spontaneous remission also is more common compared to the other PPDs. Treatment consists of topical corticosteroids and antihistamines.¹⁶

Lichen Aureus—Lichen aureus was first observed by the dermatologist R.H. Martin in 1958.¹⁷ It is clinically characterized by closely aggregated purpuric papules with a distinctive golden-brown color more often localized to the lower extremities and sometimes in a dermatomal distribution. Lichen aureus affects males and females equally, and similar to Majocchi purpura can be seen in children.⁴ Histopathologic examination reveals a prominent lichenoid plus superficial and deep perivascular lymphocytic infiltrate, extravasated erythrocytes, papillary dermal edema, hemosiderophages, and an unaffected epidermis. In rare cases, perineural infiltrates may be seen. Topical steroids usually are ineffective in lichen aureus treatment, but responses to psoralen plus UVA therapy also have been noted.¹⁷

Differential Diagnosis

COVID-19–Related Cutaneous Changes—Because COVID-19–related pathology is now a common differential diagnosis for many cutaneous eruptions, one must be mindful of the possibility for patients to have PPD, cutaneous changes from underlying COVID-19, or both.¹⁸ The microvascular changes from COVID-19 infection can be variable.¹⁹ Besides the presence of erythema along a distal digit, manifestations can include reticulated dusky erythema mimicking livedoid vasculopathy or inflammatory purpura.¹⁹

Retiform Purpura—Retiform purpura may occur in the setting of microvascular occlusion and can represent the pattern of underlying dermal vasculature. It is nonblanching and typically stellate or branching.²⁰ The microvascular occlusion may be a result of hypercoagulability or may be secondary to cutaneous vasculitis, resulting in thrombosis and subsequent vascular occlusion.²¹ There are many reasons for hypercoagulability in retiform purpura, including disseminated intravascular coagulation in the setting of COVID-19 infection.²² The treatment of retiform purpura is aimed at alleviating the underlying cause and providing symptomatic relief. Conversely, the PPDs generally are benign and require minimal workup.

Leukocytoclastic Vasculitis—The hallmark of leukocytoclastic vasculitis is palpable purpura, often appearing as nonblanchable papules, typically in a dependent distribution such as the lower extremities (Figure 3). Although it primarily affects children, Henoch-Schönlein purpura is a type of leukocytoclastic vasculitis with lesions potentially similar in appearance to those of PPD.²³ Palpable purpura may be painful and may ulcerate but rarely is pruritic. Leukocytoclastic vasculitis represents perivascular infiltrates composed of neutrophils, lymphocytes, and occasionally eosinophils, along with karyorrhexis, luminal fibrin, and fibrinoid degeneration of blood vessel walls, often resulting from immune complex deposition. Leukocytoclastic vasculitis may affect blood vessels of any size and requires further clinical and laboratory evaluation for infection (including COVID-19), hypercoagulability, autoimmune disease, or medication-related reactions.²⁴

Stasis Dermatitis—Stasis dermatitis, a chronic inflammatory condition stemming from retrograde venous flow due to incompetent venous valves, mimics PPD. Stasis dermatitis initially appears as demarcated erythematous plaques, fissures, and scaling of the lower legs bilaterally, usually involving the medial malleolus.²⁵ With time, the affected region develops overlying brawny hyperpigmentation and fibrosis (Figure 4). Pruritus or pain are common features, while fissures and superficial erosions may heal and recur, leading to lichenification.

Although both commonly appear on the lower extremities, duplex ultrasonography may be helpful to distinguish PPDs from stasis dermatitis since the latter occurs in the context of chronic venous insufficiency, varicose veins, soft tissue edema, and lymphedema.²⁵ Additionally, pruritus, lichenification, and edema often are not seen in most PPD variants, although stasis dermatitis and PPD may occur in tandem. Conservative treatment involves elevation of the extremities, compression, and topical steroids for symptomatic relief.

Cellulitis—The key characteristics of cellulitis are redness, swelling, warmth, tenderness, fever, and leukocytosis. A history of trauma, such as a prior break in the skin, and pain in the affected area suggest cellulitis. Several skin conditions present similarly to cellulitis, including PPD, and thus approximately 30% of cases are misdiagnosed.²⁶ Cellulitis rarely presents in a bilateral or diffusely scattered pattern as seen in PPDs. Rather, it is unilateral with smooth indistinct borders. Variables suggestive of cellulitis include immunosuppression, rapid progression, and previous occurrences. Hyperpigmented plaques or thickening of the skin are more indicative of a chronic process such as stasis dermatitis or lipodermatosclerosis rather than acute cellulitis. Purpura is not a typical finding in most cases of soft tissue cellulitis. Treatment may be case specific depending on severity, presence or absence of sepsis, findings on blood cultures, or other pathologic evaluation. Antibiotics are directed to the causative organism, typically Streptococcus and Staphylococcus species, although coverage against various gram-negative organisms may be indicated.²⁷

Caution With Teledermatology

COVID-19 has established the value of telemedicine in providing access to health care services for at-risk or underserved individuals. The PPDs are benign, often asymptomatic, and potentially identifiable with teledermatology alone; however, they also can easily be mistaken for COVID-19–related eruptions, vasculitis, other types of purpura, stasis dermatitis, or other complications of lower extremity stasis and lymphedema, especially in an aging population. If tissue biopsy is required, as in the workup of vasculitis, the efficacy of telemedicine becomes more questionable. It is important to delineate the potentially confusing PPDs from other potentially dangerous or life-threatening inflammatory dermatoses.²⁸

Pigmented purpuric dermatoses (PPDs) are characterized by petechiae, dusky macules representative of postinflammatory hyperpigmentation and dermal hemosiderin, and purpura generally localized to the lower extremities. They typically represent a spectrum of lymphocytic capillaritis, variable erythrocyte extravasation from papillary dermal blood vessels, and deposition of hemosiderin, yielding the classic red to orange to golden-brown findings on gross examination. Clinical overlap exists, but variants include Schamberg disease (SD), Majocchi purpura, Gougerot-Blum purpura, eczematoid purpura of Doucas and Kapetanakis (DK), and lichen aureus.¹ Other forms are rarer, including linear, granulomatous, quadrantic, transitory, and familial variants. It remains controversial whether PPD may precede or have an association with cutaneous T-cell lymphoma.² Dermoscopy usually shows copper-red pigmentation in the background, oval red dots, linear vessels, brown globules, and follicular openings. Although these findings may be useful in PPD diagnosis, they are not applicable in differentiating among the variants.

Pigmented purpuric dermatoses can easily be mistaken for stasis dermatitis or cellulitis, as these may occur concomitantly or in populations at risk for all 3 conditions, such as women older than 50 years with recent trauma or infection in the affected area. Tissue biopsy and clinical laboratory evaluation may be required to differentiate between PPD from leukocytoclastic vasculitis or the myriad causes of retiform purpura. Importantly, clinicians also should differentiate PPD from the purpuric eruptions of the lower extremities associated with COVID-19 infection.

Pigmented Purpuric Dermatoses

Schamberg Disease—In 1901, Jay Frank Schamberg, a distinguished professor of dermatology in Philadelphia, Pennsylvania, described “a peculiar progressive pigmentary disease of the skin” in a 15-year-old adolescent boy.³ Schamberg disease is the most common PPD, characterized by pruritic spots resembling cayenne pepper (Figure 1) with orange-brown pigmented macules on the legs and feet.⁴ Although platelet dysfunction, coagulation deficiencies, or dermal atrophy may contribute to hemorrhaging that manifests as petechiae or ecchymoses, SD typically is not associated with any laboratory abnormalities, and petechial eruption is not widespread.⁵ Capillary fragility can be assessed by the tourniquet test, in which pressure is applied to the forearm with a blood pressure cuff inflated between systolic and diastolic blood pressure for 5 to 10 minutes. Upon removing the cuff, a positive test is indicated by 15 or more petechiae in an area 5 cm in diameter due to poor platelet function. A positive result may be seen in SD.⁶

Histologically, SD is characterized by patchy parakeratosis, mild spongiosis of the stratum Malpighi, and lymphoid capillaritis (Figure 2).⁷ In addition to CD3⁺, CD4⁺, CD8⁺, CD1a⁺, and CD36⁺ lymphocytes, histology also may contain dendritic cells and cellular adhesion molecules (intercellular adhesion molecule 1, epithelial cell adhesion molecule 1) within the superficial perivascular infiltrate.⁸ There is no definitive therapy, but first-line interventions include emollients, topical steroids, and oral antihistamines. Nonpharmacologic management includes compression or support stockings, elevation of the lower extremities, and avoidance of offending medications (if identifiable).¹

Majocchi Purpura—Domenico Majocchi was a renowned Italian dermatologist who described an entity in 1898 that he called purpura annularis telangiectodes, now also known as Majocchi purpura.⁹ It is more common in females, young adults, and children. Majocchi purpura has rarely been reported in families with a possible autosomal-dominant inheritance.¹⁰ Typically, bluish-red annular macules with central atrophy surrounded by hyperpigmentation may be seen on the lower extremities, potentially extending to the upper extremities.¹ Treatment of Majocchi purpura remains a challenge but may respond to narrowband UVB phototherapy. Emollients and topical steroids also are used as first-line treatments. Biopsy demonstrates telangiectasia, pericapillary infiltration of mononuclear lymphocytes, and papillary dermal hemosiderin.¹¹

Gougerot-Blum Purpura—In 1925, French dermatologists Henri Gougerot and Paul Blum described a pigmented purpuric lichenoid dermatitis known as Gougerot-Blum purpura,¹² a rare PPD characterized by lichenoid papules that eventually coalesce into plaques of various colors, along with red-brown hyperpigmentation.⁴ As with other PPD variants, the legs are most involved, with rare extension to the trunk or thighs. The plaques may resemble and be mistaken for Kaposi sarcoma, cutaneous vasculitis, traumatic purpura, or mycosis fungoides. Dermoscopic examination reveals small, polygonal or round, red dots underlying brown scaly patches.¹³ Gougerot-Blum purpura is found more commonly in adult men and rarely affects children.⁴ Histologically, a lichenoid and superficial perivascular infiltrate composed of lymphocytes and macrophages is seen. Various therapies have been described, including topical steroids, antihistamines, psoralen plus UVA phototherapy, and cyclosporin A.¹⁴

Eczematoid Purpura of Doucas and Kapetanakis—In 1949, Greek dermatologists Christopher Doucas and John Kapetanakis observed several cases of purpuric dermatosis similar in form to the “pigmented purpuric lichenoid dermatitis” of Gougerot-Blum purpura¹² and to the “progressive pigmentary dermatitis” of Schamberg disease.³ After observing a gradual disappearance of the classic yellow color from hemosiderin deposition, Doucas and Kapetanakis described a new bright red eruption with lichenification.¹⁵ Eczematoid purpura of Doucas and Kapetanakis is rare and predominantly seen in middle-aged males. Hyperpigmented or dark brown macules may develop bilaterally on the legs, progressing to the thighs and upper extremities. Unlike the other types of PPD, DK is extensive and severely pruritic.⁴

Although most PPD can be drug induced, DK has shown the greatest tendency for pruritic erythematous plaques following drug usage including but not limited to amlodipine, aspirin, acetaminophen, thiamine, interferon alfa, chlordiazepoxide, and isotretinoin. Additionally, DK has been associated with a contact allergy to clothing dyes and rubber.⁴ On histology, epidermal spongiosis may be seen, correlating with the eczematoid clinical findings. Spontaneous remission also is more common compared to the other PPDs. Treatment consists of topical corticosteroids and antihistamines.¹⁶

Lichen Aureus—Lichen aureus was first observed by the dermatologist R.H. Martin in 1958.¹⁷ It is clinically characterized by closely aggregated purpuric papules with a distinctive golden-brown color more often localized to the lower extremities and sometimes in a dermatomal distribution. Lichen aureus affects males and females equally, and similar to Majocchi purpura can be seen in children.⁴ Histopathologic examination reveals a prominent lichenoid plus superficial and deep perivascular lymphocytic infiltrate, extravasated erythrocytes, papillary dermal edema, hemosiderophages, and an unaffected epidermis. In rare cases, perineural infiltrates may be seen. Topical steroids usually are ineffective in lichen aureus treatment, but responses to psoralen plus UVA therapy also have been noted.¹⁷

Differential Diagnosis

COVID-19–Related Cutaneous Changes—Because COVID-19–related pathology is now a common differential diagnosis for many cutaneous eruptions, one must be mindful of the possibility for patients to have PPD, cutaneous changes from underlying COVID-19, or both.¹⁸ The microvascular changes from COVID-19 infection can be variable.¹⁹ Besides the presence of erythema along a distal digit, manifestations can include reticulated dusky erythema mimicking livedoid vasculopathy or inflammatory purpura.¹⁹

Retiform Purpura—Retiform purpura may occur in the setting of microvascular occlusion and can represent the pattern of underlying dermal vasculature. It is nonblanching and typically stellate or branching.²⁰ The microvascular occlusion may be a result of hypercoagulability or may be secondary to cutaneous vasculitis, resulting in thrombosis and subsequent vascular occlusion.²¹ There are many reasons for hypercoagulability in retiform purpura, including disseminated intravascular coagulation in the setting of COVID-19 infection.²² The treatment of retiform purpura is aimed at alleviating the underlying cause and providing symptomatic relief. Conversely, the PPDs generally are benign and require minimal workup.

Leukocytoclastic Vasculitis—The hallmark of leukocytoclastic vasculitis is palpable purpura, often appearing as nonblanchable papules, typically in a dependent distribution such as the lower extremities (Figure 3). Although it primarily affects children, Henoch-Schönlein purpura is a type of leukocytoclastic vasculitis with lesions potentially similar in appearance to those of PPD.²³ Palpable purpura may be painful and may ulcerate but rarely is pruritic. Leukocytoclastic vasculitis represents perivascular infiltrates composed of neutrophils, lymphocytes, and occasionally eosinophils, along with karyorrhexis, luminal fibrin, and fibrinoid degeneration of blood vessel walls, often resulting from immune complex deposition. Leukocytoclastic vasculitis may affect blood vessels of any size and requires further clinical and laboratory evaluation for infection (including COVID-19), hypercoagulability, autoimmune disease, or medication-related reactions.²⁴

Stasis Dermatitis—Stasis dermatitis, a chronic inflammatory condition stemming from retrograde venous flow due to incompetent venous valves, mimics PPD. Stasis dermatitis initially appears as demarcated erythematous plaques, fissures, and scaling of the lower legs bilaterally, usually involving the medial malleolus.²⁵ With time, the affected region develops overlying brawny hyperpigmentation and fibrosis (Figure 4). Pruritus or pain are common features, while fissures and superficial erosions may heal and recur, leading to lichenification.

Although both commonly appear on the lower extremities, duplex ultrasonography may be helpful to distinguish PPDs from stasis dermatitis since the latter occurs in the context of chronic venous insufficiency, varicose veins, soft tissue edema, and lymphedema.²⁵ Additionally, pruritus, lichenification, and edema often are not seen in most PPD variants, although stasis dermatitis and PPD may occur in tandem. Conservative treatment involves elevation of the extremities, compression, and topical steroids for symptomatic relief.

Cellulitis—The key characteristics of cellulitis are redness, swelling, warmth, tenderness, fever, and leukocytosis. A history of trauma, such as a prior break in the skin, and pain in the affected area suggest cellulitis. Several skin conditions present similarly to cellulitis, including PPD, and thus approximately 30% of cases are misdiagnosed.²⁶ Cellulitis rarely presents in a bilateral or diffusely scattered pattern as seen in PPDs. Rather, it is unilateral with smooth indistinct borders. Variables suggestive of cellulitis include immunosuppression, rapid progression, and previous occurrences. Hyperpigmented plaques or thickening of the skin are more indicative of a chronic process such as stasis dermatitis or lipodermatosclerosis rather than acute cellulitis. Purpura is not a typical finding in most cases of soft tissue cellulitis. Treatment may be case specific depending on severity, presence or absence of sepsis, findings on blood cultures, or other pathologic evaluation. Antibiotics are directed to the causative organism, typically Streptococcus and Staphylococcus species, although coverage against various gram-negative organisms may be indicated.²⁷

Caution With Teledermatology

COVID-19 has established the value of telemedicine in providing access to health care services for at-risk or underserved individuals. The PPDs are benign, often asymptomatic, and potentially identifiable with teledermatology alone; however, they also can easily be mistaken for COVID-19–related eruptions, vasculitis, other types of purpura, stasis dermatitis, or other complications of lower extremity stasis and lymphedema, especially in an aging population. If tissue biopsy is required, as in the workup of vasculitis, the efficacy of telemedicine becomes more questionable. It is important to delineate the potentially confusing PPDs from other potentially dangerous or life-threatening inflammatory dermatoses.²⁸

To the Editor:

Herpes vegetans (HV) is an uncommon infection caused by human herpesvirus (HHV) in patients who are immunocompromised, such as those who are HIV positive.¹ Unlike typical HHV infection, HV can present with exophytic exudative ulcers and papillomatous vegetations. The presentation of ulcerated genital nodules, especially in an immunocompromised patient, yields an array of disorders in the differential diagnosis, including condyloma latum, condyloma acuminatum, pyogenic granuloma (PG), and verrucous carcinoma.^2,3 Histopathology of HV reveals pseudoepitheliomatous hyperplasia, plasma cell infiltration, and positivity for HHV type 1 (HHV-1) and/or HHV type 2 (HHV-2). Herpes vegetans lesions typically require a multimodal treatment approach because many cases are resistant to acyclovir. Treatment options include the nucleoside analogues foscarnet and cidofovir; immunomodulators such as topical imiquimod; and the topical antiviral trifluridine.^1,4-6 We describe a case of HV in a patient with a history of well-controlled HIV infection who presented with a painful fungating penile lesion.

A 55-year-old man presented to the hospital with a painful expanding mass on the distal aspect of the penis of 3 months’ duration. He had a history of HIV infection that was well-controlled by antiretroviral therapy, prior hepatitis B virus infection and acyclovir-resistant genital HHV-2 infection. Physical examination revealed a large, firm, circumferential, exophytic, verrucous plaque with various areas of ulceration and purulent drainage on the distal shaft and glans of the penis (Figure 1). The patient’s most recent absolute CD4 count was 425 cells/mm³ (reference range, 500–1500 cells/mm³). His HIV viral load was undetectable at less than 30 copies/mL. Histopathology with hematoxylin and eosin staining of biopsy material from the penile lesion demonstrated pseudoepitheliomatous epidermal hyperplasia with focal ulceration and a mixed inflammatory infiltrate (Figure 2A). At higher magnification, clear viral cytopathic changes of HHV were noted, including multinucleation, nuclear molding, and homogenous gray nuclei (Figure 2B). Additional staining for fungi, mycobacteria, and spirochetes was negative. In-situ hybridization was negative for human papillomavirus subtypes. A bacterial culture of swabs of the purulent drainage was positive for Staphylococcus aureus and Proteus mirabilis.

Given the patient’s known history of acyclovir-resistant HHV-2 infection, he received a 28-day course of intravenous foscarnet 40 mg/kg every 12 hours. He also was given a 14-day course of intravenous ampicillin-sulbactam 3 g every 6 hours. The patient gradually improved during a 35-day hospital stay. He was discharged with cidofovir cream 1% and oral valacyclovir; the latter was subsequently discontinued by dermatology because of his known history of acyclovir resistance. Four months after discharge, the patient underwent a circumcision performed by urology to decrease the risk for recurrence and achieve the best cosmetic outcome. At the 6-month follow-up visit, dramatic clinical improvement was evident, with complete resolution of the plaque and only isolated areas of scarring (Figure 3). The patient reported that penile function was preserved.

Herpes vegetans represents a rare infection with HHV-1 or HHV-2, typically in patients who are considerably immunosuppressed, such as those with cancer, those undergoing transplantation, and those with uncontrolled HIV infection.¹ Few cases of HV have been described in an immunocompetent patient.² Our case is unique because the patient’s HIV infection was well controlled at the time HV was diagnosed, demonstrated by his modestly low CD4 count and undetectable HIV viral load.

Patients with HV can present diagnostic and therapeutic challenges. Typically, a diagnosis of cutaneous HHV infection does not require a biopsy; most cases appear as clustered vesicular lesions, making the disease easy to diagnose clinically. However, biopsies and cultures are necessary to identify the underlying cause of atypical verrucous exophytic lesions. Other conditions with clinical features similar to HV include squamous cell carcinoma, condyloma acuminatum, and deep fungal and mycobacterial infections.^2,3 A tissue biopsy, histologic staining, and tissue culture should be performed to identify the causative pathogen and potential targets for treatment. Definitive diagnosis is vital to deliver proper treatment modalities, which often involve a multimodal multidisciplinary approach. 

Several pathogenic mechanisms of HV have been proposed. One theory suggests that in an immunocompetent patient, HHV typically triggers a lymphocytic response, which leads to activation of interferon alpha. However, in an immunocompromised patient, such as an individual with AIDS, this interferon response is diminished, which explains why these patients typically have a chronic and resistant HHV infection. HIV has an affinity for infecting dermal dendritic cells, which signals activation of tumor necrosis factor and interleukin.⁶ Both cytokines contribute to an antiapoptotic environment that promotes continued proliferation of these viral cells in the epidermis. Over time, propagation of disinhibited cells can lead to the verrucous and hyperkeratotic-appearing skin that is common in patients with HV.⁷

Another theorized mechanism underlying hypertrophic herpetic lesions was described in the context of HHV-1 infection and subsequent PG. El Hayderi et al⁸ reported that histologic and immunohistochemical examination of a patient’s lesion revealed sparse epithelial cell aggregates within PG as well as HHV-1 antigens in the nuclei and cytoplasm of normal-appearing and cytopathic epithelial cells. Immunohistochemical examination also revealed vascular endothelial growth factor within HHV-1–infected epithelial cells and PG endothelial cells, suggesting that PG formation may be indirectly driven by vascular endothelial growth factor and its proangiogenic properties. The pathogenesis of PG in the setting of HHV-1 infection displays many similarities to hyperkeratotic lesions observed in atypical cutaneous manifestations of HHV-2.⁸

The management of patients with HV continues to be complex, often requiring a multimodal regimen. Although acyclovir has been shown to be highly effective for treating and preventing most HHV infections, acyclovir resistance frequently has been reported in immunocompromised populations.⁵ Acyclovir resistance can be correlated with the severity of immunodeficiency as well as the duration of acyclovir exposure. Resistance to acyclovir often results from deficient intracellular phosphorylation, which is required for activation of the drug. If patients show resistance to acyclovir and its derivatives, alternate drug classes that do not depend on thymidine kinase phosphorylation should be considered.

Our patient received a combination of intravenous foscarnet and a course of ampicillin-sulbactam while an inpatient due to his documented history of acyclovir-resistant HHV-2 infection, and he was discharged on cidofovir cream 1%. Cidofovir is US Food and Drug Administration approved for treating cytomegalovirus retinitis in patients with AIDS. Although data are limited, topical and intralesional cidofovir have been used to treat acyclovir-resistant cases of HV with documented success.^1,9 In refractory HV or when the disease is slow to resolve, intralesional cidofovir has been documented to be an additional treatment option. Intralesional and topical cidofovir carry a much lower risk for adverse effects such as kidney dysfunction compared to intravenous cidofovir¹ and can be considered in patients with minimal clinical improvement and those at increased risk for side effects.

Our case demonstrated how a patient with HV may require a complex and prolonged hospital course for appropriate treatment. Our patient required an array of both medical and surgical modalities to reach the desired outcome. Here, a multitude of specialties including infectious disease, dermatology, and urology worked together to reach a positive clinical and cosmetic outcome for this patient. 

To the Editor:

Herpes vegetans (HV) is an uncommon infection caused by human herpesvirus (HHV) in patients who are immunocompromised, such as those who are HIV positive.¹ Unlike typical HHV infection, HV can present with exophytic exudative ulcers and papillomatous vegetations. The presentation of ulcerated genital nodules, especially in an immunocompromised patient, yields an array of disorders in the differential diagnosis, including condyloma latum, condyloma acuminatum, pyogenic granuloma (PG), and verrucous carcinoma.^2,3 Histopathology of HV reveals pseudoepitheliomatous hyperplasia, plasma cell infiltration, and positivity for HHV type 1 (HHV-1) and/or HHV type 2 (HHV-2). Herpes vegetans lesions typically require a multimodal treatment approach because many cases are resistant to acyclovir. Treatment options include the nucleoside analogues foscarnet and cidofovir; immunomodulators such as topical imiquimod; and the topical antiviral trifluridine.^1,4-6 We describe a case of HV in a patient with a history of well-controlled HIV infection who presented with a painful fungating penile lesion.

A 55-year-old man presented to the hospital with a painful expanding mass on the distal aspect of the penis of 3 months’ duration. He had a history of HIV infection that was well-controlled by antiretroviral therapy, prior hepatitis B virus infection and acyclovir-resistant genital HHV-2 infection. Physical examination revealed a large, firm, circumferential, exophytic, verrucous plaque with various areas of ulceration and purulent drainage on the distal shaft and glans of the penis (Figure 1). The patient’s most recent absolute CD4 count was 425 cells/mm³ (reference range, 500–1500 cells/mm³). His HIV viral load was undetectable at less than 30 copies/mL. Histopathology with hematoxylin and eosin staining of biopsy material from the penile lesion demonstrated pseudoepitheliomatous epidermal hyperplasia with focal ulceration and a mixed inflammatory infiltrate (Figure 2A). At higher magnification, clear viral cytopathic changes of HHV were noted, including multinucleation, nuclear molding, and homogenous gray nuclei (Figure 2B). Additional staining for fungi, mycobacteria, and spirochetes was negative. In-situ hybridization was negative for human papillomavirus subtypes. A bacterial culture of swabs of the purulent drainage was positive for Staphylococcus aureus and Proteus mirabilis.

Given the patient’s known history of acyclovir-resistant HHV-2 infection, he received a 28-day course of intravenous foscarnet 40 mg/kg every 12 hours. He also was given a 14-day course of intravenous ampicillin-sulbactam 3 g every 6 hours. The patient gradually improved during a 35-day hospital stay. He was discharged with cidofovir cream 1% and oral valacyclovir; the latter was subsequently discontinued by dermatology because of his known history of acyclovir resistance. Four months after discharge, the patient underwent a circumcision performed by urology to decrease the risk for recurrence and achieve the best cosmetic outcome. At the 6-month follow-up visit, dramatic clinical improvement was evident, with complete resolution of the plaque and only isolated areas of scarring (Figure 3). The patient reported that penile function was preserved.

Herpes vegetans represents a rare infection with HHV-1 or HHV-2, typically in patients who are considerably immunosuppressed, such as those with cancer, those undergoing transplantation, and those with uncontrolled HIV infection.¹ Few cases of HV have been described in an immunocompetent patient.² Our case is unique because the patient’s HIV infection was well controlled at the time HV was diagnosed, demonstrated by his modestly low CD4 count and undetectable HIV viral load.

Patients with HV can present diagnostic and therapeutic challenges. Typically, a diagnosis of cutaneous HHV infection does not require a biopsy; most cases appear as clustered vesicular lesions, making the disease easy to diagnose clinically. However, biopsies and cultures are necessary to identify the underlying cause of atypical verrucous exophytic lesions. Other conditions with clinical features similar to HV include squamous cell carcinoma, condyloma acuminatum, and deep fungal and mycobacterial infections.^2,3 A tissue biopsy, histologic staining, and tissue culture should be performed to identify the causative pathogen and potential targets for treatment. Definitive diagnosis is vital to deliver proper treatment modalities, which often involve a multimodal multidisciplinary approach. 

Several pathogenic mechanisms of HV have been proposed. One theory suggests that in an immunocompetent patient, HHV typically triggers a lymphocytic response, which leads to activation of interferon alpha. However, in an immunocompromised patient, such as an individual with AIDS, this interferon response is diminished, which explains why these patients typically have a chronic and resistant HHV infection. HIV has an affinity for infecting dermal dendritic cells, which signals activation of tumor necrosis factor and interleukin.⁶ Both cytokines contribute to an antiapoptotic environment that promotes continued proliferation of these viral cells in the epidermis. Over time, propagation of disinhibited cells can lead to the verrucous and hyperkeratotic-appearing skin that is common in patients with HV.⁷

Another theorized mechanism underlying hypertrophic herpetic lesions was described in the context of HHV-1 infection and subsequent PG. El Hayderi et al⁸ reported that histologic and immunohistochemical examination of a patient’s lesion revealed sparse epithelial cell aggregates within PG as well as HHV-1 antigens in the nuclei and cytoplasm of normal-appearing and cytopathic epithelial cells. Immunohistochemical examination also revealed vascular endothelial growth factor within HHV-1–infected epithelial cells and PG endothelial cells, suggesting that PG formation may be indirectly driven by vascular endothelial growth factor and its proangiogenic properties. The pathogenesis of PG in the setting of HHV-1 infection displays many similarities to hyperkeratotic lesions observed in atypical cutaneous manifestations of HHV-2.⁸

The management of patients with HV continues to be complex, often requiring a multimodal regimen. Although acyclovir has been shown to be highly effective for treating and preventing most HHV infections, acyclovir resistance frequently has been reported in immunocompromised populations.⁵ Acyclovir resistance can be correlated with the severity of immunodeficiency as well as the duration of acyclovir exposure. Resistance to acyclovir often results from deficient intracellular phosphorylation, which is required for activation of the drug. If patients show resistance to acyclovir and its derivatives, alternate drug classes that do not depend on thymidine kinase phosphorylation should be considered.

Our patient received a combination of intravenous foscarnet and a course of ampicillin-sulbactam while an inpatient due to his documented history of acyclovir-resistant HHV-2 infection, and he was discharged on cidofovir cream 1%. Cidofovir is US Food and Drug Administration approved for treating cytomegalovirus retinitis in patients with AIDS. Although data are limited, topical and intralesional cidofovir have been used to treat acyclovir-resistant cases of HV with documented success.^1,9 In refractory HV or when the disease is slow to resolve, intralesional cidofovir has been documented to be an additional treatment option. Intralesional and topical cidofovir carry a much lower risk for adverse effects such as kidney dysfunction compared to intravenous cidofovir¹ and can be considered in patients with minimal clinical improvement and those at increased risk for side effects.

Our case demonstrated how a patient with HV may require a complex and prolonged hospital course for appropriate treatment. Our patient required an array of both medical and surgical modalities to reach the desired outcome. Here, a multitude of specialties including infectious disease, dermatology, and urology worked together to reach a positive clinical and cosmetic outcome for this patient. 

To the Editor:

Herpes vegetans (HV) is an uncommon infection caused by human herpesvirus (HHV) in patients who are immunocompromised, such as those who are HIV positive.¹ Unlike typical HHV infection, HV can present with exophytic exudative ulcers and papillomatous vegetations. The presentation of ulcerated genital nodules, especially in an immunocompromised patient, yields an array of disorders in the differential diagnosis, including condyloma latum, condyloma acuminatum, pyogenic granuloma (PG), and verrucous carcinoma.^2,3 Histopathology of HV reveals pseudoepitheliomatous hyperplasia, plasma cell infiltration, and positivity for HHV type 1 (HHV-1) and/or HHV type 2 (HHV-2). Herpes vegetans lesions typically require a multimodal treatment approach because many cases are resistant to acyclovir. Treatment options include the nucleoside analogues foscarnet and cidofovir; immunomodulators such as topical imiquimod; and the topical antiviral trifluridine.^1,4-6 We describe a case of HV in a patient with a history of well-controlled HIV infection who presented with a painful fungating penile lesion.

A 55-year-old man presented to the hospital with a painful expanding mass on the distal aspect of the penis of 3 months’ duration. He had a history of HIV infection that was well-controlled by antiretroviral therapy, prior hepatitis B virus infection and acyclovir-resistant genital HHV-2 infection. Physical examination revealed a large, firm, circumferential, exophytic, verrucous plaque with various areas of ulceration and purulent drainage on the distal shaft and glans of the penis (Figure 1). The patient’s most recent absolute CD4 count was 425 cells/mm³ (reference range, 500–1500 cells/mm³). His HIV viral load was undetectable at less than 30 copies/mL. Histopathology with hematoxylin and eosin staining of biopsy material from the penile lesion demonstrated pseudoepitheliomatous epidermal hyperplasia with focal ulceration and a mixed inflammatory infiltrate (Figure 2A). At higher magnification, clear viral cytopathic changes of HHV were noted, including multinucleation, nuclear molding, and homogenous gray nuclei (Figure 2B). Additional staining for fungi, mycobacteria, and spirochetes was negative. In-situ hybridization was negative for human papillomavirus subtypes. A bacterial culture of swabs of the purulent drainage was positive for Staphylococcus aureus and Proteus mirabilis.

Given the patient’s known history of acyclovir-resistant HHV-2 infection, he received a 28-day course of intravenous foscarnet 40 mg/kg every 12 hours. He also was given a 14-day course of intravenous ampicillin-sulbactam 3 g every 6 hours. The patient gradually improved during a 35-day hospital stay. He was discharged with cidofovir cream 1% and oral valacyclovir; the latter was subsequently discontinued by dermatology because of his known history of acyclovir resistance. Four months after discharge, the patient underwent a circumcision performed by urology to decrease the risk for recurrence and achieve the best cosmetic outcome. At the 6-month follow-up visit, dramatic clinical improvement was evident, with complete resolution of the plaque and only isolated areas of scarring (Figure 3). The patient reported that penile function was preserved.

Herpes vegetans represents a rare infection with HHV-1 or HHV-2, typically in patients who are considerably immunosuppressed, such as those with cancer, those undergoing transplantation, and those with uncontrolled HIV infection.¹ Few cases of HV have been described in an immunocompetent patient.² Our case is unique because the patient’s HIV infection was well controlled at the time HV was diagnosed, demonstrated by his modestly low CD4 count and undetectable HIV viral load.

Patients with HV can present diagnostic and therapeutic challenges. Typically, a diagnosis of cutaneous HHV infection does not require a biopsy; most cases appear as clustered vesicular lesions, making the disease easy to diagnose clinically. However, biopsies and cultures are necessary to identify the underlying cause of atypical verrucous exophytic lesions. Other conditions with clinical features similar to HV include squamous cell carcinoma, condyloma acuminatum, and deep fungal and mycobacterial infections.^2,3 A tissue biopsy, histologic staining, and tissue culture should be performed to identify the causative pathogen and potential targets for treatment. Definitive diagnosis is vital to deliver proper treatment modalities, which often involve a multimodal multidisciplinary approach. 

Several pathogenic mechanisms of HV have been proposed. One theory suggests that in an immunocompetent patient, HHV typically triggers a lymphocytic response, which leads to activation of interferon alpha. However, in an immunocompromised patient, such as an individual with AIDS, this interferon response is diminished, which explains why these patients typically have a chronic and resistant HHV infection. HIV has an affinity for infecting dermal dendritic cells, which signals activation of tumor necrosis factor and interleukin.⁶ Both cytokines contribute to an antiapoptotic environment that promotes continued proliferation of these viral cells in the epidermis. Over time, propagation of disinhibited cells can lead to the verrucous and hyperkeratotic-appearing skin that is common in patients with HV.⁷

Another theorized mechanism underlying hypertrophic herpetic lesions was described in the context of HHV-1 infection and subsequent PG. El Hayderi et al⁸ reported that histologic and immunohistochemical examination of a patient’s lesion revealed sparse epithelial cell aggregates within PG as well as HHV-1 antigens in the nuclei and cytoplasm of normal-appearing and cytopathic epithelial cells. Immunohistochemical examination also revealed vascular endothelial growth factor within HHV-1–infected epithelial cells and PG endothelial cells, suggesting that PG formation may be indirectly driven by vascular endothelial growth factor and its proangiogenic properties. The pathogenesis of PG in the setting of HHV-1 infection displays many similarities to hyperkeratotic lesions observed in atypical cutaneous manifestations of HHV-2.⁸

The management of patients with HV continues to be complex, often requiring a multimodal regimen. Although acyclovir has been shown to be highly effective for treating and preventing most HHV infections, acyclovir resistance frequently has been reported in immunocompromised populations.⁵ Acyclovir resistance can be correlated with the severity of immunodeficiency as well as the duration of acyclovir exposure. Resistance to acyclovir often results from deficient intracellular phosphorylation, which is required for activation of the drug. If patients show resistance to acyclovir and its derivatives, alternate drug classes that do not depend on thymidine kinase phosphorylation should be considered.

Our patient received a combination of intravenous foscarnet and a course of ampicillin-sulbactam while an inpatient due to his documented history of acyclovir-resistant HHV-2 infection, and he was discharged on cidofovir cream 1%. Cidofovir is US Food and Drug Administration approved for treating cytomegalovirus retinitis in patients with AIDS. Although data are limited, topical and intralesional cidofovir have been used to treat acyclovir-resistant cases of HV with documented success.^1,9 In refractory HV or when the disease is slow to resolve, intralesional cidofovir has been documented to be an additional treatment option. Intralesional and topical cidofovir carry a much lower risk for adverse effects such as kidney dysfunction compared to intravenous cidofovir¹ and can be considered in patients with minimal clinical improvement and those at increased risk for side effects.

Our case demonstrated how a patient with HV may require a complex and prolonged hospital course for appropriate treatment. Our patient required an array of both medical and surgical modalities to reach the desired outcome. Here, a multitude of specialties including infectious disease, dermatology, and urology worked together to reach a positive clinical and cosmetic outcome for this patient. 

To the Editor:

Most cutaneous squamous cell carcinomas (cSCCs) are successfully treated with standard modalities such as surgical excision; however, a subset of tumors is not amenable to surgical resection.^1,2 Patients who are not able to undergo surgical treatment may instead receive radiation therapy, topical 5-fluorouracil (5-FU), imiquimod, cryosurgery, photodynamic therapy, or systemic treatment (eg, immunotherapy) in addition to intralesional approaches for localized disease.^1-4 However, the adverse effects associated with these treatments and their modest effect in preventing the recurrence of cutaneous lesions limit their efficacy against unresectable cSCC.^4-6 We present a case that demonstrates the efficacy of electrodesiccation and curettage (ED&C) followed by topical 5-FU for an invasive cSCC not amenable to surgical therapy.

A 58-year-old woman presented for evaluation of a 3.5×3.4-cm, incisional biopsy–proven, invasive stage T2a cSCC (Brigham and Women’s Hospital tumor staging system [Boston, Massachusetts]) on the dorsal aspect of the left foot, which had developed over several months (Figure 1A). She had a history of treatment with psoralen plus UV light therapy for erythroderma of unknown cause and peripheral neuropathy. She was not a surgical candidate because of suspected underlying cutaneous sclerosis and a history of poor wound healing on the lower legs.

Prior to presentation to dermatology, the patient had been treated with intralesional methotrexate, intralesional 5-FU, and the antiangiogenic and antiproliferative combination agent OLCAT-005³—consisting of equal parts [by volume] of diclofenac gel 3%, imiquimod cream 5%, hydrocortisone valerate cream 0.2%, calcipotriene cream 0.005%, and tretinoin cream 0.05—which failed, and the patient reported that OLCAT-005 made the pain from the cSCC worse.

Upon growth of the lesion over several months, the patient was referred to the High-Risk Skin Cancer Clinic at Massachusetts General Hospital (Boston, Massachusetts). A repeat biopsy demonstrated an invasive well-differentiated cSCC (Figure 2). The size and invasive features of the lesion on clinical examination prompted a referral to surgical oncology for a wide local excision. However, surgical oncology concluded she was not a surgical candidate.

Magnetic resonance imaging showed no deep invasion of the cSCC to the tendons or bones. Electrodesiccation and curettage was performed to debulk the tumor, followed by twice-daily application of topical 5-FU for 4 weeks to improve the odds of tumor clearance (Figure 1B). Fourteen weeks after completion of 5-FU treatment, the cSCC showed complete clinical regression (Figure 1C). No recurrence has been detected clinically more than 3 years following treatment.

Prior to the advent of Mohs micrographic surgery, ED&C commonly was used to treat skin cancer, with a lower cost and a cure rate close to 95%.^7,8 We postulate that the mechanism of tumor regression in our patient was ED&C-mediated removal and necrosis of neoplastic tissue combined with 5-FU–induced cancer-cell DNA damage and apoptosis. An antitumor immune response also may have contributed to the complete regression of the cSCC.

Although antiangiogenic and antiproliferative agents are suitable for primary cSCC treatment, it is possible that this patient’s prior therapies alone—in the absence of debulking by ED&C to sufficiently reduce disease burden—did not allow for tumor clearance and were ineffective. Many clinicians are reluctant to apply 5-FU to a wound bed because it can impede wound healing.⁹ In this case, re-epithelialization likely occurred primarily after completion of 5-FU treatment.

We recommend consideration of ED&C with 5-FU for similar malignant lesions that are not amenable to surgical excision. Nevertheless, Mohs micrographic surgery and wide local excision remain the gold standards for definitive treatment of invasive skin cancer in a patient who is a candidate for surgical treatment.

To the Editor:

Most cutaneous squamous cell carcinomas (cSCCs) are successfully treated with standard modalities such as surgical excision; however, a subset of tumors is not amenable to surgical resection.^1,2 Patients who are not able to undergo surgical treatment may instead receive radiation therapy, topical 5-fluorouracil (5-FU), imiquimod, cryosurgery, photodynamic therapy, or systemic treatment (eg, immunotherapy) in addition to intralesional approaches for localized disease.^1-4 However, the adverse effects associated with these treatments and their modest effect in preventing the recurrence of cutaneous lesions limit their efficacy against unresectable cSCC.^4-6 We present a case that demonstrates the efficacy of electrodesiccation and curettage (ED&C) followed by topical 5-FU for an invasive cSCC not amenable to surgical therapy.

A 58-year-old woman presented for evaluation of a 3.5×3.4-cm, incisional biopsy–proven, invasive stage T2a cSCC (Brigham and Women’s Hospital tumor staging system [Boston, Massachusetts]) on the dorsal aspect of the left foot, which had developed over several months (Figure 1A). She had a history of treatment with psoralen plus UV light therapy for erythroderma of unknown cause and peripheral neuropathy. She was not a surgical candidate because of suspected underlying cutaneous sclerosis and a history of poor wound healing on the lower legs.

Prior to presentation to dermatology, the patient had been treated with intralesional methotrexate, intralesional 5-FU, and the antiangiogenic and antiproliferative combination agent OLCAT-005³—consisting of equal parts [by volume] of diclofenac gel 3%, imiquimod cream 5%, hydrocortisone valerate cream 0.2%, calcipotriene cream 0.005%, and tretinoin cream 0.05—which failed, and the patient reported that OLCAT-005 made the pain from the cSCC worse.

Upon growth of the lesion over several months, the patient was referred to the High-Risk Skin Cancer Clinic at Massachusetts General Hospital (Boston, Massachusetts). A repeat biopsy demonstrated an invasive well-differentiated cSCC (Figure 2). The size and invasive features of the lesion on clinical examination prompted a referral to surgical oncology for a wide local excision. However, surgical oncology concluded she was not a surgical candidate.

Magnetic resonance imaging showed no deep invasion of the cSCC to the tendons or bones. Electrodesiccation and curettage was performed to debulk the tumor, followed by twice-daily application of topical 5-FU for 4 weeks to improve the odds of tumor clearance (Figure 1B). Fourteen weeks after completion of 5-FU treatment, the cSCC showed complete clinical regression (Figure 1C). No recurrence has been detected clinically more than 3 years following treatment.

Prior to the advent of Mohs micrographic surgery, ED&C commonly was used to treat skin cancer, with a lower cost and a cure rate close to 95%.^7,8 We postulate that the mechanism of tumor regression in our patient was ED&C-mediated removal and necrosis of neoplastic tissue combined with 5-FU–induced cancer-cell DNA damage and apoptosis. An antitumor immune response also may have contributed to the complete regression of the cSCC.

Although antiangiogenic and antiproliferative agents are suitable for primary cSCC treatment, it is possible that this patient’s prior therapies alone—in the absence of debulking by ED&C to sufficiently reduce disease burden—did not allow for tumor clearance and were ineffective. Many clinicians are reluctant to apply 5-FU to a wound bed because it can impede wound healing.⁹ In this case, re-epithelialization likely occurred primarily after completion of 5-FU treatment.

We recommend consideration of ED&C with 5-FU for similar malignant lesions that are not amenable to surgical excision. Nevertheless, Mohs micrographic surgery and wide local excision remain the gold standards for definitive treatment of invasive skin cancer in a patient who is a candidate for surgical treatment.

To the Editor:

Most cutaneous squamous cell carcinomas (cSCCs) are successfully treated with standard modalities such as surgical excision; however, a subset of tumors is not amenable to surgical resection.^1,2 Patients who are not able to undergo surgical treatment may instead receive radiation therapy, topical 5-fluorouracil (5-FU), imiquimod, cryosurgery, photodynamic therapy, or systemic treatment (eg, immunotherapy) in addition to intralesional approaches for localized disease.^1-4 However, the adverse effects associated with these treatments and their modest effect in preventing the recurrence of cutaneous lesions limit their efficacy against unresectable cSCC.^4-6 We present a case that demonstrates the efficacy of electrodesiccation and curettage (ED&C) followed by topical 5-FU for an invasive cSCC not amenable to surgical therapy.

A 58-year-old woman presented for evaluation of a 3.5×3.4-cm, incisional biopsy–proven, invasive stage T2a cSCC (Brigham and Women’s Hospital tumor staging system [Boston, Massachusetts]) on the dorsal aspect of the left foot, which had developed over several months (Figure 1A). She had a history of treatment with psoralen plus UV light therapy for erythroderma of unknown cause and peripheral neuropathy. She was not a surgical candidate because of suspected underlying cutaneous sclerosis and a history of poor wound healing on the lower legs.

Prior to presentation to dermatology, the patient had been treated with intralesional methotrexate, intralesional 5-FU, and the antiangiogenic and antiproliferative combination agent OLCAT-005³—consisting of equal parts [by volume] of diclofenac gel 3%, imiquimod cream 5%, hydrocortisone valerate cream 0.2%, calcipotriene cream 0.005%, and tretinoin cream 0.05—which failed, and the patient reported that OLCAT-005 made the pain from the cSCC worse.

Upon growth of the lesion over several months, the patient was referred to the High-Risk Skin Cancer Clinic at Massachusetts General Hospital (Boston, Massachusetts). A repeat biopsy demonstrated an invasive well-differentiated cSCC (Figure 2). The size and invasive features of the lesion on clinical examination prompted a referral to surgical oncology for a wide local excision. However, surgical oncology concluded she was not a surgical candidate.

Magnetic resonance imaging showed no deep invasion of the cSCC to the tendons or bones. Electrodesiccation and curettage was performed to debulk the tumor, followed by twice-daily application of topical 5-FU for 4 weeks to improve the odds of tumor clearance (Figure 1B). Fourteen weeks after completion of 5-FU treatment, the cSCC showed complete clinical regression (Figure 1C). No recurrence has been detected clinically more than 3 years following treatment.

Prior to the advent of Mohs micrographic surgery, ED&C commonly was used to treat skin cancer, with a lower cost and a cure rate close to 95%.^7,8 We postulate that the mechanism of tumor regression in our patient was ED&C-mediated removal and necrosis of neoplastic tissue combined with 5-FU–induced cancer-cell DNA damage and apoptosis. An antitumor immune response also may have contributed to the complete regression of the cSCC.

Although antiangiogenic and antiproliferative agents are suitable for primary cSCC treatment, it is possible that this patient’s prior therapies alone—in the absence of debulking by ED&C to sufficiently reduce disease burden—did not allow for tumor clearance and were ineffective. Many clinicians are reluctant to apply 5-FU to a wound bed because it can impede wound healing.⁹ In this case, re-epithelialization likely occurred primarily after completion of 5-FU treatment.

We recommend consideration of ED&C with 5-FU for similar malignant lesions that are not amenable to surgical excision. Nevertheless, Mohs micrographic surgery and wide local excision remain the gold standards for definitive treatment of invasive skin cancer in a patient who is a candidate for surgical treatment.

The best-selling drug Humira (adalimumab) now faces competition in the United States after a 20-year monopoly. The first adalimumab biosimilar, Amjevita, launched in the United States on January 31, and in July, seven additional biosimilars became available. These drugs have the potential to lower prescription drug prices, but when and by how much remains to be seen.

Here’s what you need to know about adalimumab biosimilars.
 

What Humira biosimilars are now available?

Eight different biosimilars have launched in 2023 with discounts as large at 85% from Humira’s list price of $6,922. A few companies also offer two price points.

Three of these biosimilars – Hadlima, Hyrimoz, and Yuflyma – are available in high concentration formulations. This high concentration formulation makes up 85% of Humira prescriptions, according to a report from Goodroot, a collection of companies focused on lowering health care costs.

Cyltezo is currently the only adalimumab biosimilar with an interchangeability designation, meaning that a pharmacist can substitute the biosimilar for an equivalent Humira prescription without the intervention of a clinician. A total of 47 states allow for these substitutions without prior approval from a clinician, according to Goodroot, and the clinician must be notified of the switch within a certain time frame. A total of 40 states require that patients be notified of the switch before substitution.

However, it’s not clear if this interchangeability designation will prove an advantage for Cyltezo, as it is interchangeable with the lower concentration version of Humira that makes up just 15% of prescriptions.

Most of the companies behind these biosimilars are pursuing interchangeability designations for their drugs, except for Fresenius Kabi (Idacio) and Coherus (Yusimry).

A ninth biosimilar, Pfizer’s adalimumab-afzb (Abrilada), is not yet on the market and is currently awaiting an approval decision from the Food and Drug Administration to add an interchangeability designation to its prior approval for a low-concentration formulation.
 

Why are they priced differently?

The two price points offer different deals to payers. Pharmacy benefit managers make confidential agreements with drug manufacturers to get a discount – called a rebate – to get the drug on the PBM’s formulary. The PBM keeps a portion of that rebate, and the rest is passed on to the insurance company and patients. Biosimilars at a higher price point will likely offer larger rebates. Biosimilars offered at lower price points incorporate this discount up front in their list pricing and likely will not offer large rebates.

Will biosimilars be covered by payers?

Currently, biosimilars are being offered on formularies at parity with Humira, meaning they are on the same tier. The PBM companies OptumRx and Cigna Group’s Express Scripts will offer Amjevita (at both price points), Cyltezo, and Hyrimoz (at both price points).

“This decision allows our clients flexibility to provide access to the lower list price, so members in high-deductible plans and benefit designs with coinsurance can experience lower out-of-pocket costs,” said OptumRx spokesperson Isaac Sorensen in an email.

Mark Cuban Cost Plus Drug Company, which uses a direct-to-consumer model, will offer Yusimry for $567.27 on its website. SmithRx, a PBM based in San Francisco, announced it would partner with Cost Plus Drugs to offer Yusimry, adding that SmithRx members can use their insurance benefits to further reduce out-of-pocket costs. RxPreferred, another PBM, will also offer Yusimry through its partnership with Cuban’s company.

The news website Formulary Watch previously reported that CVS Caremark, another of the biggest PBMs, will be offering Amjevita, but as a nonpreferred brand, while Humira remains the preferred brand. CVS Caremark did not respond to a request for comment.
 

Will patients pay less?

Biosimilars have been touted as a potential solution to lower spending on biologic drugs, but it’s unknown if patients will ultimately benefit with lower out-of-pocket costs. It’s “impossible to predict” if the discount that third-party payers pay will be passed on to consumers, said Mark Fendrick, MD, who directs the University of Michigan Center for Value-based Insurance Design in Ann Arbor.

Michigan Medicine

Generally, a consumer’s copay is a percentage of a drug’s list price, so it stands to reason that a low drug price would result in lower out-of-pocket payments. While this is mostly true, Humira has a successful copay assistance program to lower prescription costs for consumers. According to a 2022 IQVIA report, 82% of commercial prescriptions cost patients less than $10 for Humira because of this program.

To appeal to patients, biosimilar companies will need to offer similar savings, Dr. Fendrick added. “There will be some discontent if patients are actually asked to pay more out-of-pocket for a less expensive drug,” he said.

All eight companies behind these biosimilars are offering or will be launching copay saving programs, many which advertise copays as low as $0 per month for eligible patients.
 

How will Humira respond?

Marta Wosińska, PhD, a health care economist at the Brookings Institute, Washington, predicts payers will use these lower biosimilar prices to negotiate better deals with AbbVie, Humira’s manufacturer. “We have a lot of players coming into [the market] right now, so the competition is really fierce,” she said. In response, AbbVie will need to increase rebates on Humira and/or lower its price to compete with these biosimilars. 

“The ball is in AbbVie’s court,” she said. “If [the company] is not willing to drop price sufficiently, then payers will start switching to biosimilars.”

Dr. Fendrick reported past financial relationships and consulting arrangements with AbbVie, Amgen, Arnold Ventures, Bayer, CareFirst, BlueCross BlueShield, and many other companies. Dr. Wosińska has received funding from Arnold Ventures and serves as an expert witness on antitrust cases involving generic medication.

A version of this article first appeared on Medscape.com.

The best-selling drug Humira (adalimumab) now faces competition in the United States after a 20-year monopoly. The first adalimumab biosimilar, Amjevita, launched in the United States on January 31, and in July, seven additional biosimilars became available. These drugs have the potential to lower prescription drug prices, but when and by how much remains to be seen.

Here’s what you need to know about adalimumab biosimilars.
 

What Humira biosimilars are now available?

Eight different biosimilars have launched in 2023 with discounts as large at 85% from Humira’s list price of $6,922. A few companies also offer two price points.

Three of these biosimilars – Hadlima, Hyrimoz, and Yuflyma – are available in high concentration formulations. This high concentration formulation makes up 85% of Humira prescriptions, according to a report from Goodroot, a collection of companies focused on lowering health care costs.

Cyltezo is currently the only adalimumab biosimilar with an interchangeability designation, meaning that a pharmacist can substitute the biosimilar for an equivalent Humira prescription without the intervention of a clinician. A total of 47 states allow for these substitutions without prior approval from a clinician, according to Goodroot, and the clinician must be notified of the switch within a certain time frame. A total of 40 states require that patients be notified of the switch before substitution.

However, it’s not clear if this interchangeability designation will prove an advantage for Cyltezo, as it is interchangeable with the lower concentration version of Humira that makes up just 15% of prescriptions.

Most of the companies behind these biosimilars are pursuing interchangeability designations for their drugs, except for Fresenius Kabi (Idacio) and Coherus (Yusimry).

A ninth biosimilar, Pfizer’s adalimumab-afzb (Abrilada), is not yet on the market and is currently awaiting an approval decision from the Food and Drug Administration to add an interchangeability designation to its prior approval for a low-concentration formulation.
 

Why are they priced differently?

The two price points offer different deals to payers. Pharmacy benefit managers make confidential agreements with drug manufacturers to get a discount – called a rebate – to get the drug on the PBM’s formulary. The PBM keeps a portion of that rebate, and the rest is passed on to the insurance company and patients. Biosimilars at a higher price point will likely offer larger rebates. Biosimilars offered at lower price points incorporate this discount up front in their list pricing and likely will not offer large rebates.

Will biosimilars be covered by payers?

Currently, biosimilars are being offered on formularies at parity with Humira, meaning they are on the same tier. The PBM companies OptumRx and Cigna Group’s Express Scripts will offer Amjevita (at both price points), Cyltezo, and Hyrimoz (at both price points).

“This decision allows our clients flexibility to provide access to the lower list price, so members in high-deductible plans and benefit designs with coinsurance can experience lower out-of-pocket costs,” said OptumRx spokesperson Isaac Sorensen in an email.

Mark Cuban Cost Plus Drug Company, which uses a direct-to-consumer model, will offer Yusimry for $567.27 on its website. SmithRx, a PBM based in San Francisco, announced it would partner with Cost Plus Drugs to offer Yusimry, adding that SmithRx members can use their insurance benefits to further reduce out-of-pocket costs. RxPreferred, another PBM, will also offer Yusimry through its partnership with Cuban’s company.

The news website Formulary Watch previously reported that CVS Caremark, another of the biggest PBMs, will be offering Amjevita, but as a nonpreferred brand, while Humira remains the preferred brand. CVS Caremark did not respond to a request for comment.
 

Will patients pay less?

Biosimilars have been touted as a potential solution to lower spending on biologic drugs, but it’s unknown if patients will ultimately benefit with lower out-of-pocket costs. It’s “impossible to predict” if the discount that third-party payers pay will be passed on to consumers, said Mark Fendrick, MD, who directs the University of Michigan Center for Value-based Insurance Design in Ann Arbor.

Michigan Medicine

Generally, a consumer’s copay is a percentage of a drug’s list price, so it stands to reason that a low drug price would result in lower out-of-pocket payments. While this is mostly true, Humira has a successful copay assistance program to lower prescription costs for consumers. According to a 2022 IQVIA report, 82% of commercial prescriptions cost patients less than $10 for Humira because of this program.

To appeal to patients, biosimilar companies will need to offer similar savings, Dr. Fendrick added. “There will be some discontent if patients are actually asked to pay more out-of-pocket for a less expensive drug,” he said.

All eight companies behind these biosimilars are offering or will be launching copay saving programs, many which advertise copays as low as $0 per month for eligible patients.
 

How will Humira respond?

Marta Wosińska, PhD, a health care economist at the Brookings Institute, Washington, predicts payers will use these lower biosimilar prices to negotiate better deals with AbbVie, Humira’s manufacturer. “We have a lot of players coming into [the market] right now, so the competition is really fierce,” she said. In response, AbbVie will need to increase rebates on Humira and/or lower its price to compete with these biosimilars. 

“The ball is in AbbVie’s court,” she said. “If [the company] is not willing to drop price sufficiently, then payers will start switching to biosimilars.”

Dr. Fendrick reported past financial relationships and consulting arrangements with AbbVie, Amgen, Arnold Ventures, Bayer, CareFirst, BlueCross BlueShield, and many other companies. Dr. Wosińska has received funding from Arnold Ventures and serves as an expert witness on antitrust cases involving generic medication.

A version of this article first appeared on Medscape.com.

The best-selling drug Humira (adalimumab) now faces competition in the United States after a 20-year monopoly. The first adalimumab biosimilar, Amjevita, launched in the United States on January 31, and in July, seven additional biosimilars became available. These drugs have the potential to lower prescription drug prices, but when and by how much remains to be seen.

Here’s what you need to know about adalimumab biosimilars.
 

What Humira biosimilars are now available?

Eight different biosimilars have launched in 2023 with discounts as large at 85% from Humira’s list price of $6,922. A few companies also offer two price points.

Three of these biosimilars – Hadlima, Hyrimoz, and Yuflyma – are available in high concentration formulations. This high concentration formulation makes up 85% of Humira prescriptions, according to a report from Goodroot, a collection of companies focused on lowering health care costs.

Cyltezo is currently the only adalimumab biosimilar with an interchangeability designation, meaning that a pharmacist can substitute the biosimilar for an equivalent Humira prescription without the intervention of a clinician. A total of 47 states allow for these substitutions without prior approval from a clinician, according to Goodroot, and the clinician must be notified of the switch within a certain time frame. A total of 40 states require that patients be notified of the switch before substitution.

However, it’s not clear if this interchangeability designation will prove an advantage for Cyltezo, as it is interchangeable with the lower concentration version of Humira that makes up just 15% of prescriptions.

Most of the companies behind these biosimilars are pursuing interchangeability designations for their drugs, except for Fresenius Kabi (Idacio) and Coherus (Yusimry).

A ninth biosimilar, Pfizer’s adalimumab-afzb (Abrilada), is not yet on the market and is currently awaiting an approval decision from the Food and Drug Administration to add an interchangeability designation to its prior approval for a low-concentration formulation.
 

Why are they priced differently?

The two price points offer different deals to payers. Pharmacy benefit managers make confidential agreements with drug manufacturers to get a discount – called a rebate – to get the drug on the PBM’s formulary. The PBM keeps a portion of that rebate, and the rest is passed on to the insurance company and patients. Biosimilars at a higher price point will likely offer larger rebates. Biosimilars offered at lower price points incorporate this discount up front in their list pricing and likely will not offer large rebates.

Will biosimilars be covered by payers?

Currently, biosimilars are being offered on formularies at parity with Humira, meaning they are on the same tier. The PBM companies OptumRx and Cigna Group’s Express Scripts will offer Amjevita (at both price points), Cyltezo, and Hyrimoz (at both price points).

“This decision allows our clients flexibility to provide access to the lower list price, so members in high-deductible plans and benefit designs with coinsurance can experience lower out-of-pocket costs,” said OptumRx spokesperson Isaac Sorensen in an email.

Mark Cuban Cost Plus Drug Company, which uses a direct-to-consumer model, will offer Yusimry for $567.27 on its website. SmithRx, a PBM based in San Francisco, announced it would partner with Cost Plus Drugs to offer Yusimry, adding that SmithRx members can use their insurance benefits to further reduce out-of-pocket costs. RxPreferred, another PBM, will also offer Yusimry through its partnership with Cuban’s company.

The news website Formulary Watch previously reported that CVS Caremark, another of the biggest PBMs, will be offering Amjevita, but as a nonpreferred brand, while Humira remains the preferred brand. CVS Caremark did not respond to a request for comment.
 

Will patients pay less?

Biosimilars have been touted as a potential solution to lower spending on biologic drugs, but it’s unknown if patients will ultimately benefit with lower out-of-pocket costs. It’s “impossible to predict” if the discount that third-party payers pay will be passed on to consumers, said Mark Fendrick, MD, who directs the University of Michigan Center for Value-based Insurance Design in Ann Arbor.

Michigan Medicine

Generally, a consumer’s copay is a percentage of a drug’s list price, so it stands to reason that a low drug price would result in lower out-of-pocket payments. While this is mostly true, Humira has a successful copay assistance program to lower prescription costs for consumers. According to a 2022 IQVIA report, 82% of commercial prescriptions cost patients less than $10 for Humira because of this program.

To appeal to patients, biosimilar companies will need to offer similar savings, Dr. Fendrick added. “There will be some discontent if patients are actually asked to pay more out-of-pocket for a less expensive drug,” he said.

All eight companies behind these biosimilars are offering or will be launching copay saving programs, many which advertise copays as low as $0 per month for eligible patients.
 

How will Humira respond?

Marta Wosińska, PhD, a health care economist at the Brookings Institute, Washington, predicts payers will use these lower biosimilar prices to negotiate better deals with AbbVie, Humira’s manufacturer. “We have a lot of players coming into [the market] right now, so the competition is really fierce,” she said. In response, AbbVie will need to increase rebates on Humira and/or lower its price to compete with these biosimilars. 

“The ball is in AbbVie’s court,” she said. “If [the company] is not willing to drop price sufficiently, then payers will start switching to biosimilars.”

Dr. Fendrick reported past financial relationships and consulting arrangements with AbbVie, Amgen, Arnold Ventures, Bayer, CareFirst, BlueCross BlueShield, and many other companies. Dr. Wosińska has received funding from Arnold Ventures and serves as an expert witness on antitrust cases involving generic medication.

A version of this article first appeared on Medscape.com.

Church architecture describes visually the idea of the sacred, which is a fundamental need of man.

– Mario Botta, Swiss architect

My parents are visiting the Holy See today – prima volta in Italia! My mom waited years for this. She isn’t meeting the Pope or attending Mass. Yet, in the Whatsapp pics they sent me, you can see tears well up as she experiences St. Peter’s Basilica. It’s a visceral response to what is just a building and a poignant example of the significance of spaces.

More than just appreciating an edifice’s grandeur or exquisiteness, we are wired to connect with spaces emotionally. Beautiful or significant buildings move us, they make us feel something. Churches, synagogues, or mosques are good examples. They combine spiritual and aesthetic allure. But so too do gorgeous hotels, Apple stores, and posh restaurants. We crave the richness of an environment experienced through our five senses. The glory of sunlight through stained glass, the smell of luxurious scent pumped into a lobby, the weight of a silky new iPhone in your hand. We also have a sixth sense, that feeling we get from knowing that we are standing in a sacred place. A physical space that connects us with something wider and deeper than ourselves.

Dr. Jeffrey Benabio

Every day when I cover patient messages, I offer some patients an immediate, free solution to their problem. Just today I exchanged emails with a patient thinking I had addressed her concern by reassuring her that it was a benign seborrheic keratosis. Done. She then replied, “Thanks so much, Dr. Benabio! I still would like to schedule an appointment to come in person.” So much for the efficiency of digital medicine.

Before dismissing these patients as Luddites, understand what they want is the doctor’s office experience. The sights, the smells, the sacredness of what happens here. It is no coincidence that the first clinics were temples. In ancient Greece and Rome, the sick and the gashed made pilgrimages to one of at least 300 Asclepieia, temples of healing. During the medieval period, monasteries doubled as housing for the sick until the church began constructing stand-alone hospitals, often in cross-shaped design with an altar in the middle (eventually that became the nurses station, but without the wine).

Patients entrust us with their lives and their loved ones’ lives and a visit takes on far more significance than a simple service transaction. Forty years on, I can recall visits to Dr. Bellin’s office. He saw pediatric patients out of his Victorian home office with broad, creaky hardwood floors, stained glass, and cast iron radiators. The scent of isopropyl soaked cotton balls and typewriter ink is unforgettable. Far from sterile, it was warm, safe. It was a sacred place, one for which we still sometimes drive by when doing the tour of where I grew up.

We shall forge ahead and continue to offer virtual channels to serve our patients just as any service industry. But don’t force them there. At the same time Starbucks has been building its digital app, it is also building Starbucks Reserve Roasteries. Immense cathedral edifices with warm woods and luxurious brass, the smell of roasting coffee and warm leather perfuming the air. It is where patrons will travel long distances and endure long waits to pay a lot more for a cup of coffee.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Church architecture describes visually the idea of the sacred, which is a fundamental need of man.

– Mario Botta, Swiss architect

My parents are visiting the Holy See today – prima volta in Italia! My mom waited years for this. She isn’t meeting the Pope or attending Mass. Yet, in the Whatsapp pics they sent me, you can see tears well up as she experiences St. Peter’s Basilica. It’s a visceral response to what is just a building and a poignant example of the significance of spaces.

More than just appreciating an edifice’s grandeur or exquisiteness, we are wired to connect with spaces emotionally. Beautiful or significant buildings move us, they make us feel something. Churches, synagogues, or mosques are good examples. They combine spiritual and aesthetic allure. But so too do gorgeous hotels, Apple stores, and posh restaurants. We crave the richness of an environment experienced through our five senses. The glory of sunlight through stained glass, the smell of luxurious scent pumped into a lobby, the weight of a silky new iPhone in your hand. We also have a sixth sense, that feeling we get from knowing that we are standing in a sacred place. A physical space that connects us with something wider and deeper than ourselves.

Dr. Jeffrey Benabio

Every day when I cover patient messages, I offer some patients an immediate, free solution to their problem. Just today I exchanged emails with a patient thinking I had addressed her concern by reassuring her that it was a benign seborrheic keratosis. Done. She then replied, “Thanks so much, Dr. Benabio! I still would like to schedule an appointment to come in person.” So much for the efficiency of digital medicine.

Before dismissing these patients as Luddites, understand what they want is the doctor’s office experience. The sights, the smells, the sacredness of what happens here. It is no coincidence that the first clinics were temples. In ancient Greece and Rome, the sick and the gashed made pilgrimages to one of at least 300 Asclepieia, temples of healing. During the medieval period, monasteries doubled as housing for the sick until the church began constructing stand-alone hospitals, often in cross-shaped design with an altar in the middle (eventually that became the nurses station, but without the wine).

Patients entrust us with their lives and their loved ones’ lives and a visit takes on far more significance than a simple service transaction. Forty years on, I can recall visits to Dr. Bellin’s office. He saw pediatric patients out of his Victorian home office with broad, creaky hardwood floors, stained glass, and cast iron radiators. The scent of isopropyl soaked cotton balls and typewriter ink is unforgettable. Far from sterile, it was warm, safe. It was a sacred place, one for which we still sometimes drive by when doing the tour of where I grew up.

We shall forge ahead and continue to offer virtual channels to serve our patients just as any service industry. But don’t force them there. At the same time Starbucks has been building its digital app, it is also building Starbucks Reserve Roasteries. Immense cathedral edifices with warm woods and luxurious brass, the smell of roasting coffee and warm leather perfuming the air. It is where patrons will travel long distances and endure long waits to pay a lot more for a cup of coffee.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Church architecture describes visually the idea of the sacred, which is a fundamental need of man.

– Mario Botta, Swiss architect

My parents are visiting the Holy See today – prima volta in Italia! My mom waited years for this. She isn’t meeting the Pope or attending Mass. Yet, in the Whatsapp pics they sent me, you can see tears well up as she experiences St. Peter’s Basilica. It’s a visceral response to what is just a building and a poignant example of the significance of spaces.

More than just appreciating an edifice’s grandeur or exquisiteness, we are wired to connect with spaces emotionally. Beautiful or significant buildings move us, they make us feel something. Churches, synagogues, or mosques are good examples. They combine spiritual and aesthetic allure. But so too do gorgeous hotels, Apple stores, and posh restaurants. We crave the richness of an environment experienced through our five senses. The glory of sunlight through stained glass, the smell of luxurious scent pumped into a lobby, the weight of a silky new iPhone in your hand. We also have a sixth sense, that feeling we get from knowing that we are standing in a sacred place. A physical space that connects us with something wider and deeper than ourselves.

Dr. Jeffrey Benabio

Every day when I cover patient messages, I offer some patients an immediate, free solution to their problem. Just today I exchanged emails with a patient thinking I had addressed her concern by reassuring her that it was a benign seborrheic keratosis. Done. She then replied, “Thanks so much, Dr. Benabio! I still would like to schedule an appointment to come in person.” So much for the efficiency of digital medicine.

Before dismissing these patients as Luddites, understand what they want is the doctor’s office experience. The sights, the smells, the sacredness of what happens here. It is no coincidence that the first clinics were temples. In ancient Greece and Rome, the sick and the gashed made pilgrimages to one of at least 300 Asclepieia, temples of healing. During the medieval period, monasteries doubled as housing for the sick until the church began constructing stand-alone hospitals, often in cross-shaped design with an altar in the middle (eventually that became the nurses station, but without the wine).

Patients entrust us with their lives and their loved ones’ lives and a visit takes on far more significance than a simple service transaction. Forty years on, I can recall visits to Dr. Bellin’s office. He saw pediatric patients out of his Victorian home office with broad, creaky hardwood floors, stained glass, and cast iron radiators. The scent of isopropyl soaked cotton balls and typewriter ink is unforgettable. Far from sterile, it was warm, safe. It was a sacred place, one for which we still sometimes drive by when doing the tour of where I grew up.

We shall forge ahead and continue to offer virtual channels to serve our patients just as any service industry. But don’t force them there. At the same time Starbucks has been building its digital app, it is also building Starbucks Reserve Roasteries. Immense cathedral edifices with warm woods and luxurious brass, the smell of roasting coffee and warm leather perfuming the air. It is where patrons will travel long distances and endure long waits to pay a lot more for a cup of coffee.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

A U.S. Food and Drug Administration investigation of injection-site necrosis in some people who received the 23-valent pneumococcal vaccine has concluded that the benefits of the vaccine outweigh the risks.

No similar safety signal has been detected for the more recently approved 15-valent and 20-valent pneumococcal conjugate vaccines, explain the investigators, led by Brendan Day, MD, MPH, from the FDA’s Center for Biologics Evaluation and Research, in their report published online in JAMA Internal Medicine.

Reports of injection-site necrosis emerged after the vaccine (Pneumovax 23, Merck) had been approved by the FDA and was administered to a large, diverse, real-world population.

Rare safety events can emerge after FDA approval, as clinical trials may not be able to detect them in a study-group population.

Therefore, “postmarketing safety surveillance is critical to further characterize the safety profile of licensed vaccines,” the investigators point out.

The FDA and the Centers for Disease Control and Prevention monitor the postmarketing safety of licensed vaccines using the Vaccine Adverse Event Reporting System (VAERS), which relies on people who get the vaccines to report adverse events.
 

Real-world finding

After reports indicated a safety signal in 2020, the researchers conducted a case-series review, calculated the reporting rate, and did a PubMed search for similar reports.

They found that the reporting rate for injection-site necrosis was less than 0.2 cases per 1 million vaccine doses administered. The PubMed search yielded two cases of injection-site necrosis after the vaccine.

The 23-valent vaccine helps protect people from pneumococcus bacterial infection. The manufacturer reports that it is for people at least 50 years of age and for children who are at least 2 years of age with medical conditions that put them at elevated risk for infection.

The U.S. package insert has been updated, in the Post-Marketing Experience section, to include injection-site necrosis.

Of the 104 VAERS reports identified by the researchers, 48 met the case definition. Of those cases, most were for skin necrosis (n = 43), five of which also included fat necrosis. The remaining five cases of necrosis affected fascia (n = 2); fat and fascia (n = 1); fat, fascia, and muscle (n = 1); and muscle (n = 1).

In 23 of the 48 cases (47.9%), the reactions were serious and included one death (unrelated to vaccination).

Seventeen patients (35.4%) were hospitalized and 26 (54.2%) required surgery, most commonly debridement. Eight patients (16.7%) underwent multiple surgical procedures and three (6.3%) required a skin graft.

For patients with skin necrosis (n = 43), the median age was 67 years, and most patients were female (n = 36). Twelve patients were immunocompromised.

Concomitant vaccinations were reported in 10 patients, five of whom got the shot in the same arm as the 23-valent pneumococcal vaccine. A concurrent diagnosis of cellulitis was reported in 16 patients and an abscess was reported in three patients. There were too few cases of fat, fascia, or muscle necrosis to draw conclusions, the researchers report.

Often, skin necrosis was seen after a progression of symptoms, such as redness, pain, or swelling.

“These reports are consistent with published descriptions of injection-site necrosis, which has been reported as a rare complication for many vaccines and injectable drugs,” the investigators report.

Although the researchers couldn’t conclude from the VAERS reports alone that the vaccine injection caused the necrosis, “the timing and the location of reactions at the injection site suggest a possible causal association with the vaccine,” they explain. However, they add, patient comorbidities and poor injection technique may also be contributors.

A version of this article first appeared on Medscape.com.

A U.S. Food and Drug Administration investigation of injection-site necrosis in some people who received the 23-valent pneumococcal vaccine has concluded that the benefits of the vaccine outweigh the risks.

No similar safety signal has been detected for the more recently approved 15-valent and 20-valent pneumococcal conjugate vaccines, explain the investigators, led by Brendan Day, MD, MPH, from the FDA’s Center for Biologics Evaluation and Research, in their report published online in JAMA Internal Medicine.

Reports of injection-site necrosis emerged after the vaccine (Pneumovax 23, Merck) had been approved by the FDA and was administered to a large, diverse, real-world population.

Rare safety events can emerge after FDA approval, as clinical trials may not be able to detect them in a study-group population.

Therefore, “postmarketing safety surveillance is critical to further characterize the safety profile of licensed vaccines,” the investigators point out.

The FDA and the Centers for Disease Control and Prevention monitor the postmarketing safety of licensed vaccines using the Vaccine Adverse Event Reporting System (VAERS), which relies on people who get the vaccines to report adverse events.
 

Real-world finding

After reports indicated a safety signal in 2020, the researchers conducted a case-series review, calculated the reporting rate, and did a PubMed search for similar reports.

They found that the reporting rate for injection-site necrosis was less than 0.2 cases per 1 million vaccine doses administered. The PubMed search yielded two cases of injection-site necrosis after the vaccine.

The 23-valent vaccine helps protect people from pneumococcus bacterial infection. The manufacturer reports that it is for people at least 50 years of age and for children who are at least 2 years of age with medical conditions that put them at elevated risk for infection.

The U.S. package insert has been updated, in the Post-Marketing Experience section, to include injection-site necrosis.

Of the 104 VAERS reports identified by the researchers, 48 met the case definition. Of those cases, most were for skin necrosis (n = 43), five of which also included fat necrosis. The remaining five cases of necrosis affected fascia (n = 2); fat and fascia (n = 1); fat, fascia, and muscle (n = 1); and muscle (n = 1).

In 23 of the 48 cases (47.9%), the reactions were serious and included one death (unrelated to vaccination).

Seventeen patients (35.4%) were hospitalized and 26 (54.2%) required surgery, most commonly debridement. Eight patients (16.7%) underwent multiple surgical procedures and three (6.3%) required a skin graft.

For patients with skin necrosis (n = 43), the median age was 67 years, and most patients were female (n = 36). Twelve patients were immunocompromised.

Concomitant vaccinations were reported in 10 patients, five of whom got the shot in the same arm as the 23-valent pneumococcal vaccine. A concurrent diagnosis of cellulitis was reported in 16 patients and an abscess was reported in three patients. There were too few cases of fat, fascia, or muscle necrosis to draw conclusions, the researchers report.

Often, skin necrosis was seen after a progression of symptoms, such as redness, pain, or swelling.

“These reports are consistent with published descriptions of injection-site necrosis, which has been reported as a rare complication for many vaccines and injectable drugs,” the investigators report.

Although the researchers couldn’t conclude from the VAERS reports alone that the vaccine injection caused the necrosis, “the timing and the location of reactions at the injection site suggest a possible causal association with the vaccine,” they explain. However, they add, patient comorbidities and poor injection technique may also be contributors.

A version of this article first appeared on Medscape.com.

A U.S. Food and Drug Administration investigation of injection-site necrosis in some people who received the 23-valent pneumococcal vaccine has concluded that the benefits of the vaccine outweigh the risks.

No similar safety signal has been detected for the more recently approved 15-valent and 20-valent pneumococcal conjugate vaccines, explain the investigators, led by Brendan Day, MD, MPH, from the FDA’s Center for Biologics Evaluation and Research, in their report published online in JAMA Internal Medicine.

Reports of injection-site necrosis emerged after the vaccine (Pneumovax 23, Merck) had been approved by the FDA and was administered to a large, diverse, real-world population.

Rare safety events can emerge after FDA approval, as clinical trials may not be able to detect them in a study-group population.

Therefore, “postmarketing safety surveillance is critical to further characterize the safety profile of licensed vaccines,” the investigators point out.

The FDA and the Centers for Disease Control and Prevention monitor the postmarketing safety of licensed vaccines using the Vaccine Adverse Event Reporting System (VAERS), which relies on people who get the vaccines to report adverse events.
 

Real-world finding

After reports indicated a safety signal in 2020, the researchers conducted a case-series review, calculated the reporting rate, and did a PubMed search for similar reports.

They found that the reporting rate for injection-site necrosis was less than 0.2 cases per 1 million vaccine doses administered. The PubMed search yielded two cases of injection-site necrosis after the vaccine.

The 23-valent vaccine helps protect people from pneumococcus bacterial infection. The manufacturer reports that it is for people at least 50 years of age and for children who are at least 2 years of age with medical conditions that put them at elevated risk for infection.

The U.S. package insert has been updated, in the Post-Marketing Experience section, to include injection-site necrosis.

Of the 104 VAERS reports identified by the researchers, 48 met the case definition. Of those cases, most were for skin necrosis (n = 43), five of which also included fat necrosis. The remaining five cases of necrosis affected fascia (n = 2); fat and fascia (n = 1); fat, fascia, and muscle (n = 1); and muscle (n = 1).

In 23 of the 48 cases (47.9%), the reactions were serious and included one death (unrelated to vaccination).

Seventeen patients (35.4%) were hospitalized and 26 (54.2%) required surgery, most commonly debridement. Eight patients (16.7%) underwent multiple surgical procedures and three (6.3%) required a skin graft.

For patients with skin necrosis (n = 43), the median age was 67 years, and most patients were female (n = 36). Twelve patients were immunocompromised.

Concomitant vaccinations were reported in 10 patients, five of whom got the shot in the same arm as the 23-valent pneumococcal vaccine. A concurrent diagnosis of cellulitis was reported in 16 patients and an abscess was reported in three patients. There were too few cases of fat, fascia, or muscle necrosis to draw conclusions, the researchers report.

Often, skin necrosis was seen after a progression of symptoms, such as redness, pain, or swelling.

“These reports are consistent with published descriptions of injection-site necrosis, which has been reported as a rare complication for many vaccines and injectable drugs,” the investigators report.

Although the researchers couldn’t conclude from the VAERS reports alone that the vaccine injection caused the necrosis, “the timing and the location of reactions at the injection site suggest a possible causal association with the vaccine,” they explain. However, they add, patient comorbidities and poor injection technique may also be contributors.

A version of this article first appeared on Medscape.com.

Choosing the right partner to add to your practice takes planning and strategic decision-making. When the match is right, the benefits can be significant: more hands to share the load of running a medical practice, and increased revenue and expanded patient population. A partner can bring in new, complementary strengths and skills. Adding a partner is also a way to prepare for the future by setting your practice up for a smooth transition if you or another partner is looking toward retirement.

But a mismatched partnership can cost you time and money, not to mention endless amount of conflict, dysfunction, and liability. Mutual trust and a long-term commitment on both sides are critical.

“Just like with marriage, it can be very difficult, traumatic, and expensive to break up with a partner,” said Clifton Straughn, MD, partner at Direct Access MD, a concierge-service model family practice in Anderson, S.C. “So, do your due diligence and take your time.” Picking the right partner is essential.
 

The basics

Before you begin the process of partnership with a physician, be sure you know what you need, the skill sets you’re looking for to complement your practice, and the personality characteristics and values that are important to you so the person you choose can check all the boxes and not just add a name to the letterhead.

“A lot of times, doctors go into this with just a general idea that they need more doctors or that they would like to be bigger or have more clout,” said Tim Boden, a certified medical practice executive with over 40 years of experience. “But you have to understand that to a certain degree, if you’re bringing somebody in who has basically an identical clinical profile to yours, you’re going to be sacrificing a bit of your lunch for a while until that person builds a name for himself or herself. A new partner’s skill set should match the need that you’re trying to fill.”

Figure out and discuss with your current partners how much it will cost to bring in a partner between their compensation and additional practice expenses. How much revenue will you expect the partner to generate? Will your practice break even the first year or the second? And how will you cover any shortfall?

It’s also essential to understand how the day-to-day operation of your practice will change after you add another partner.

• Will the new partner’s percentage of ownership be the same as that of the other partners?
• Will their ownership include a percentage of the facility, equipment, supplies, and accounts receivable?
• How will you split call and work hours?
• How will decision-making work?
• How would buyout work if a partner were to leave the practice, and is there a minimum obligation, such as a 5-year commitment?

As a team, you may also want to discuss “soft skills,” or the way you’d hope a partner would represent your practice to patients and the community.

“These can be harder to quantify,” said Dr. Straughn. “Evaluating them can take artful questions and simple observation over time.”
 

It’s a slow process

Many practices offer paths to partnership rather than bringing in a partner straight away. With this process, an incoming physician works toward that goal. If you’re going this route, discuss this during the hiring process, so that both sides are clear about the process. Rule No. 1 is to make sure that new hires understand that partnership is possible, although it’s not a given. The typical partnership track is 2-3 years, but you can set the timeline that works best for your practice.

Mr. Boden recommends at least a year for this period so as to allow you the opportunity to evaluate the new member, how they work, and how they fit with your team. The partnership track method is typically for young or fairly new physicians.

“I would avoid ever promising an ownership position to a recruit,” said Mr. Boden. “I would only show them how it can happen and what it would look like if they qualify.”
 

Consider professional help

If you want to be sure you weigh all the pros and cons of your new partner, a medical practice consultant may be the way to go. A consultant can identify many situations that you might overlook.

Some services offer a medical practice assessment to help you see where you need the most help and what skills might be best to bring to the table. They might also be able to take over some of the administrative work of a new hire if you like, so you and the other partners can focus solely on interacting with and observing the clinical abilities of a potential partner.

A health care attorney can help you build a sound agreement regarding decision-making and how the fees/costs will be divided and can put legal protections in place for everyone involved.

You’ll need a buy-sell agreement (also called a partnership or shareholder agreement) that spells out the terms and conditions, including buying into and selling out of the practice. A fair agreement respects all parties, while a poor one that offers the new partner a minority share or lessor profit may favor the practice’s current partners but could breed resentment, undermining the practice’s culture and morale.
 

Takeaway

Ideally, you’ll select someone with excellent credentials and experience with similar goals for the practice who blends well with your staff. It’s best to find someone who fits well culturally with your office and who practices medicine with a similar patient philosophy.

To that end, Mr. Boden encourages out-of-the-box questions for interviews, such as what a potential partner wants to make sure they have room for in their life, or what their ideal work and family life looks like. The more you can assess components such as emotional intelligence, =the fuller picture you’ll get.

“You’re going to be spending major hours every week with this person, and your destiny is going to be tied up with theirs to some degree,” said Mr. Boden. You can teach somebody the job, but if you don’t genuinely like and respect them and want to work with them daily, it may not be the right fit.

A version of this article first appeared on Medscape.com.

Choosing the right partner to add to your practice takes planning and strategic decision-making. When the match is right, the benefits can be significant: more hands to share the load of running a medical practice, and increased revenue and expanded patient population. A partner can bring in new, complementary strengths and skills. Adding a partner is also a way to prepare for the future by setting your practice up for a smooth transition if you or another partner is looking toward retirement.

But a mismatched partnership can cost you time and money, not to mention endless amount of conflict, dysfunction, and liability. Mutual trust and a long-term commitment on both sides are critical.

“Just like with marriage, it can be very difficult, traumatic, and expensive to break up with a partner,” said Clifton Straughn, MD, partner at Direct Access MD, a concierge-service model family practice in Anderson, S.C. “So, do your due diligence and take your time.” Picking the right partner is essential.
 

The basics

Before you begin the process of partnership with a physician, be sure you know what you need, the skill sets you’re looking for to complement your practice, and the personality characteristics and values that are important to you so the person you choose can check all the boxes and not just add a name to the letterhead.

“A lot of times, doctors go into this with just a general idea that they need more doctors or that they would like to be bigger or have more clout,” said Tim Boden, a certified medical practice executive with over 40 years of experience. “But you have to understand that to a certain degree, if you’re bringing somebody in who has basically an identical clinical profile to yours, you’re going to be sacrificing a bit of your lunch for a while until that person builds a name for himself or herself. A new partner’s skill set should match the need that you’re trying to fill.”

Figure out and discuss with your current partners how much it will cost to bring in a partner between their compensation and additional practice expenses. How much revenue will you expect the partner to generate? Will your practice break even the first year or the second? And how will you cover any shortfall?

It’s also essential to understand how the day-to-day operation of your practice will change after you add another partner.

• Will the new partner’s percentage of ownership be the same as that of the other partners?
• Will their ownership include a percentage of the facility, equipment, supplies, and accounts receivable?
• How will you split call and work hours?
• How will decision-making work?
• How would buyout work if a partner were to leave the practice, and is there a minimum obligation, such as a 5-year commitment?

As a team, you may also want to discuss “soft skills,” or the way you’d hope a partner would represent your practice to patients and the community.

“These can be harder to quantify,” said Dr. Straughn. “Evaluating them can take artful questions and simple observation over time.”
 

It’s a slow process

Many practices offer paths to partnership rather than bringing in a partner straight away. With this process, an incoming physician works toward that goal. If you’re going this route, discuss this during the hiring process, so that both sides are clear about the process. Rule No. 1 is to make sure that new hires understand that partnership is possible, although it’s not a given. The typical partnership track is 2-3 years, but you can set the timeline that works best for your practice.

Mr. Boden recommends at least a year for this period so as to allow you the opportunity to evaluate the new member, how they work, and how they fit with your team. The partnership track method is typically for young or fairly new physicians.

“I would avoid ever promising an ownership position to a recruit,” said Mr. Boden. “I would only show them how it can happen and what it would look like if they qualify.”
 

Consider professional help

If you want to be sure you weigh all the pros and cons of your new partner, a medical practice consultant may be the way to go. A consultant can identify many situations that you might overlook.

Some services offer a medical practice assessment to help you see where you need the most help and what skills might be best to bring to the table. They might also be able to take over some of the administrative work of a new hire if you like, so you and the other partners can focus solely on interacting with and observing the clinical abilities of a potential partner.

A health care attorney can help you build a sound agreement regarding decision-making and how the fees/costs will be divided and can put legal protections in place for everyone involved.

You’ll need a buy-sell agreement (also called a partnership or shareholder agreement) that spells out the terms and conditions, including buying into and selling out of the practice. A fair agreement respects all parties, while a poor one that offers the new partner a minority share or lessor profit may favor the practice’s current partners but could breed resentment, undermining the practice’s culture and morale.
 

Takeaway

Ideally, you’ll select someone with excellent credentials and experience with similar goals for the practice who blends well with your staff. It’s best to find someone who fits well culturally with your office and who practices medicine with a similar patient philosophy.

To that end, Mr. Boden encourages out-of-the-box questions for interviews, such as what a potential partner wants to make sure they have room for in their life, or what their ideal work and family life looks like. The more you can assess components such as emotional intelligence, =the fuller picture you’ll get.

“You’re going to be spending major hours every week with this person, and your destiny is going to be tied up with theirs to some degree,” said Mr. Boden. You can teach somebody the job, but if you don’t genuinely like and respect them and want to work with them daily, it may not be the right fit.

A version of this article first appeared on Medscape.com.

Choosing the right partner to add to your practice takes planning and strategic decision-making. When the match is right, the benefits can be significant: more hands to share the load of running a medical practice, and increased revenue and expanded patient population. A partner can bring in new, complementary strengths and skills. Adding a partner is also a way to prepare for the future by setting your practice up for a smooth transition if you or another partner is looking toward retirement.

But a mismatched partnership can cost you time and money, not to mention endless amount of conflict, dysfunction, and liability. Mutual trust and a long-term commitment on both sides are critical.

“Just like with marriage, it can be very difficult, traumatic, and expensive to break up with a partner,” said Clifton Straughn, MD, partner at Direct Access MD, a concierge-service model family practice in Anderson, S.C. “So, do your due diligence and take your time.” Picking the right partner is essential.
 

The basics

Before you begin the process of partnership with a physician, be sure you know what you need, the skill sets you’re looking for to complement your practice, and the personality characteristics and values that are important to you so the person you choose can check all the boxes and not just add a name to the letterhead.

“A lot of times, doctors go into this with just a general idea that they need more doctors or that they would like to be bigger or have more clout,” said Tim Boden, a certified medical practice executive with over 40 years of experience. “But you have to understand that to a certain degree, if you’re bringing somebody in who has basically an identical clinical profile to yours, you’re going to be sacrificing a bit of your lunch for a while until that person builds a name for himself or herself. A new partner’s skill set should match the need that you’re trying to fill.”

Figure out and discuss with your current partners how much it will cost to bring in a partner between their compensation and additional practice expenses. How much revenue will you expect the partner to generate? Will your practice break even the first year or the second? And how will you cover any shortfall?

It’s also essential to understand how the day-to-day operation of your practice will change after you add another partner.

• Will the new partner’s percentage of ownership be the same as that of the other partners?
• Will their ownership include a percentage of the facility, equipment, supplies, and accounts receivable?
• How will you split call and work hours?
• How will decision-making work?
• How would buyout work if a partner were to leave the practice, and is there a minimum obligation, such as a 5-year commitment?

As a team, you may also want to discuss “soft skills,” or the way you’d hope a partner would represent your practice to patients and the community.

“These can be harder to quantify,” said Dr. Straughn. “Evaluating them can take artful questions and simple observation over time.”
 

It’s a slow process

Many practices offer paths to partnership rather than bringing in a partner straight away. With this process, an incoming physician works toward that goal. If you’re going this route, discuss this during the hiring process, so that both sides are clear about the process. Rule No. 1 is to make sure that new hires understand that partnership is possible, although it’s not a given. The typical partnership track is 2-3 years, but you can set the timeline that works best for your practice.

Mr. Boden recommends at least a year for this period so as to allow you the opportunity to evaluate the new member, how they work, and how they fit with your team. The partnership track method is typically for young or fairly new physicians.

“I would avoid ever promising an ownership position to a recruit,” said Mr. Boden. “I would only show them how it can happen and what it would look like if they qualify.”
 

Consider professional help

If you want to be sure you weigh all the pros and cons of your new partner, a medical practice consultant may be the way to go. A consultant can identify many situations that you might overlook.

Some services offer a medical practice assessment to help you see where you need the most help and what skills might be best to bring to the table. They might also be able to take over some of the administrative work of a new hire if you like, so you and the other partners can focus solely on interacting with and observing the clinical abilities of a potential partner.

A health care attorney can help you build a sound agreement regarding decision-making and how the fees/costs will be divided and can put legal protections in place for everyone involved.

You’ll need a buy-sell agreement (also called a partnership or shareholder agreement) that spells out the terms and conditions, including buying into and selling out of the practice. A fair agreement respects all parties, while a poor one that offers the new partner a minority share or lessor profit may favor the practice’s current partners but could breed resentment, undermining the practice’s culture and morale.
 

Takeaway

Ideally, you’ll select someone with excellent credentials and experience with similar goals for the practice who blends well with your staff. It’s best to find someone who fits well culturally with your office and who practices medicine with a similar patient philosophy.

To that end, Mr. Boden encourages out-of-the-box questions for interviews, such as what a potential partner wants to make sure they have room for in their life, or what their ideal work and family life looks like. The more you can assess components such as emotional intelligence, =the fuller picture you’ll get.

“You’re going to be spending major hours every week with this person, and your destiny is going to be tied up with theirs to some degree,” said Mr. Boden. You can teach somebody the job, but if you don’t genuinely like and respect them and want to work with them daily, it may not be the right fit.

A version of this article first appeared on Medscape.com.

In a test of one of the nation’s most restrictive laws limiting noncompete clauses in medicine, an Indiana pediatric critical-care physician is suing to stop his former hospital employer from controlling his future employment prospects.

David Lankford, DO, acknowledges that he signed a contract with the Lutheran Health Network that included a noncompete clause. However, he claims in a lawsuit filed July 5 in Allen County Superior Court that an Indiana law that took effect 4 days earlier nullifies the clause because he quit his job with cause. 

Indiana’s law is notable among states because if a physician terminates his/her job for cause, the noncompete may be considered unenforceable.

“When you have physicians who are unable to work in their community, it creates a barrier for access to care for patients,” Dr. Lankford said in an interview. “I’m fighting to decrease barriers and continue to have patients be able to see their doctors in their own hometown or their own county.”

Lutheran Health’s media relations department did not respond to requests for comment.
 

Noncompete clauses ‘extremely common’

Non-compete clauses – which typically restrict when and where employees can take future jobs – are common in physician contracts, Anu Murthy, JD, who reviews employee contracts for a firm called Contract Diagnostics, said in an interview.

However, the tide has been turning against them.

About a dozen states and the District of Columbia have enacted legislation to limit the use of noncompetes in employment contracts, and about half of states have pending legislation that could dilute noncompete clauses, Ms. Murthy said. In June, the state of New York sent a noncompete ban bill to the governor’s desk.

For more about state-by-state restrictions on noncompete clauses, check this chart.

In his lawsuit, Dr. Lankford said he was hired in 2017 to work at Lutheran Hospital in Fort Wayne.

Dr. Lankford signed an employee renewal contract in 2020 that included a noncompete clause; his attorneys declined to provide details about the clause because of confidentiality restrictions. 

In 2022, the lawsuit says, Lutheran Hospital told Dr. Lankford that he’d need to take on more work due to layoffs of pediatric hospitalists. His patient load subsequently grew by 4-5 times, and he quit as of Jan. 7, 2023. 

Dr. Lankford wrote that he found a new job at Parkview Regional Medical Center in Fort Wayne, but his former employer threatened to take action under the noncompete clause, and Parkview withdrew its offer.

Among other things, the new Indiana law says that the clauses are not enforceable “if physician terminates the physician’s employment for cause.”

The lawsuit asks for a judge to prevent Lutheran Health Network from enforcing the clause.
 

Impact on patients

The new Indiana law also bans noncompete clauses for primary care physicians. Kathleen A. DeLaney, JD, one of Dr. Lankford’s attorneys, said in an interview that this provision came about because rural legislators didn’t want to add to the challenges of attracting primary care doctors to move to their communities.  

State legislators have become less friendly to noncompete clauses in medicine because they’re wary of the negative effects on patients, Evan Starr, PhD, said in an interview. The clauses prevent doctors from taking new jobs where they could continue to treat their previous patients, said Dr. Starr, associate professor in the department of management and organization at the University of Maryland.

However, he said, hospitals are fighting to preserve the clauses, arguing that they provide a base of patients to physicians in return for their agreement not to go work for a competitor.

The legal landscape may change even more. The Federal Trade Commission has proposed banning the clauses nationally, and a decision is expected in 2024. However, it’s an election year, which may delay a decision, attorney Ms. Murthy said, “and there is also language in the proposed rule that could exempt nonprofit hospitals, which further complicates the issues.”

For now, Ms. Murthy said, “we are still seeing noncompetes and other restrictive covenants in almost every contract we review in all 50 states and across all specialties. We explicitly explain to every client that they should only sign the agreement with the expectation that their specific noncompete will be enforced as written. Large employer groups, including hospital systems, will likely fight any kind of restriction or dilution of noncompetes, and these types of legal challenges could be tied up in court for many years.”
 

A version of this article first appeared on Medscape.com.

In a test of one of the nation’s most restrictive laws limiting noncompete clauses in medicine, an Indiana pediatric critical-care physician is suing to stop his former hospital employer from controlling his future employment prospects.

David Lankford, DO, acknowledges that he signed a contract with the Lutheran Health Network that included a noncompete clause. However, he claims in a lawsuit filed July 5 in Allen County Superior Court that an Indiana law that took effect 4 days earlier nullifies the clause because he quit his job with cause. 

Indiana’s law is notable among states because if a physician terminates his/her job for cause, the noncompete may be considered unenforceable.

“When you have physicians who are unable to work in their community, it creates a barrier for access to care for patients,” Dr. Lankford said in an interview. “I’m fighting to decrease barriers and continue to have patients be able to see their doctors in their own hometown or their own county.”

Lutheran Health’s media relations department did not respond to requests for comment.
 

Noncompete clauses ‘extremely common’

Non-compete clauses – which typically restrict when and where employees can take future jobs – are common in physician contracts, Anu Murthy, JD, who reviews employee contracts for a firm called Contract Diagnostics, said in an interview.

However, the tide has been turning against them.

About a dozen states and the District of Columbia have enacted legislation to limit the use of noncompetes in employment contracts, and about half of states have pending legislation that could dilute noncompete clauses, Ms. Murthy said. In June, the state of New York sent a noncompete ban bill to the governor’s desk.

For more about state-by-state restrictions on noncompete clauses, check this chart.

In his lawsuit, Dr. Lankford said he was hired in 2017 to work at Lutheran Hospital in Fort Wayne.

Dr. Lankford signed an employee renewal contract in 2020 that included a noncompete clause; his attorneys declined to provide details about the clause because of confidentiality restrictions. 

In 2022, the lawsuit says, Lutheran Hospital told Dr. Lankford that he’d need to take on more work due to layoffs of pediatric hospitalists. His patient load subsequently grew by 4-5 times, and he quit as of Jan. 7, 2023. 

Dr. Lankford wrote that he found a new job at Parkview Regional Medical Center in Fort Wayne, but his former employer threatened to take action under the noncompete clause, and Parkview withdrew its offer.

Among other things, the new Indiana law says that the clauses are not enforceable “if physician terminates the physician’s employment for cause.”

The lawsuit asks for a judge to prevent Lutheran Health Network from enforcing the clause.
 

Impact on patients

The new Indiana law also bans noncompete clauses for primary care physicians. Kathleen A. DeLaney, JD, one of Dr. Lankford’s attorneys, said in an interview that this provision came about because rural legislators didn’t want to add to the challenges of attracting primary care doctors to move to their communities.  

State legislators have become less friendly to noncompete clauses in medicine because they’re wary of the negative effects on patients, Evan Starr, PhD, said in an interview. The clauses prevent doctors from taking new jobs where they could continue to treat their previous patients, said Dr. Starr, associate professor in the department of management and organization at the University of Maryland.

However, he said, hospitals are fighting to preserve the clauses, arguing that they provide a base of patients to physicians in return for their agreement not to go work for a competitor.

The legal landscape may change even more. The Federal Trade Commission has proposed banning the clauses nationally, and a decision is expected in 2024. However, it’s an election year, which may delay a decision, attorney Ms. Murthy said, “and there is also language in the proposed rule that could exempt nonprofit hospitals, which further complicates the issues.”

For now, Ms. Murthy said, “we are still seeing noncompetes and other restrictive covenants in almost every contract we review in all 50 states and across all specialties. We explicitly explain to every client that they should only sign the agreement with the expectation that their specific noncompete will be enforced as written. Large employer groups, including hospital systems, will likely fight any kind of restriction or dilution of noncompetes, and these types of legal challenges could be tied up in court for many years.”
 

A version of this article first appeared on Medscape.com.

In a test of one of the nation’s most restrictive laws limiting noncompete clauses in medicine, an Indiana pediatric critical-care physician is suing to stop his former hospital employer from controlling his future employment prospects.

David Lankford, DO, acknowledges that he signed a contract with the Lutheran Health Network that included a noncompete clause. However, he claims in a lawsuit filed July 5 in Allen County Superior Court that an Indiana law that took effect 4 days earlier nullifies the clause because he quit his job with cause. 

Indiana’s law is notable among states because if a physician terminates his/her job for cause, the noncompete may be considered unenforceable.

“When you have physicians who are unable to work in their community, it creates a barrier for access to care for patients,” Dr. Lankford said in an interview. “I’m fighting to decrease barriers and continue to have patients be able to see their doctors in their own hometown or their own county.”

Lutheran Health’s media relations department did not respond to requests for comment.
 

Noncompete clauses ‘extremely common’

Non-compete clauses – which typically restrict when and where employees can take future jobs – are common in physician contracts, Anu Murthy, JD, who reviews employee contracts for a firm called Contract Diagnostics, said in an interview.

However, the tide has been turning against them.

About a dozen states and the District of Columbia have enacted legislation to limit the use of noncompetes in employment contracts, and about half of states have pending legislation that could dilute noncompete clauses, Ms. Murthy said. In June, the state of New York sent a noncompete ban bill to the governor’s desk.

For more about state-by-state restrictions on noncompete clauses, check this chart.

In his lawsuit, Dr. Lankford said he was hired in 2017 to work at Lutheran Hospital in Fort Wayne.

Dr. Lankford signed an employee renewal contract in 2020 that included a noncompete clause; his attorneys declined to provide details about the clause because of confidentiality restrictions. 

In 2022, the lawsuit says, Lutheran Hospital told Dr. Lankford that he’d need to take on more work due to layoffs of pediatric hospitalists. His patient load subsequently grew by 4-5 times, and he quit as of Jan. 7, 2023. 

Dr. Lankford wrote that he found a new job at Parkview Regional Medical Center in Fort Wayne, but his former employer threatened to take action under the noncompete clause, and Parkview withdrew its offer.

Among other things, the new Indiana law says that the clauses are not enforceable “if physician terminates the physician’s employment for cause.”

The lawsuit asks for a judge to prevent Lutheran Health Network from enforcing the clause.
 

Impact on patients

The new Indiana law also bans noncompete clauses for primary care physicians. Kathleen A. DeLaney, JD, one of Dr. Lankford’s attorneys, said in an interview that this provision came about because rural legislators didn’t want to add to the challenges of attracting primary care doctors to move to their communities.  

State legislators have become less friendly to noncompete clauses in medicine because they’re wary of the negative effects on patients, Evan Starr, PhD, said in an interview. The clauses prevent doctors from taking new jobs where they could continue to treat their previous patients, said Dr. Starr, associate professor in the department of management and organization at the University of Maryland.

However, he said, hospitals are fighting to preserve the clauses, arguing that they provide a base of patients to physicians in return for their agreement not to go work for a competitor.

The legal landscape may change even more. The Federal Trade Commission has proposed banning the clauses nationally, and a decision is expected in 2024. However, it’s an election year, which may delay a decision, attorney Ms. Murthy said, “and there is also language in the proposed rule that could exempt nonprofit hospitals, which further complicates the issues.”

For now, Ms. Murthy said, “we are still seeing noncompetes and other restrictive covenants in almost every contract we review in all 50 states and across all specialties. We explicitly explain to every client that they should only sign the agreement with the expectation that their specific noncompete will be enforced as written. Large employer groups, including hospital systems, will likely fight any kind of restriction or dilution of noncompetes, and these types of legal challenges could be tied up in court for many years.”
 

A version of this article first appeared on Medscape.com.

It’s interesting how questions often arrive in clusters. This week, my inbox is packed with queries about paid sick leave and paid time off (PTO); what is the difference, which is preferable, what is required, and how does one implement a fair and legal time-off policy for a medical office?

First, the difference: Paid sick leave is the time off allotted to each employee for illness or injury, whereas PTO is an all-encompassing bundle that includes vacation and any other miscellaneous time benefits in addition to sick leave.

Which is preferable? That depends on whom you ask, and sometimes, on the legal situation in your state. Employees generally like the PTO concept, because most never use all of their sick leave. The ability to take the difference as extra vacation time makes them happy and makes your office more attractive to excellent prospects. They also appreciate making their own decisions about taking time off.

Many employers like PTO because there is less paperwork involved and less abuse of sick leave – and they don’t have to make any decisions about whether an employee is actually sick. Reasons for absences are now irrelevant, so feigned illnesses are a thing of the past. If an employee requests a day off with adequate notice, and there is adequate coverage of that employee’s duties, you don’t need to know (or care) about the reason for the request.

Critics of PTO say employees are absent more often, since employees who never used their full allotment of sick leave will typically use all of their PTO; but that, in a sense, is the idea. Time off is necessary and important for good office morale, and should be taken by all employees, as well as by all employers. (Remember Eastern’s First Law: Your last words will NOT be, “I wish I had spent more time in the office.”)

Moreover, you should be suspicious of any employee who refuses to take vacations. They may be embezzlers who fear that their illicit modus operandi will be discovered during their absence.

Another common criticism of PTO is the possibility that employees will not stay home when they are truly sick because some employees may view all PTO as vacation time, and don’t want to “waste” any of it on illness. You should make it very clear that sick employees should stay home – and will be sent home if they come to work sick. You have an obligation to protect your other employees – and of course your patients, particularly those who are elderly or immunocompromised – from a staff member with a potentially communicable illness.

The legal requirements of time off are variable. There are currently no federal laws requiring employers to offer paid time off, but each state has its own PTO and sick leave requirements, so you will need to check your state’s specific guidelines before creating or updating a time off policy.

When drafting your policy, make sure everyone knows they will have to request PTO in advance, except for emergencies. Start with defining “in advance” (72 hours? A week?), and then “emergency”; and put these definitions in writing. Illnesses are emergencies, of course, but what about waking up with a bad hangover? A sick child qualifies if your employee is the only available caregiver, but what if the employee’s car has broken down? Some circumstances will have to be decided on a case-by-case basis; but you will have fewer hassles if you anticipate and settle more situations in advance.

What about allowing employees to take salary in exchange for unused PTO, or to roll it over into the next year? We don’t permit either in my office, but some states (for instance, California, Montana, and Nebraska) prohibit use-it-or-lose-it policies.

When an employee leaves or is terminated, do you have to pay accrued PTO? No federal law requires it, but some states do.

What about employees who use up their allotted PTO and request unpaid time off? In my office, we require employees to submit a written request, explaining why they need it, and why it’s a special situation and won’t be a regular occurrence. Even if you (almost) always approve such requests, forcing your employees to jump through a hoop or two makes it less likely that anyone will abuse the privilege. Moreover, this allows you to make judgments on a case-by-case basis, while still being able to honestly say you offer it as a blanket policy to all your employees.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

It’s interesting how questions often arrive in clusters. This week, my inbox is packed with queries about paid sick leave and paid time off (PTO); what is the difference, which is preferable, what is required, and how does one implement a fair and legal time-off policy for a medical office?

First, the difference: Paid sick leave is the time off allotted to each employee for illness or injury, whereas PTO is an all-encompassing bundle that includes vacation and any other miscellaneous time benefits in addition to sick leave.

Which is preferable? That depends on whom you ask, and sometimes, on the legal situation in your state. Employees generally like the PTO concept, because most never use all of their sick leave. The ability to take the difference as extra vacation time makes them happy and makes your office more attractive to excellent prospects. They also appreciate making their own decisions about taking time off.

Many employers like PTO because there is less paperwork involved and less abuse of sick leave – and they don’t have to make any decisions about whether an employee is actually sick. Reasons for absences are now irrelevant, so feigned illnesses are a thing of the past. If an employee requests a day off with adequate notice, and there is adequate coverage of that employee’s duties, you don’t need to know (or care) about the reason for the request.

Critics of PTO say employees are absent more often, since employees who never used their full allotment of sick leave will typically use all of their PTO; but that, in a sense, is the idea. Time off is necessary and important for good office morale, and should be taken by all employees, as well as by all employers. (Remember Eastern’s First Law: Your last words will NOT be, “I wish I had spent more time in the office.”)

Moreover, you should be suspicious of any employee who refuses to take vacations. They may be embezzlers who fear that their illicit modus operandi will be discovered during their absence.

Another common criticism of PTO is the possibility that employees will not stay home when they are truly sick because some employees may view all PTO as vacation time, and don’t want to “waste” any of it on illness. You should make it very clear that sick employees should stay home – and will be sent home if they come to work sick. You have an obligation to protect your other employees – and of course your patients, particularly those who are elderly or immunocompromised – from a staff member with a potentially communicable illness.

The legal requirements of time off are variable. There are currently no federal laws requiring employers to offer paid time off, but each state has its own PTO and sick leave requirements, so you will need to check your state’s specific guidelines before creating or updating a time off policy.

When drafting your policy, make sure everyone knows they will have to request PTO in advance, except for emergencies. Start with defining “in advance” (72 hours? A week?), and then “emergency”; and put these definitions in writing. Illnesses are emergencies, of course, but what about waking up with a bad hangover? A sick child qualifies if your employee is the only available caregiver, but what if the employee’s car has broken down? Some circumstances will have to be decided on a case-by-case basis; but you will have fewer hassles if you anticipate and settle more situations in advance.

What about allowing employees to take salary in exchange for unused PTO, or to roll it over into the next year? We don’t permit either in my office, but some states (for instance, California, Montana, and Nebraska) prohibit use-it-or-lose-it policies.

When an employee leaves or is terminated, do you have to pay accrued PTO? No federal law requires it, but some states do.

What about employees who use up their allotted PTO and request unpaid time off? In my office, we require employees to submit a written request, explaining why they need it, and why it’s a special situation and won’t be a regular occurrence. Even if you (almost) always approve such requests, forcing your employees to jump through a hoop or two makes it less likely that anyone will abuse the privilege. Moreover, this allows you to make judgments on a case-by-case basis, while still being able to honestly say you offer it as a blanket policy to all your employees.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

It’s interesting how questions often arrive in clusters. This week, my inbox is packed with queries about paid sick leave and paid time off (PTO); what is the difference, which is preferable, what is required, and how does one implement a fair and legal time-off policy for a medical office?

First, the difference: Paid sick leave is the time off allotted to each employee for illness or injury, whereas PTO is an all-encompassing bundle that includes vacation and any other miscellaneous time benefits in addition to sick leave.

Which is preferable? That depends on whom you ask, and sometimes, on the legal situation in your state. Employees generally like the PTO concept, because most never use all of their sick leave. The ability to take the difference as extra vacation time makes them happy and makes your office more attractive to excellent prospects. They also appreciate making their own decisions about taking time off.

Many employers like PTO because there is less paperwork involved and less abuse of sick leave – and they don’t have to make any decisions about whether an employee is actually sick. Reasons for absences are now irrelevant, so feigned illnesses are a thing of the past. If an employee requests a day off with adequate notice, and there is adequate coverage of that employee’s duties, you don’t need to know (or care) about the reason for the request.

Critics of PTO say employees are absent more often, since employees who never used their full allotment of sick leave will typically use all of their PTO; but that, in a sense, is the idea. Time off is necessary and important for good office morale, and should be taken by all employees, as well as by all employers. (Remember Eastern’s First Law: Your last words will NOT be, “I wish I had spent more time in the office.”)

Moreover, you should be suspicious of any employee who refuses to take vacations. They may be embezzlers who fear that their illicit modus operandi will be discovered during their absence.

Another common criticism of PTO is the possibility that employees will not stay home when they are truly sick because some employees may view all PTO as vacation time, and don’t want to “waste” any of it on illness. You should make it very clear that sick employees should stay home – and will be sent home if they come to work sick. You have an obligation to protect your other employees – and of course your patients, particularly those who are elderly or immunocompromised – from a staff member with a potentially communicable illness.

The legal requirements of time off are variable. There are currently no federal laws requiring employers to offer paid time off, but each state has its own PTO and sick leave requirements, so you will need to check your state’s specific guidelines before creating or updating a time off policy.

When drafting your policy, make sure everyone knows they will have to request PTO in advance, except for emergencies. Start with defining “in advance” (72 hours? A week?), and then “emergency”; and put these definitions in writing. Illnesses are emergencies, of course, but what about waking up with a bad hangover? A sick child qualifies if your employee is the only available caregiver, but what if the employee’s car has broken down? Some circumstances will have to be decided on a case-by-case basis; but you will have fewer hassles if you anticipate and settle more situations in advance.

What about allowing employees to take salary in exchange for unused PTO, or to roll it over into the next year? We don’t permit either in my office, but some states (for instance, California, Montana, and Nebraska) prohibit use-it-or-lose-it policies.

When an employee leaves or is terminated, do you have to pay accrued PTO? No federal law requires it, but some states do.

What about employees who use up their allotted PTO and request unpaid time off? In my office, we require employees to submit a written request, explaining why they need it, and why it’s a special situation and won’t be a regular occurrence. Even if you (almost) always approve such requests, forcing your employees to jump through a hoop or two makes it less likely that anyone will abuse the privilege. Moreover, this allows you to make judgments on a case-by-case basis, while still being able to honestly say you offer it as a blanket policy to all your employees.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

DUBLIN – A multidisciplinary team (MDT) approach using videoconferencing to discuss the management of patients with difficult-to-treat psoriatic arthritis (PsA) can help rheumatologists to improve outcomes, according to presenters at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

In the same session at the meeting, GRAPPA also announced a new initiative to define difficult-to-treat PsA.

Deepak Jadon, MBBCh, PhD, a rheumatologist with Cambridge (England) University Hospitals NHS Foundation Trust, described his experience of running a clinic for patients with difficult-to-treat PsA in eastern England, covering a catchment area of approximately 6 million people between six and seven hospitals. He discussed how the MDT in his region operates to discuss the management of such patients, whose treatment options may also have indications for comorbidities such as inflammatory bowel disease or uveitis, or have complicating factors such as metabolic syndrome.

“You have to have an interested and engaged colleague to form that collaboration,” Dr. Jadon said. “If you are working in isolation, without your colleagues in the same building, that becomes harder. We have been running remote multispecialty meetings without the patient being present, and I have had the good fortune of having medical students brought into our practice. We discussed approximately 220 patients, initially in our psoriasis-spondyloarthritis MDT and subsequently in our inflammatory bowel disease–spondyloarthritis MDT.”

There are also MDTs with hepatologist colleagues carried out on an ad hoc basis to discuss patients with nonalcoholic fatty liver disease, as well as patients with hepatitis or a transplanted liver, who have psoriatic disease.

This difficult-to-treat cohort is discussed in MDT meetings conducted on Zoom. At MDT meetings, carried out with frequencies ranging from monthly to bimonthly, Dr. Jadon said there would be two dermatologists, two rheumatologists, one to four dermatology and rheumatology trainees and fellows, one to four specialist nurses, one to three research nurses, and one biologics pharmacist. They record the meetings and discuss anywhere from 4 to 18 patients, reviewing items in their electronic medical record, calling or writing patients and/or their primary care clinician as needed. They take about an hour to meet, with a half hour of prep time and another 1.5 hours to undertake necessary actions.

“Generally, the question is, how can we change treatment to best cover the domains of disease?” Dr. Jadon said. “Progressively, more patients are being put onto biologics as a result of these conversations, and I do feel that it has helped our patients and us to consolidate their management plan. Naturally, as all clinicians do, we doubt ourselves and wonder if we are missing something. Is there an aspect of the disease [being missed]? Is there a treatment that I haven’t been using? [The meetings have] been reassuring in that regard. I also learn from my colleagues who have earlier access to treatments, especially in dermatology.”

In a small number of patients, some combinations of advanced therapies, such as combining a Janus kinase inhibitor with a biologic, have been used as a result of these collaborations, “and to discuss this in an MDT has been reassuring, including from a medico-legal perspective,” Dr. Jadon said. “One of the main things we found to be useful is having a brief referral pro forma. Usually, by the time patients reach this forum, they have used a lot of treatments, and it can be difficult to remember that on the spot. It is also important to focus on what the actual question is. Naturally, in these discussions, where you talk about the complexities and various facets of disease, you can get a bit lost and sometimes you actually don’t address the original question.”

He also said it has been very beneficial to use screen sharing in the remote MDTs so that different disciplines can review images together, such as with radiology colleagues. “There are varying skill sets among our colleagues, especially in radiology, and it has been quite nice to review their peripheral imaging, their axial imaging, laboratory markers, and skin lesions together.”

New GRAPPA project to provide clarity

A new GRAPPA project has been devised to help physicians identify and define difficult-to-treat and difficult-to-manage PsA in order to help physicians to categorize and treat these patients.

“We have a growing treatment armamentarium ... but we still do not reach all the patients that we would like to,” said Fabian Proft, MD, of Charité University Medicine, Berlin. “We set our targets, but we see in the real world that we are only reaching them in 40% or 50% of our patients. So, we need to do better, and in order to do better, we need to understand better.”

“We should not only make a definition of difficult-to-treat PsA, which is nonresponse to treatment with objective signs of inflammation, but also we need to address and acknowledge difficult-to-manage [patients],” Dr. Proft said. “We should not stop as soon as we come up with a definition. This will be a working definition and will need to be validated.”

The speakers reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

DUBLIN – A multidisciplinary team (MDT) approach using videoconferencing to discuss the management of patients with difficult-to-treat psoriatic arthritis (PsA) can help rheumatologists to improve outcomes, according to presenters at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

In the same session at the meeting, GRAPPA also announced a new initiative to define difficult-to-treat PsA.

Deepak Jadon, MBBCh, PhD, a rheumatologist with Cambridge (England) University Hospitals NHS Foundation Trust, described his experience of running a clinic for patients with difficult-to-treat PsA in eastern England, covering a catchment area of approximately 6 million people between six and seven hospitals. He discussed how the MDT in his region operates to discuss the management of such patients, whose treatment options may also have indications for comorbidities such as inflammatory bowel disease or uveitis, or have complicating factors such as metabolic syndrome.

“You have to have an interested and engaged colleague to form that collaboration,” Dr. Jadon said. “If you are working in isolation, without your colleagues in the same building, that becomes harder. We have been running remote multispecialty meetings without the patient being present, and I have had the good fortune of having medical students brought into our practice. We discussed approximately 220 patients, initially in our psoriasis-spondyloarthritis MDT and subsequently in our inflammatory bowel disease–spondyloarthritis MDT.”

There are also MDTs with hepatologist colleagues carried out on an ad hoc basis to discuss patients with nonalcoholic fatty liver disease, as well as patients with hepatitis or a transplanted liver, who have psoriatic disease.

This difficult-to-treat cohort is discussed in MDT meetings conducted on Zoom. At MDT meetings, carried out with frequencies ranging from monthly to bimonthly, Dr. Jadon said there would be two dermatologists, two rheumatologists, one to four dermatology and rheumatology trainees and fellows, one to four specialist nurses, one to three research nurses, and one biologics pharmacist. They record the meetings and discuss anywhere from 4 to 18 patients, reviewing items in their electronic medical record, calling or writing patients and/or their primary care clinician as needed. They take about an hour to meet, with a half hour of prep time and another 1.5 hours to undertake necessary actions.

“Generally, the question is, how can we change treatment to best cover the domains of disease?” Dr. Jadon said. “Progressively, more patients are being put onto biologics as a result of these conversations, and I do feel that it has helped our patients and us to consolidate their management plan. Naturally, as all clinicians do, we doubt ourselves and wonder if we are missing something. Is there an aspect of the disease [being missed]? Is there a treatment that I haven’t been using? [The meetings have] been reassuring in that regard. I also learn from my colleagues who have earlier access to treatments, especially in dermatology.”

In a small number of patients, some combinations of advanced therapies, such as combining a Janus kinase inhibitor with a biologic, have been used as a result of these collaborations, “and to discuss this in an MDT has been reassuring, including from a medico-legal perspective,” Dr. Jadon said. “One of the main things we found to be useful is having a brief referral pro forma. Usually, by the time patients reach this forum, they have used a lot of treatments, and it can be difficult to remember that on the spot. It is also important to focus on what the actual question is. Naturally, in these discussions, where you talk about the complexities and various facets of disease, you can get a bit lost and sometimes you actually don’t address the original question.”

He also said it has been very beneficial to use screen sharing in the remote MDTs so that different disciplines can review images together, such as with radiology colleagues. “There are varying skill sets among our colleagues, especially in radiology, and it has been quite nice to review their peripheral imaging, their axial imaging, laboratory markers, and skin lesions together.”

New GRAPPA project to provide clarity

A new GRAPPA project has been devised to help physicians identify and define difficult-to-treat and difficult-to-manage PsA in order to help physicians to categorize and treat these patients.

“We have a growing treatment armamentarium ... but we still do not reach all the patients that we would like to,” said Fabian Proft, MD, of Charité University Medicine, Berlin. “We set our targets, but we see in the real world that we are only reaching them in 40% or 50% of our patients. So, we need to do better, and in order to do better, we need to understand better.”

“We should not only make a definition of difficult-to-treat PsA, which is nonresponse to treatment with objective signs of inflammation, but also we need to address and acknowledge difficult-to-manage [patients],” Dr. Proft said. “We should not stop as soon as we come up with a definition. This will be a working definition and will need to be validated.”

The speakers reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

DUBLIN – A multidisciplinary team (MDT) approach using videoconferencing to discuss the management of patients with difficult-to-treat psoriatic arthritis (PsA) can help rheumatologists to improve outcomes, according to presenters at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

In the same session at the meeting, GRAPPA also announced a new initiative to define difficult-to-treat PsA.

Deepak Jadon, MBBCh, PhD, a rheumatologist with Cambridge (England) University Hospitals NHS Foundation Trust, described his experience of running a clinic for patients with difficult-to-treat PsA in eastern England, covering a catchment area of approximately 6 million people between six and seven hospitals. He discussed how the MDT in his region operates to discuss the management of such patients, whose treatment options may also have indications for comorbidities such as inflammatory bowel disease or uveitis, or have complicating factors such as metabolic syndrome.

“You have to have an interested and engaged colleague to form that collaboration,” Dr. Jadon said. “If you are working in isolation, without your colleagues in the same building, that becomes harder. We have been running remote multispecialty meetings without the patient being present, and I have had the good fortune of having medical students brought into our practice. We discussed approximately 220 patients, initially in our psoriasis-spondyloarthritis MDT and subsequently in our inflammatory bowel disease–spondyloarthritis MDT.”

There are also MDTs with hepatologist colleagues carried out on an ad hoc basis to discuss patients with nonalcoholic fatty liver disease, as well as patients with hepatitis or a transplanted liver, who have psoriatic disease.

This difficult-to-treat cohort is discussed in MDT meetings conducted on Zoom. At MDT meetings, carried out with frequencies ranging from monthly to bimonthly, Dr. Jadon said there would be two dermatologists, two rheumatologists, one to four dermatology and rheumatology trainees and fellows, one to four specialist nurses, one to three research nurses, and one biologics pharmacist. They record the meetings and discuss anywhere from 4 to 18 patients, reviewing items in their electronic medical record, calling or writing patients and/or their primary care clinician as needed. They take about an hour to meet, with a half hour of prep time and another 1.5 hours to undertake necessary actions.

“Generally, the question is, how can we change treatment to best cover the domains of disease?” Dr. Jadon said. “Progressively, more patients are being put onto biologics as a result of these conversations, and I do feel that it has helped our patients and us to consolidate their management plan. Naturally, as all clinicians do, we doubt ourselves and wonder if we are missing something. Is there an aspect of the disease [being missed]? Is there a treatment that I haven’t been using? [The meetings have] been reassuring in that regard. I also learn from my colleagues who have earlier access to treatments, especially in dermatology.”

In a small number of patients, some combinations of advanced therapies, such as combining a Janus kinase inhibitor with a biologic, have been used as a result of these collaborations, “and to discuss this in an MDT has been reassuring, including from a medico-legal perspective,” Dr. Jadon said. “One of the main things we found to be useful is having a brief referral pro forma. Usually, by the time patients reach this forum, they have used a lot of treatments, and it can be difficult to remember that on the spot. It is also important to focus on what the actual question is. Naturally, in these discussions, where you talk about the complexities and various facets of disease, you can get a bit lost and sometimes you actually don’t address the original question.”

He also said it has been very beneficial to use screen sharing in the remote MDTs so that different disciplines can review images together, such as with radiology colleagues. “There are varying skill sets among our colleagues, especially in radiology, and it has been quite nice to review their peripheral imaging, their axial imaging, laboratory markers, and skin lesions together.”

New GRAPPA project to provide clarity

A new GRAPPA project has been devised to help physicians identify and define difficult-to-treat and difficult-to-manage PsA in order to help physicians to categorize and treat these patients.

“We have a growing treatment armamentarium ... but we still do not reach all the patients that we would like to,” said Fabian Proft, MD, of Charité University Medicine, Berlin. “We set our targets, but we see in the real world that we are only reaching them in 40% or 50% of our patients. So, we need to do better, and in order to do better, we need to understand better.”

“We should not only make a definition of difficult-to-treat PsA, which is nonresponse to treatment with objective signs of inflammation, but also we need to address and acknowledge difficult-to-manage [patients],” Dr. Proft said. “We should not stop as soon as we come up with a definition. This will be a working definition and will need to be validated.”

The speakers reported no relevant financial relationships.

A version of this article appeared on Medscape.com.