The Role of Inpatient Dermatology Consultations

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The Role of Inpatient Dermatology Consultations
In Partnership With the Society of Dermatology Hospitalists

Dermatology is an often-underutilized resource in the hospital setting. As the health care landscape has evolved, so has the role of the inpatient dermatologist.1-3 Structural changes in the health system and advances in therapies have shifted dermatology from an admitting service to an almost exclusively outpatient practice. Improved treatment modalities led to decreases in the number of patients requiring admission for chronic dermatoses, and outpatient clinics began offering therapies once limited to hospitals.1,4 Inpatient dermatology consultations emerged and continue to have profound effects on hospitalized patients regardless of their reason for admission.1-11

Inpatient dermatologists supply knowledge in areas primary medical teams lack, and there is evidence that dermatology consultations improve the quality of care while decreasing cost.2,5-7 Establishing correct diagnoses, preventing exposure to unnecessary medications, and reducing hospitalization duration and readmission rates are a few ways dermatology consultations positively impact hospitalized patients.2,5-7,9,10 This study highlights the role of the dermatologist in the care of hospitalized patients at a large academic medical center in an urban setting and reveals how consultation supports the efficiency and efficacy of other services.

Materials and Methods

Study Design—This single-institution, cross-sectional retrospective study included all hospitalized patients at the Thomas Jefferson University Hospital (Philadelphia, Pennsylvania), who received an inpatient dermatology consultation completed by physicians of Jefferson Dermatology Associates between January 1, 2019, and December 31, 2019. The institutional review board at Thomas Jefferson University approved this study.

Data Collection—A list of all inpatient dermatology consultations in 2019 was provided by Jefferson Dermatology Associates. Through a retrospective chart review, data regarding the consultations were collected from the electronic medical record (Epic Systems) and recorded into the Research Electronic Data Capture system. Data on patient demographics, the primary medical team, the dermatology evaluation, and the hospital course of the patient were collected.

Results

Patient Characteristics—Dermatology received 253 inpatient consultation requests during this time period; 53% of patients were female and 47% were male, with a mean age of 55 years. Most patients were White (57%), while 34% were Black. Five percent and 4% of patients were Asian and Hispanic or Latino, respectively (Table 1). The mean duration of hospitalization for all patients was 15 days, and the average number of days to discharge following the first encounter with dermatology was 10 days.

Requesting Team and Reason for Consultation—Internal medicine consulted dermatology most frequently (34% of all consultations), followed by emergency medicine (14%) and a variety of other services (Table 1). Most dermatology consultations were placed to assist in achieving a diagnosis of a cutaneous condition (77%), while a minority were to assist in the management of a previously diagnosed disease (22%). A small fraction of consultations (5%) were to complete full-body skin examinations (FBSEs) to rule out infection or malignancy in candidates for organ transplantation, left ventricular assist devices, or certain chemotherapies. One FBSE was conducted to search for a primary tumor in a patient diagnosed with metastatic melanoma.

Most Common Final Diagnoses and Consultation Impact—Table 2 lists the most common final diagnosis categories, as well as the effects of the consultation on diagnosis, management, biopsies, hospitalization, and clinical improvement as documented by the primary medical provider. The most common final diagnoses were inflammatory and autoimmune (39%), such as contact dermatitis and seborrheic dermatitis; infectious (23%), such as varicella (primary or zoster) and bacterial furunculosis; drug reactions (20%), such as morbilliform drug eruptions; vascular (8%), such as vasculitis and calciphylaxis; neoplastic (7%), such as keratinocyte carcinomas and leukemia cutis; and other (15%), such as xerosis, keratosis pilaris, and miliaria rubra.

 

 

Impact on Diagnosis—Fifty-six percent of all consultations resulted in a change in diagnosis. When dermatology was consulted specifically to assist in the diagnosis of a patient (195 consultations), the working diagnosis of the primary team was changed 69% of the time. Thirty-five of these consultation requests had no preliminary diagnosis, and the primary team listed the working diagnosis as either rash or a morphologic description of the lesion(s). Sixty-three percent of suspected drug eruptions ended with a diagnosis of a form of drug eruption, while 20% of consultations for suspected cellulitis or bacterial infections were confirmed to be cellulitis or soft tissue infections.

Impact on Management—Regardless of the reason for the consultation, most consultations (86%) resulted in a change in management. The remaining 14% consisted of FBSEs with benign findings; cases of cutaneous metastases and leukemia cutis managed by oncology; as well as select cases of purpura fulminans, postfebrile desquamation, and postinflammatory hyperpigmentation.

Changes in management included alterations in medications, requests for additional laboratory work or imaging, additional consultation requests, biopsies, or specific wound care instructions. Seventy-five percent of all consultations were given specific medication recommendations by dermatology. Most (61%) were recommended to be given a topical steroid, antibiotic, or both. However, 45% of all consultations were recommended to initiate a systemic medication, most commonly antihistamines, antibiotics, steroids, antivirals, or immunomodulators. Dermatology recommended discontinuing specific medications in 16% of all consultations, with antibiotics being the most frequent culprit (17 antibiotics discontinued), owing to drug eruptions or misdiagnosed infections. Vancomycin, piperacillin-tazobactam, and trimethoprim-sulfamethoxazole were the most frequently discontinued antibiotics.

Dermatology was consulted for assistance in management of previously diagnosed cutaneous conditions 56 times (22% of all consultations), often regarding complicated cases of hidradenitis suppurativa (9 cases), pyoderma gangrenosum (5 cases), bullous pemphigoid (4 cases), or erythroderma (4 cases). Most of these cases required a single dermatology encounter to provide recommendations (71%), and 21% required 1 additional follow-up. Sixty-three percent of patients consulted for management assistance were noted to have improvement in their cutaneous condition by time of discharge, as documented by the primary provider in the medical record.

Twenty-eight percent of all consultations required at least 1 biopsy. Seventy-two percent of all biopsies were consistent with the dermatologist’s working diagnosis or highest-ranked differential diagnosis, and 16% of biopsy results were consistent with the second- or third-ranked diagnosis. The primary teams requested a biopsy 38 times to assist in diagnosis, as documented in the progress note or consultation request. Only 21 of these consultations (55% of requests) received at least 1 biopsy, as the remaining consultations did not require a biopsy to establish a diagnosis. The most common final diagnoses of consultations receiving biopsies included drug eruptions (5), leukemia cutis (4), vasculopathies (4), vasculitis (4), and calciphylaxis (3).

 

 

Impact on Hospitalization and Efficacy—Dermatology performed 217 consultations regarding patients already admitted to the hospital, and 92% remained hospitalized either due to comorbidities or complicated cutaneous conditions following the consultation. The remaining 8% were cleared for discharge. Dermatology received 36 consultation requests from emergency medicine physicians. Fifty-three percent of these patients were admitted, while the remaining 47% were discharged from the emergency department or its observation unit following evaluation.

Fifty-one percent of all consultations were noted to have improvement in their cutaneous condition by the time of discharge, as noted in the physical examination, progress note, or discharge summary of the primary team. Thirty percent of cases remained stable, where improvement was not noted in in the medical record. Most of these cases involved keratinocyte carcinomas scheduled for outpatient excision, benign melanocytic nevi found on FBSE, and benign etiologies that led to immediate discharge following consultation. Three percent of all consultations were noted to have worsened following consultation, including cases of calciphylaxis, vasculopathies, and purpura fulminans, as well as patients who elected for palliative care and hospice. The cutaneous condition by the time of discharge could not be determined from the medical record in 16% of all consultations.

Eighty-five percent of all consultations required a single encounter with dermatology. An additional 10% required a single follow-up with dermatology, while only 5% of patients required 3 or more encounters. Notably, these cases included patients with 1 or more severe cutaneous diseases, such as Sweet syndrome, calciphylaxis, Stevens-Johnson syndrome/toxic epidermal necrolysis, and hidradenitis suppurativa.

 

Comment

Although dermatology often is viewed as an outpatient specialty, this study provides a glimpse into the ways inpatient dermatology consultations optimize the care of hospitalized patients. Most consultations involved assistance in diagnosing an unknown condition, but several regarded pre-existing skin disorders requiring management aid. As a variety of medical specialties requested consultations, dermatology was able to provide care to a diverse group of patients with conditions varying in complexity and severity. Several specialties benefited from niche dermatologic expertise: hematology and oncology frequently requested dermatology to assist in diagnosis and management of the toxic effects of chemotherapy, cutaneous metastasis, or suspected cutaneous infections in immunocompromised patients. Cardiology patients were frequently evaluated for potential malignancy or infection prior to heart transplantation and initiation of antirejection immunosuppressants. Dermatology was consulted to differentiate cutaneous manifestations of critical illness from underlying systemic disease in the intensive care unit, and patients presenting to the emergency department often were examined to determine if hospital admission was necessary, with 47% of these consultations resulting in a discharge following evaluation by a dermatologist.

Our results were consistent with prior studies1,5,6 that have reported frequent changes in final diagnosis following dermatology consultation, with 69% of working diagnoses changed in this study when consultation was requested for diagnostic assistance. When dermatology was consulted for diagnostic assistance, several of these cases lacked a preliminary differential diagnosis. Although the absence of a documented differential diagnosis may not necessarily reflect a lack of suspicion for a particular etiology, 86% of all consultations included a ranked differential or working diagnosis either in the consultation request or progress note prior to consultation. The final diagnoses of consultations without a preliminary diagnosis varied from the mild and localized to systemic and severe, further suggesting these cases reflected knowledge gaps of the primary medical team.

 

 

Integration of dermatology into the care of hospitalized patients could provide an opportunity for education of primary medical teams. With frequent consultation, primary medical teams may become more comfortable diagnosing and managing common cutaneous conditions specific to their specialty or extended hospitalizations.

Several consultations were requested to aid in management of cases of hidradenitis suppurativa, pyoderma gangrenosum, or bullous pemphigoid that either failed outpatient therapy or were complicated by superinfections. Despite the ranges in complexity, the majority of all consultations required a single encounter and led to improvement by the time of discharge, demonstrating the efficacy and efficiency of inpatient dermatologists.

Dermatology consultations often led to changes in management involving medications and additional workup. Changes in management also extended to specific wound care instructions provided by dermatology, as expected for cases of Stevens-Johnson syndrome/toxic epidermal necrolysis, Sweet syndrome, hidradenitis suppurativa, and pyoderma gangrenosum. However, patients with the sequelae of extended hospitalizations, such as chronic wounds, pressure ulcers, and edema bullae, also benefited from this expertise.

When patients required a biopsy, the final diagnoses were consistent with the dermatologist’s number one differential diagnosis or top 3 differential diagnoses 72% and 88% of the time, respectively. Only 55% of cases where the primary team requested a biopsy ultimately required a biopsy, as many involved clinical diagnoses such as urticaria. Not only was dermatology accurate in their preliminary diagnoses, but they decreased cost and morbidity by avoiding unnecessary procedures.

This study provided additional evidence to support the integration of dermatology into the hospital setting for the benefit of patients, primary medical teams, and hospital systems. Dermatology offers high-value care through the efficient diagnosis and management of hospitalized patients, which contributes to decreased cost and improved outcomes.2,5-7,9,10 This study highlighted lesser-known areas of impact, such as the various specialty-specific services dermatology provides as well as the high rates of reported improvement following consultation. Future studies should continue to explore the field’s unique impact on hospitalized medicine as well as other avenues of care delivery, such as telemedicine, that may encourage dermatologists to participate in consultations and increase the volume of patients who may benefit from their care.

References
  1. Madigan LM, Fox LP. Where are we now with inpatient consultative dermatology?: assessing the value and evolution of this subspecialty over the past decade. J Am Acad Dermatol. 2019;80:1804-1808. doi:10.1016/j.jaad.2019.01.031
  2. Noe MH, Rosenbach M. Inpatient dermatologists—crucial for the management of skin diseases in hospitalized patients [editorial]. JAMA Dermatol. 2018;154:524-525. doi:10.1001/jamadermatol.2017.6195
  3. Strowd LC. Inpatient dermatology: a paradigm shift in the management of skin disease in the hospital. Br J Dermatol. 2019;180:966-967. doi:10.1111/bjd.17778
  4. Kirsner RS, Yang DG, Kerdel FA. The changing status of inpatient dermatology at American academic dermatology programs. J Am Acad Dermatol. 1999;40:755-757. doi:10.1016/s0190-9622(99)70158-1
  5. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480. doi:10.1001/jamadermatol.2015.5098
  6. Ko LN, Garza-Mayers AC, St John J, et al. Effect of dermatology consultation on outcomes for patients with presumed cellulitis. JAMA Dermatol. 2018;154:529-533. doi:10.1001/jamadermatol.2017.6196
  7. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543. doi:10.1001/jamadermatol.2017.6197
  8. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528. doi:10.1001/jamadermatol.2016.6130
  9. Imadojemu S, Rosenbach M. Dermatologists must take an active role in the diagnosis of cellulitis. JAMA Dermatol. 2017;153:134-135. doi:10.1001/jamadermatol.2016.4230
  10. Hughey LC. The impact dermatologists can have on misdiagnosis of cellulitis and overuse of antibiotics: closing the gap. JAMA Dermatol. 2014;150:1061-1062. doi:10.1001/jamadermatol.2014.1164
  11. Ko LN, Kroshinsky D. Dermatology hospitalists: a multicenter survey study characterizing the infrastructure of consultative dermatology in select American hospitals. Int J Dermatol. 2018;57:553-558. doi:10.1111/ijd.13939
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From the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Sidney Kimmel Medical College, Philadelphia, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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From the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Sidney Kimmel Medical College, Philadelphia, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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From the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Sidney Kimmel Medical College, Philadelphia, Pennsylvania.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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In Partnership With the Society of Dermatology Hospitalists
In Partnership With the Society of Dermatology Hospitalists

Dermatology is an often-underutilized resource in the hospital setting. As the health care landscape has evolved, so has the role of the inpatient dermatologist.1-3 Structural changes in the health system and advances in therapies have shifted dermatology from an admitting service to an almost exclusively outpatient practice. Improved treatment modalities led to decreases in the number of patients requiring admission for chronic dermatoses, and outpatient clinics began offering therapies once limited to hospitals.1,4 Inpatient dermatology consultations emerged and continue to have profound effects on hospitalized patients regardless of their reason for admission.1-11

Inpatient dermatologists supply knowledge in areas primary medical teams lack, and there is evidence that dermatology consultations improve the quality of care while decreasing cost.2,5-7 Establishing correct diagnoses, preventing exposure to unnecessary medications, and reducing hospitalization duration and readmission rates are a few ways dermatology consultations positively impact hospitalized patients.2,5-7,9,10 This study highlights the role of the dermatologist in the care of hospitalized patients at a large academic medical center in an urban setting and reveals how consultation supports the efficiency and efficacy of other services.

Materials and Methods

Study Design—This single-institution, cross-sectional retrospective study included all hospitalized patients at the Thomas Jefferson University Hospital (Philadelphia, Pennsylvania), who received an inpatient dermatology consultation completed by physicians of Jefferson Dermatology Associates between January 1, 2019, and December 31, 2019. The institutional review board at Thomas Jefferson University approved this study.

Data Collection—A list of all inpatient dermatology consultations in 2019 was provided by Jefferson Dermatology Associates. Through a retrospective chart review, data regarding the consultations were collected from the electronic medical record (Epic Systems) and recorded into the Research Electronic Data Capture system. Data on patient demographics, the primary medical team, the dermatology evaluation, and the hospital course of the patient were collected.

Results

Patient Characteristics—Dermatology received 253 inpatient consultation requests during this time period; 53% of patients were female and 47% were male, with a mean age of 55 years. Most patients were White (57%), while 34% were Black. Five percent and 4% of patients were Asian and Hispanic or Latino, respectively (Table 1). The mean duration of hospitalization for all patients was 15 days, and the average number of days to discharge following the first encounter with dermatology was 10 days.

Requesting Team and Reason for Consultation—Internal medicine consulted dermatology most frequently (34% of all consultations), followed by emergency medicine (14%) and a variety of other services (Table 1). Most dermatology consultations were placed to assist in achieving a diagnosis of a cutaneous condition (77%), while a minority were to assist in the management of a previously diagnosed disease (22%). A small fraction of consultations (5%) were to complete full-body skin examinations (FBSEs) to rule out infection or malignancy in candidates for organ transplantation, left ventricular assist devices, or certain chemotherapies. One FBSE was conducted to search for a primary tumor in a patient diagnosed with metastatic melanoma.

Most Common Final Diagnoses and Consultation Impact—Table 2 lists the most common final diagnosis categories, as well as the effects of the consultation on diagnosis, management, biopsies, hospitalization, and clinical improvement as documented by the primary medical provider. The most common final diagnoses were inflammatory and autoimmune (39%), such as contact dermatitis and seborrheic dermatitis; infectious (23%), such as varicella (primary or zoster) and bacterial furunculosis; drug reactions (20%), such as morbilliform drug eruptions; vascular (8%), such as vasculitis and calciphylaxis; neoplastic (7%), such as keratinocyte carcinomas and leukemia cutis; and other (15%), such as xerosis, keratosis pilaris, and miliaria rubra.

 

 

Impact on Diagnosis—Fifty-six percent of all consultations resulted in a change in diagnosis. When dermatology was consulted specifically to assist in the diagnosis of a patient (195 consultations), the working diagnosis of the primary team was changed 69% of the time. Thirty-five of these consultation requests had no preliminary diagnosis, and the primary team listed the working diagnosis as either rash or a morphologic description of the lesion(s). Sixty-three percent of suspected drug eruptions ended with a diagnosis of a form of drug eruption, while 20% of consultations for suspected cellulitis or bacterial infections were confirmed to be cellulitis or soft tissue infections.

Impact on Management—Regardless of the reason for the consultation, most consultations (86%) resulted in a change in management. The remaining 14% consisted of FBSEs with benign findings; cases of cutaneous metastases and leukemia cutis managed by oncology; as well as select cases of purpura fulminans, postfebrile desquamation, and postinflammatory hyperpigmentation.

Changes in management included alterations in medications, requests for additional laboratory work or imaging, additional consultation requests, biopsies, or specific wound care instructions. Seventy-five percent of all consultations were given specific medication recommendations by dermatology. Most (61%) were recommended to be given a topical steroid, antibiotic, or both. However, 45% of all consultations were recommended to initiate a systemic medication, most commonly antihistamines, antibiotics, steroids, antivirals, or immunomodulators. Dermatology recommended discontinuing specific medications in 16% of all consultations, with antibiotics being the most frequent culprit (17 antibiotics discontinued), owing to drug eruptions or misdiagnosed infections. Vancomycin, piperacillin-tazobactam, and trimethoprim-sulfamethoxazole were the most frequently discontinued antibiotics.

Dermatology was consulted for assistance in management of previously diagnosed cutaneous conditions 56 times (22% of all consultations), often regarding complicated cases of hidradenitis suppurativa (9 cases), pyoderma gangrenosum (5 cases), bullous pemphigoid (4 cases), or erythroderma (4 cases). Most of these cases required a single dermatology encounter to provide recommendations (71%), and 21% required 1 additional follow-up. Sixty-three percent of patients consulted for management assistance were noted to have improvement in their cutaneous condition by time of discharge, as documented by the primary provider in the medical record.

Twenty-eight percent of all consultations required at least 1 biopsy. Seventy-two percent of all biopsies were consistent with the dermatologist’s working diagnosis or highest-ranked differential diagnosis, and 16% of biopsy results were consistent with the second- or third-ranked diagnosis. The primary teams requested a biopsy 38 times to assist in diagnosis, as documented in the progress note or consultation request. Only 21 of these consultations (55% of requests) received at least 1 biopsy, as the remaining consultations did not require a biopsy to establish a diagnosis. The most common final diagnoses of consultations receiving biopsies included drug eruptions (5), leukemia cutis (4), vasculopathies (4), vasculitis (4), and calciphylaxis (3).

 

 

Impact on Hospitalization and Efficacy—Dermatology performed 217 consultations regarding patients already admitted to the hospital, and 92% remained hospitalized either due to comorbidities or complicated cutaneous conditions following the consultation. The remaining 8% were cleared for discharge. Dermatology received 36 consultation requests from emergency medicine physicians. Fifty-three percent of these patients were admitted, while the remaining 47% were discharged from the emergency department or its observation unit following evaluation.

Fifty-one percent of all consultations were noted to have improvement in their cutaneous condition by the time of discharge, as noted in the physical examination, progress note, or discharge summary of the primary team. Thirty percent of cases remained stable, where improvement was not noted in in the medical record. Most of these cases involved keratinocyte carcinomas scheduled for outpatient excision, benign melanocytic nevi found on FBSE, and benign etiologies that led to immediate discharge following consultation. Three percent of all consultations were noted to have worsened following consultation, including cases of calciphylaxis, vasculopathies, and purpura fulminans, as well as patients who elected for palliative care and hospice. The cutaneous condition by the time of discharge could not be determined from the medical record in 16% of all consultations.

Eighty-five percent of all consultations required a single encounter with dermatology. An additional 10% required a single follow-up with dermatology, while only 5% of patients required 3 or more encounters. Notably, these cases included patients with 1 or more severe cutaneous diseases, such as Sweet syndrome, calciphylaxis, Stevens-Johnson syndrome/toxic epidermal necrolysis, and hidradenitis suppurativa.

 

Comment

Although dermatology often is viewed as an outpatient specialty, this study provides a glimpse into the ways inpatient dermatology consultations optimize the care of hospitalized patients. Most consultations involved assistance in diagnosing an unknown condition, but several regarded pre-existing skin disorders requiring management aid. As a variety of medical specialties requested consultations, dermatology was able to provide care to a diverse group of patients with conditions varying in complexity and severity. Several specialties benefited from niche dermatologic expertise: hematology and oncology frequently requested dermatology to assist in diagnosis and management of the toxic effects of chemotherapy, cutaneous metastasis, or suspected cutaneous infections in immunocompromised patients. Cardiology patients were frequently evaluated for potential malignancy or infection prior to heart transplantation and initiation of antirejection immunosuppressants. Dermatology was consulted to differentiate cutaneous manifestations of critical illness from underlying systemic disease in the intensive care unit, and patients presenting to the emergency department often were examined to determine if hospital admission was necessary, with 47% of these consultations resulting in a discharge following evaluation by a dermatologist.

Our results were consistent with prior studies1,5,6 that have reported frequent changes in final diagnosis following dermatology consultation, with 69% of working diagnoses changed in this study when consultation was requested for diagnostic assistance. When dermatology was consulted for diagnostic assistance, several of these cases lacked a preliminary differential diagnosis. Although the absence of a documented differential diagnosis may not necessarily reflect a lack of suspicion for a particular etiology, 86% of all consultations included a ranked differential or working diagnosis either in the consultation request or progress note prior to consultation. The final diagnoses of consultations without a preliminary diagnosis varied from the mild and localized to systemic and severe, further suggesting these cases reflected knowledge gaps of the primary medical team.

 

 

Integration of dermatology into the care of hospitalized patients could provide an opportunity for education of primary medical teams. With frequent consultation, primary medical teams may become more comfortable diagnosing and managing common cutaneous conditions specific to their specialty or extended hospitalizations.

Several consultations were requested to aid in management of cases of hidradenitis suppurativa, pyoderma gangrenosum, or bullous pemphigoid that either failed outpatient therapy or were complicated by superinfections. Despite the ranges in complexity, the majority of all consultations required a single encounter and led to improvement by the time of discharge, demonstrating the efficacy and efficiency of inpatient dermatologists.

Dermatology consultations often led to changes in management involving medications and additional workup. Changes in management also extended to specific wound care instructions provided by dermatology, as expected for cases of Stevens-Johnson syndrome/toxic epidermal necrolysis, Sweet syndrome, hidradenitis suppurativa, and pyoderma gangrenosum. However, patients with the sequelae of extended hospitalizations, such as chronic wounds, pressure ulcers, and edema bullae, also benefited from this expertise.

When patients required a biopsy, the final diagnoses were consistent with the dermatologist’s number one differential diagnosis or top 3 differential diagnoses 72% and 88% of the time, respectively. Only 55% of cases where the primary team requested a biopsy ultimately required a biopsy, as many involved clinical diagnoses such as urticaria. Not only was dermatology accurate in their preliminary diagnoses, but they decreased cost and morbidity by avoiding unnecessary procedures.

This study provided additional evidence to support the integration of dermatology into the hospital setting for the benefit of patients, primary medical teams, and hospital systems. Dermatology offers high-value care through the efficient diagnosis and management of hospitalized patients, which contributes to decreased cost and improved outcomes.2,5-7,9,10 This study highlighted lesser-known areas of impact, such as the various specialty-specific services dermatology provides as well as the high rates of reported improvement following consultation. Future studies should continue to explore the field’s unique impact on hospitalized medicine as well as other avenues of care delivery, such as telemedicine, that may encourage dermatologists to participate in consultations and increase the volume of patients who may benefit from their care.

Dermatology is an often-underutilized resource in the hospital setting. As the health care landscape has evolved, so has the role of the inpatient dermatologist.1-3 Structural changes in the health system and advances in therapies have shifted dermatology from an admitting service to an almost exclusively outpatient practice. Improved treatment modalities led to decreases in the number of patients requiring admission for chronic dermatoses, and outpatient clinics began offering therapies once limited to hospitals.1,4 Inpatient dermatology consultations emerged and continue to have profound effects on hospitalized patients regardless of their reason for admission.1-11

Inpatient dermatologists supply knowledge in areas primary medical teams lack, and there is evidence that dermatology consultations improve the quality of care while decreasing cost.2,5-7 Establishing correct diagnoses, preventing exposure to unnecessary medications, and reducing hospitalization duration and readmission rates are a few ways dermatology consultations positively impact hospitalized patients.2,5-7,9,10 This study highlights the role of the dermatologist in the care of hospitalized patients at a large academic medical center in an urban setting and reveals how consultation supports the efficiency and efficacy of other services.

Materials and Methods

Study Design—This single-institution, cross-sectional retrospective study included all hospitalized patients at the Thomas Jefferson University Hospital (Philadelphia, Pennsylvania), who received an inpatient dermatology consultation completed by physicians of Jefferson Dermatology Associates between January 1, 2019, and December 31, 2019. The institutional review board at Thomas Jefferson University approved this study.

Data Collection—A list of all inpatient dermatology consultations in 2019 was provided by Jefferson Dermatology Associates. Through a retrospective chart review, data regarding the consultations were collected from the electronic medical record (Epic Systems) and recorded into the Research Electronic Data Capture system. Data on patient demographics, the primary medical team, the dermatology evaluation, and the hospital course of the patient were collected.

Results

Patient Characteristics—Dermatology received 253 inpatient consultation requests during this time period; 53% of patients were female and 47% were male, with a mean age of 55 years. Most patients were White (57%), while 34% were Black. Five percent and 4% of patients were Asian and Hispanic or Latino, respectively (Table 1). The mean duration of hospitalization for all patients was 15 days, and the average number of days to discharge following the first encounter with dermatology was 10 days.

Requesting Team and Reason for Consultation—Internal medicine consulted dermatology most frequently (34% of all consultations), followed by emergency medicine (14%) and a variety of other services (Table 1). Most dermatology consultations were placed to assist in achieving a diagnosis of a cutaneous condition (77%), while a minority were to assist in the management of a previously diagnosed disease (22%). A small fraction of consultations (5%) were to complete full-body skin examinations (FBSEs) to rule out infection or malignancy in candidates for organ transplantation, left ventricular assist devices, or certain chemotherapies. One FBSE was conducted to search for a primary tumor in a patient diagnosed with metastatic melanoma.

Most Common Final Diagnoses and Consultation Impact—Table 2 lists the most common final diagnosis categories, as well as the effects of the consultation on diagnosis, management, biopsies, hospitalization, and clinical improvement as documented by the primary medical provider. The most common final diagnoses were inflammatory and autoimmune (39%), such as contact dermatitis and seborrheic dermatitis; infectious (23%), such as varicella (primary or zoster) and bacterial furunculosis; drug reactions (20%), such as morbilliform drug eruptions; vascular (8%), such as vasculitis and calciphylaxis; neoplastic (7%), such as keratinocyte carcinomas and leukemia cutis; and other (15%), such as xerosis, keratosis pilaris, and miliaria rubra.

 

 

Impact on Diagnosis—Fifty-six percent of all consultations resulted in a change in diagnosis. When dermatology was consulted specifically to assist in the diagnosis of a patient (195 consultations), the working diagnosis of the primary team was changed 69% of the time. Thirty-five of these consultation requests had no preliminary diagnosis, and the primary team listed the working diagnosis as either rash or a morphologic description of the lesion(s). Sixty-three percent of suspected drug eruptions ended with a diagnosis of a form of drug eruption, while 20% of consultations for suspected cellulitis or bacterial infections were confirmed to be cellulitis or soft tissue infections.

Impact on Management—Regardless of the reason for the consultation, most consultations (86%) resulted in a change in management. The remaining 14% consisted of FBSEs with benign findings; cases of cutaneous metastases and leukemia cutis managed by oncology; as well as select cases of purpura fulminans, postfebrile desquamation, and postinflammatory hyperpigmentation.

Changes in management included alterations in medications, requests for additional laboratory work or imaging, additional consultation requests, biopsies, or specific wound care instructions. Seventy-five percent of all consultations were given specific medication recommendations by dermatology. Most (61%) were recommended to be given a topical steroid, antibiotic, or both. However, 45% of all consultations were recommended to initiate a systemic medication, most commonly antihistamines, antibiotics, steroids, antivirals, or immunomodulators. Dermatology recommended discontinuing specific medications in 16% of all consultations, with antibiotics being the most frequent culprit (17 antibiotics discontinued), owing to drug eruptions or misdiagnosed infections. Vancomycin, piperacillin-tazobactam, and trimethoprim-sulfamethoxazole were the most frequently discontinued antibiotics.

Dermatology was consulted for assistance in management of previously diagnosed cutaneous conditions 56 times (22% of all consultations), often regarding complicated cases of hidradenitis suppurativa (9 cases), pyoderma gangrenosum (5 cases), bullous pemphigoid (4 cases), or erythroderma (4 cases). Most of these cases required a single dermatology encounter to provide recommendations (71%), and 21% required 1 additional follow-up. Sixty-three percent of patients consulted for management assistance were noted to have improvement in their cutaneous condition by time of discharge, as documented by the primary provider in the medical record.

Twenty-eight percent of all consultations required at least 1 biopsy. Seventy-two percent of all biopsies were consistent with the dermatologist’s working diagnosis or highest-ranked differential diagnosis, and 16% of biopsy results were consistent with the second- or third-ranked diagnosis. The primary teams requested a biopsy 38 times to assist in diagnosis, as documented in the progress note or consultation request. Only 21 of these consultations (55% of requests) received at least 1 biopsy, as the remaining consultations did not require a biopsy to establish a diagnosis. The most common final diagnoses of consultations receiving biopsies included drug eruptions (5), leukemia cutis (4), vasculopathies (4), vasculitis (4), and calciphylaxis (3).

 

 

Impact on Hospitalization and Efficacy—Dermatology performed 217 consultations regarding patients already admitted to the hospital, and 92% remained hospitalized either due to comorbidities or complicated cutaneous conditions following the consultation. The remaining 8% were cleared for discharge. Dermatology received 36 consultation requests from emergency medicine physicians. Fifty-three percent of these patients were admitted, while the remaining 47% were discharged from the emergency department or its observation unit following evaluation.

Fifty-one percent of all consultations were noted to have improvement in their cutaneous condition by the time of discharge, as noted in the physical examination, progress note, or discharge summary of the primary team. Thirty percent of cases remained stable, where improvement was not noted in in the medical record. Most of these cases involved keratinocyte carcinomas scheduled for outpatient excision, benign melanocytic nevi found on FBSE, and benign etiologies that led to immediate discharge following consultation. Three percent of all consultations were noted to have worsened following consultation, including cases of calciphylaxis, vasculopathies, and purpura fulminans, as well as patients who elected for palliative care and hospice. The cutaneous condition by the time of discharge could not be determined from the medical record in 16% of all consultations.

Eighty-five percent of all consultations required a single encounter with dermatology. An additional 10% required a single follow-up with dermatology, while only 5% of patients required 3 or more encounters. Notably, these cases included patients with 1 or more severe cutaneous diseases, such as Sweet syndrome, calciphylaxis, Stevens-Johnson syndrome/toxic epidermal necrolysis, and hidradenitis suppurativa.

 

Comment

Although dermatology often is viewed as an outpatient specialty, this study provides a glimpse into the ways inpatient dermatology consultations optimize the care of hospitalized patients. Most consultations involved assistance in diagnosing an unknown condition, but several regarded pre-existing skin disorders requiring management aid. As a variety of medical specialties requested consultations, dermatology was able to provide care to a diverse group of patients with conditions varying in complexity and severity. Several specialties benefited from niche dermatologic expertise: hematology and oncology frequently requested dermatology to assist in diagnosis and management of the toxic effects of chemotherapy, cutaneous metastasis, or suspected cutaneous infections in immunocompromised patients. Cardiology patients were frequently evaluated for potential malignancy or infection prior to heart transplantation and initiation of antirejection immunosuppressants. Dermatology was consulted to differentiate cutaneous manifestations of critical illness from underlying systemic disease in the intensive care unit, and patients presenting to the emergency department often were examined to determine if hospital admission was necessary, with 47% of these consultations resulting in a discharge following evaluation by a dermatologist.

Our results were consistent with prior studies1,5,6 that have reported frequent changes in final diagnosis following dermatology consultation, with 69% of working diagnoses changed in this study when consultation was requested for diagnostic assistance. When dermatology was consulted for diagnostic assistance, several of these cases lacked a preliminary differential diagnosis. Although the absence of a documented differential diagnosis may not necessarily reflect a lack of suspicion for a particular etiology, 86% of all consultations included a ranked differential or working diagnosis either in the consultation request or progress note prior to consultation. The final diagnoses of consultations without a preliminary diagnosis varied from the mild and localized to systemic and severe, further suggesting these cases reflected knowledge gaps of the primary medical team.

 

 

Integration of dermatology into the care of hospitalized patients could provide an opportunity for education of primary medical teams. With frequent consultation, primary medical teams may become more comfortable diagnosing and managing common cutaneous conditions specific to their specialty or extended hospitalizations.

Several consultations were requested to aid in management of cases of hidradenitis suppurativa, pyoderma gangrenosum, or bullous pemphigoid that either failed outpatient therapy or were complicated by superinfections. Despite the ranges in complexity, the majority of all consultations required a single encounter and led to improvement by the time of discharge, demonstrating the efficacy and efficiency of inpatient dermatologists.

Dermatology consultations often led to changes in management involving medications and additional workup. Changes in management also extended to specific wound care instructions provided by dermatology, as expected for cases of Stevens-Johnson syndrome/toxic epidermal necrolysis, Sweet syndrome, hidradenitis suppurativa, and pyoderma gangrenosum. However, patients with the sequelae of extended hospitalizations, such as chronic wounds, pressure ulcers, and edema bullae, also benefited from this expertise.

When patients required a biopsy, the final diagnoses were consistent with the dermatologist’s number one differential diagnosis or top 3 differential diagnoses 72% and 88% of the time, respectively. Only 55% of cases where the primary team requested a biopsy ultimately required a biopsy, as many involved clinical diagnoses such as urticaria. Not only was dermatology accurate in their preliminary diagnoses, but they decreased cost and morbidity by avoiding unnecessary procedures.

This study provided additional evidence to support the integration of dermatology into the hospital setting for the benefit of patients, primary medical teams, and hospital systems. Dermatology offers high-value care through the efficient diagnosis and management of hospitalized patients, which contributes to decreased cost and improved outcomes.2,5-7,9,10 This study highlighted lesser-known areas of impact, such as the various specialty-specific services dermatology provides as well as the high rates of reported improvement following consultation. Future studies should continue to explore the field’s unique impact on hospitalized medicine as well as other avenues of care delivery, such as telemedicine, that may encourage dermatologists to participate in consultations and increase the volume of patients who may benefit from their care.

References
  1. Madigan LM, Fox LP. Where are we now with inpatient consultative dermatology?: assessing the value and evolution of this subspecialty over the past decade. J Am Acad Dermatol. 2019;80:1804-1808. doi:10.1016/j.jaad.2019.01.031
  2. Noe MH, Rosenbach M. Inpatient dermatologists—crucial for the management of skin diseases in hospitalized patients [editorial]. JAMA Dermatol. 2018;154:524-525. doi:10.1001/jamadermatol.2017.6195
  3. Strowd LC. Inpatient dermatology: a paradigm shift in the management of skin disease in the hospital. Br J Dermatol. 2019;180:966-967. doi:10.1111/bjd.17778
  4. Kirsner RS, Yang DG, Kerdel FA. The changing status of inpatient dermatology at American academic dermatology programs. J Am Acad Dermatol. 1999;40:755-757. doi:10.1016/s0190-9622(99)70158-1
  5. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480. doi:10.1001/jamadermatol.2015.5098
  6. Ko LN, Garza-Mayers AC, St John J, et al. Effect of dermatology consultation on outcomes for patients with presumed cellulitis. JAMA Dermatol. 2018;154:529-533. doi:10.1001/jamadermatol.2017.6196
  7. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543. doi:10.1001/jamadermatol.2017.6197
  8. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528. doi:10.1001/jamadermatol.2016.6130
  9. Imadojemu S, Rosenbach M. Dermatologists must take an active role in the diagnosis of cellulitis. JAMA Dermatol. 2017;153:134-135. doi:10.1001/jamadermatol.2016.4230
  10. Hughey LC. The impact dermatologists can have on misdiagnosis of cellulitis and overuse of antibiotics: closing the gap. JAMA Dermatol. 2014;150:1061-1062. doi:10.1001/jamadermatol.2014.1164
  11. Ko LN, Kroshinsky D. Dermatology hospitalists: a multicenter survey study characterizing the infrastructure of consultative dermatology in select American hospitals. Int J Dermatol. 2018;57:553-558. doi:10.1111/ijd.13939
References
  1. Madigan LM, Fox LP. Where are we now with inpatient consultative dermatology?: assessing the value and evolution of this subspecialty over the past decade. J Am Acad Dermatol. 2019;80:1804-1808. doi:10.1016/j.jaad.2019.01.031
  2. Noe MH, Rosenbach M. Inpatient dermatologists—crucial for the management of skin diseases in hospitalized patients [editorial]. JAMA Dermatol. 2018;154:524-525. doi:10.1001/jamadermatol.2017.6195
  3. Strowd LC. Inpatient dermatology: a paradigm shift in the management of skin disease in the hospital. Br J Dermatol. 2019;180:966-967. doi:10.1111/bjd.17778
  4. Kirsner RS, Yang DG, Kerdel FA. The changing status of inpatient dermatology at American academic dermatology programs. J Am Acad Dermatol. 1999;40:755-757. doi:10.1016/s0190-9622(99)70158-1
  5. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480. doi:10.1001/jamadermatol.2015.5098
  6. Ko LN, Garza-Mayers AC, St John J, et al. Effect of dermatology consultation on outcomes for patients with presumed cellulitis. JAMA Dermatol. 2018;154:529-533. doi:10.1001/jamadermatol.2017.6196
  7. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543. doi:10.1001/jamadermatol.2017.6197
  8. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528. doi:10.1001/jamadermatol.2016.6130
  9. Imadojemu S, Rosenbach M. Dermatologists must take an active role in the diagnosis of cellulitis. JAMA Dermatol. 2017;153:134-135. doi:10.1001/jamadermatol.2016.4230
  10. Hughey LC. The impact dermatologists can have on misdiagnosis of cellulitis and overuse of antibiotics: closing the gap. JAMA Dermatol. 2014;150:1061-1062. doi:10.1001/jamadermatol.2014.1164
  11. Ko LN, Kroshinsky D. Dermatology hospitalists: a multicenter survey study characterizing the infrastructure of consultative dermatology in select American hospitals. Int J Dermatol. 2018;57:553-558. doi:10.1111/ijd.13939
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  • Integration of inpatient dermatology consultations can prevent unnecessary hospital admissions and medication administration.
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Imatinib Mesylate–Induced Lichenoid Drug Eruption

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Imatinib Mesylate–Induced Lichenoid Drug Eruption

Imatinib mesylate is a tyrosine kinase inhibitor initially approved by the US Food and Drug Administration in 2001 for chronic myeloid leukemia (CML). The indications for imatinib have expanded since its initial approval. It is increasingly important that dermatologists recognize adverse cutaneous manifestations associated with imatinib and are aware of their management and outcomes to avoid unnecessarily discontinuing a potentially lifesaving medication.

Adverse cutaneous manifestations in response to imatinib are not infrequent, accounting for 7% to 21% of all side effects.1 The most frequent cutaneous manifestations of imatinib are dry skin, alopecia, facial edema, and photosensitivity rash, respectively.1 Other less common manifestations include exfoliative dermatitis, nail disorders, psoriasis, folliculitis, hypotrichosis, urticaria, petechiae, Stevens-Johnson syndrome, erythema multiforme, Sweet syndrome, and leukocytoclastic vasculitis.

We report a case of imatinib-induced lichenoid drug eruption (LDE), a rare cutaneous side effect of imatinib use, along with a review of the literature.

Case Report

An 86-year-old man with a history of gastrointestinal stromal tumors (GISTs) and myelodysplastic syndrome presented with diffuse hyperpigmented skin lesions on the trunk, arms, legs, and lower lip of 2 weeks’ duration. He had been taking imatinib 400 mg once daily for 5 months for GIST. Although the oncologist stopped the medication 2 weeks prior, the lesions were persistent and gradually expanded to involve the trunk, arms, legs, and lower lip. He denied any pain or pruritus. Physical examination revealed multiple ill-defined, brown to violaceous, slightly scaly macules and patches on the trunk (Figures 1A and 1B), arms, and legs (Figure 1C), as well as violaceous to erythematous patches on the mucosal aspect of the lower lip (Figure 2). Two 4-mm punch biopsies were performed from the chest and back, which revealed an atrophic epidermis, lichenoid infiltration, and multiple melanophages in the upper dermis consistent with LDE (Figure 3). Direct immunofluorescence was negative. Therefore, based on the clinicopathologic correlation, the diagnosis of imatinib-induced LDE was made. He was treated with clobetasol ointment twice daily for 3 weeks with some improvement. His GIST was stable on follow-up computed tomography 3 months after presentation, and imatinib was resumed 1 month later with continued rash that was stable with topical corticosteroid treatment.

Figure 1. Widespread violaceous, hyperpigmented, slightly scaly macules and patches on the chest (A), back (B), and leg (C).

Figure 2. Lacy, violaceous to erythematous patches on the mucosal surface of the lower lip.

Figure 3. Atrophic epidermis, lichenoid infiltration of lymphocytes, and multiple melanophages in the upper dermis on histopathology (A and B)(H&E, original magnifications ×40 and ×100).

 

 

Comment

In addition to CML, imatinib has been approved for acute lymphoblastic leukemia, myelodysplastic syndromes, aggressive systemic mastocytosis, hypereosinophilic syndrome, chronic eosinophilic leukemia, dermatofibrosarcoma protuberans, and GIST. Moreover, off-label use of imatinib for various other tyrosine kinase–positive cancers and rheumatologic conditions have been documented.2,3 With the expanding use of imatinib, there will be more occasions for dermatologists to encounter cutaneous manifestations associated with its use.

According to a PubMed search of articles indexed for MEDLINE using the terms imatinib mesylate lichenoid drug, there have been few case reports of LDE associated with imatinib in the literature (eTable).4-24 Compared to classic LDE, imatinib-induced LDE has a few characteristic findings. Classic LDE frequently spares the oral mucosa and genitalia, but imatinib-induced LDE with manifestations on the oral mucosa and genitalia as well as cutaneous eruptions have been reported.4-9 In fact, the first known case of imatinib-induced LDE was an oral eruption in a patient with CML.4 In patients with oral involvement, lesions have been described as lacy reticular macules and violaceous papules, erosions, and ulcers.4,5,12 Interestingly, of those cases manifesting as concomitant oral and cutaneous LDE, the oral eruptions recurred more frequently, with 3 of 12 patients having recurrence of oral lesions after the cutaneous manifestations resolved.8,16 Genital manifestations of imatinib-induced LDE were much less common.9,11

To date, subsequent reports of imatinib-induced LDE have documented skin manifestations consistent with classic LDE occurring in a diffuse, bilateral, photodistributed pattern.10,15,16 One case presented with diffuse hyperpigmentation associated with LDE in a Japanese patient.20 The authors suggested this finding may be more prominent in patients with skin of color,20 which is consistent with the current case. Nail findings such as subungual hyperkeratosis and longitudinal ridging also have been reported.9,11

The latency period between initiation of imat-inib and onset of LDE generally ranges from 1 to 12 months, with onset most commonly occurring between 2 to 5 months or with dosage increase (eTable). Imatinib-induced LDE primarily has been documented with a 400-mg dose, with 1 case of a 600-mg dose and 1 case of an 800-mg dose, which suggests dose dependency. Furthermore, reports exist of several patients responding well to dose reduction with subsequent recurrence on dose reescalation.13,15

Historically, LDE resolves with discontinuation of the drug after a few weeks to months. When discontinuation of imatinib is unfavorable or patients report symptoms including severe pruritus or pain, treatment should be considered. Topical or oral corticosteroids can be used to treat imatinib-induced LDE, similar to lichen planus. When oral corticosteroids are contraindicated (eg, due to poor patient tolerance), oral acitretin at 25 to 35 mg once daily for 6 to 12 weeks has been reported as an alternative treatment.25

In the majority of cases of imatinib-induced LDE, it was undesirable to stop imatinib (eTable). Notably, in half the reported cases, imatinib was able to be continued and patients were treated symptomatically with either oral and/or topical steroids and/or acitretin with complete remission or tolerable recurrences. Dalmau et al9 reported 3 patients who responded poorly to topical and oral steroids and were subsequently treated with acitretin 25 mg once daily; 2 of 3 patients responded favorably to treatment and imatinib was able to be continued. In the current case imatinib initially helped, but because his rash was relatively asymptomatic, imatinib was restarted with control of rash with topical steroids. He developed some pancytopenia, which required intermittent stoppage of the imatinib.

Conclusion

We present a case of imatinib-induced cutaneous and oral LDE in a patient with GIST. Topical corticosteroids, oral acitretin, and oral steroids all may be reasonable treatment options if discontinuing imatinib is not possible in a symptomatic patient. If these therapies fail and the eruption is extensive or intolerable, dosage adjustment is another option to consider before discontinuation of imatinib.

References
  1. Scheinfeld N. Imatinib mesylate and dermatology part 2: a review of the cutaneous side effects of imatinib mesylate. J Drugs Dermatol. 2006;5:228-231.
  2. Kim H, Kim NH, Kang HJ, et al. Successful long-term use of imatinib mesylate in pediatric patients with sclerodermatous chronic GVHD. Pediatr Transplant. 2012;16:910-912.
  3. Prey S, Ezzedine K, Doussau A, et al. Imatinib mesylate in scleroderma-associated diffuse skin fibrosis: a phase II multicentre randomized double-blinded controlled trial. Br J Dermatol. 2012;167:1138-1144.
  4. Lim DS, Muir J. Oral lichenoid reaction to imatinib (STI 571, gleevec). Dermatology. 2002;205:169-171.
  5. Ena P, Chiarolini F, Siddi GM, et al. Oral lichenoid eruption secondary to imatinib (glivec). J Dermatolog Treat. 2004;15:253-255.
  6. Roux C, Boisseau-Garsaud AM, Saint-Cyr I, et al. Lichenoid cutaneous reaction to imatinib. Ann Dermatol Venereol. 2004;131:571-573.
  7. Prabhash K, Doval DC. Lichenoid eruption due to imat-inib. Indian J Dermatol Venereol Leprol. 2005;71:287-288.
  8. Pascual JC, Matarredona J, Miralles J, et al. Oral and cutaneous lichenoid reaction secondary to imatinib: report of two cases. Int J Dermatol. 2006;45:1471-1473.
  9. Dalmau J, Peramiquel L, Puig L, et al. Imatinib-associated lichenoid eruption: acitretin treatment allows maintained antineoplastic effect. Br J Dermatol. 2006;154:1213-1216.
  10. Chan CY, Browning J, Smith-Zagone MJ, et al. Cutaneous lichenoid dermatitis associated with imatinib mesylate. Dermatol Online J. 2007;13:29.
  11. Wahiduzzaman M, Pubalan M. Oral and cutaneous lichenoid reaction with nail changes secondary to imatinib: report of a case and literature review. Dermatol Online J. 2008;14:14.
  12. Basso FG, Boer CC, Correa ME, et al. Skin and oral lesions associated to imatinib mesylate therapy. Support Care Cancer. 2009;17:465-468.
  13. Kawakami T, Kawanabe T, Soma Y. Cutaneous lichenoid eruption caused by imatinib mesylate in a Japanese patient with chronic myeloid leukaemia. Acta Derm Venereol. 2009;89:325-326.
  14. Sendagorta E, Herranz P, Feito M, et al. Lichenoid drug eruption related to imatinib: report of a new case and review of the literature. Clin Exp Dermatol. 2009;34:E315-E316.
  15. Kuraishi N, Nagai Y, Hasegawa M, et al. Lichenoid drug eruption with palmoplantar hyperkeratosis due to imatinib mesylate: a case report and a review of the literature. Acta Derm Venereol. 2010;90:73-76.
  16. Brazzelli V, Muzio F, Manna G, et al. Photo-induced dermatitis and oral lichenoid reaction in a chronic myeloid leukemia patient treated with imatinib mesylate. Photodermatol Photoimmunol Photomed. 2012;28:2-5.
  17. Ghosh SK. Generalized lichenoid drug eruption associated with imatinib mesylate therapy. Indian J Dermatol. 2013;58:388-392.
  18. Lee J, Chung J, Jung M, et al. Lichenoid drug eruption after low-dose imatinib mesylate therapy. Ann Dermatol. 2013;25:500-502.
  19. Machaczka M, Gossart M. Multiple skin lesions caused by imatinib mesylate treatment of chronic myeloid leukemia. Pol Arch Med Wewn. 2013;123:251-252.
  20. Kagimoto Y, Mizuashi M, Kikuchi K, et al. Lichenoid drug eruption with hyperpigmentation caused by imatinib mesylate [published online June 20, 2013]. Int J Dermatol. 2014;53:E161-E162.
  21. Arshdeep, De D, Malhotra P, et al. Imatinib mesylate-induced severe lichenoid rash. Indian J Dermatol Venereol Leprol. 2014;80:93-95.
  22. Lau YM, Lam YK, Leung KH, et al. Trachyonychia in a patient with chronic myeloid leukaemia after imatinib mesylate. Hong Kong Med J. 2014;20:464.e2.
  23. Bhatia A, Kanish B, Chaudhary P. Lichenoid drug eruption due to imatinib mesylate. Int J Appl Basic Med Res. 2015;5:68-69.
  24. Luo JR, Xiang XJ, Xiong JP. Lichenoid drug eruption caused by imatinib mesylate in a Chinese patient with gastrointestinal stromal tumor. Int J Clin Pharmacol Ther. 2016;54:719-722.
  25. Laurberg G, Geiger JM, Hjorth N, et al. Treatment of lichen planus with acitretin. a double-blind, placebo-controlled study in 65 patients. J Am Acad Dermatol. 1991;24:434-437.
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Dr. Penn is from Jefferson Medical College, Philadelphia, Pennsylvania. Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia.

The authors report no conflict of interest.

The eTable is available in the Appendix in the PDF.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Dr. Penn is from Jefferson Medical College, Philadelphia, Pennsylvania. Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia.

The authors report no conflict of interest.

The eTable is available in the Appendix in the PDF.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

Author and Disclosure Information

Dr. Penn is from Jefferson Medical College, Philadelphia, Pennsylvania. Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia.

The authors report no conflict of interest.

The eTable is available in the Appendix in the PDF.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Imatinib mesylate is a tyrosine kinase inhibitor initially approved by the US Food and Drug Administration in 2001 for chronic myeloid leukemia (CML). The indications for imatinib have expanded since its initial approval. It is increasingly important that dermatologists recognize adverse cutaneous manifestations associated with imatinib and are aware of their management and outcomes to avoid unnecessarily discontinuing a potentially lifesaving medication.

Adverse cutaneous manifestations in response to imatinib are not infrequent, accounting for 7% to 21% of all side effects.1 The most frequent cutaneous manifestations of imatinib are dry skin, alopecia, facial edema, and photosensitivity rash, respectively.1 Other less common manifestations include exfoliative dermatitis, nail disorders, psoriasis, folliculitis, hypotrichosis, urticaria, petechiae, Stevens-Johnson syndrome, erythema multiforme, Sweet syndrome, and leukocytoclastic vasculitis.

We report a case of imatinib-induced lichenoid drug eruption (LDE), a rare cutaneous side effect of imatinib use, along with a review of the literature.

Case Report

An 86-year-old man with a history of gastrointestinal stromal tumors (GISTs) and myelodysplastic syndrome presented with diffuse hyperpigmented skin lesions on the trunk, arms, legs, and lower lip of 2 weeks’ duration. He had been taking imatinib 400 mg once daily for 5 months for GIST. Although the oncologist stopped the medication 2 weeks prior, the lesions were persistent and gradually expanded to involve the trunk, arms, legs, and lower lip. He denied any pain or pruritus. Physical examination revealed multiple ill-defined, brown to violaceous, slightly scaly macules and patches on the trunk (Figures 1A and 1B), arms, and legs (Figure 1C), as well as violaceous to erythematous patches on the mucosal aspect of the lower lip (Figure 2). Two 4-mm punch biopsies were performed from the chest and back, which revealed an atrophic epidermis, lichenoid infiltration, and multiple melanophages in the upper dermis consistent with LDE (Figure 3). Direct immunofluorescence was negative. Therefore, based on the clinicopathologic correlation, the diagnosis of imatinib-induced LDE was made. He was treated with clobetasol ointment twice daily for 3 weeks with some improvement. His GIST was stable on follow-up computed tomography 3 months after presentation, and imatinib was resumed 1 month later with continued rash that was stable with topical corticosteroid treatment.

Figure 1. Widespread violaceous, hyperpigmented, slightly scaly macules and patches on the chest (A), back (B), and leg (C).

Figure 2. Lacy, violaceous to erythematous patches on the mucosal surface of the lower lip.

Figure 3. Atrophic epidermis, lichenoid infiltration of lymphocytes, and multiple melanophages in the upper dermis on histopathology (A and B)(H&E, original magnifications ×40 and ×100).

 

 

Comment

In addition to CML, imatinib has been approved for acute lymphoblastic leukemia, myelodysplastic syndromes, aggressive systemic mastocytosis, hypereosinophilic syndrome, chronic eosinophilic leukemia, dermatofibrosarcoma protuberans, and GIST. Moreover, off-label use of imatinib for various other tyrosine kinase–positive cancers and rheumatologic conditions have been documented.2,3 With the expanding use of imatinib, there will be more occasions for dermatologists to encounter cutaneous manifestations associated with its use.

According to a PubMed search of articles indexed for MEDLINE using the terms imatinib mesylate lichenoid drug, there have been few case reports of LDE associated with imatinib in the literature (eTable).4-24 Compared to classic LDE, imatinib-induced LDE has a few characteristic findings. Classic LDE frequently spares the oral mucosa and genitalia, but imatinib-induced LDE with manifestations on the oral mucosa and genitalia as well as cutaneous eruptions have been reported.4-9 In fact, the first known case of imatinib-induced LDE was an oral eruption in a patient with CML.4 In patients with oral involvement, lesions have been described as lacy reticular macules and violaceous papules, erosions, and ulcers.4,5,12 Interestingly, of those cases manifesting as concomitant oral and cutaneous LDE, the oral eruptions recurred more frequently, with 3 of 12 patients having recurrence of oral lesions after the cutaneous manifestations resolved.8,16 Genital manifestations of imatinib-induced LDE were much less common.9,11

To date, subsequent reports of imatinib-induced LDE have documented skin manifestations consistent with classic LDE occurring in a diffuse, bilateral, photodistributed pattern.10,15,16 One case presented with diffuse hyperpigmentation associated with LDE in a Japanese patient.20 The authors suggested this finding may be more prominent in patients with skin of color,20 which is consistent with the current case. Nail findings such as subungual hyperkeratosis and longitudinal ridging also have been reported.9,11

The latency period between initiation of imat-inib and onset of LDE generally ranges from 1 to 12 months, with onset most commonly occurring between 2 to 5 months or with dosage increase (eTable). Imatinib-induced LDE primarily has been documented with a 400-mg dose, with 1 case of a 600-mg dose and 1 case of an 800-mg dose, which suggests dose dependency. Furthermore, reports exist of several patients responding well to dose reduction with subsequent recurrence on dose reescalation.13,15

Historically, LDE resolves with discontinuation of the drug after a few weeks to months. When discontinuation of imatinib is unfavorable or patients report symptoms including severe pruritus or pain, treatment should be considered. Topical or oral corticosteroids can be used to treat imatinib-induced LDE, similar to lichen planus. When oral corticosteroids are contraindicated (eg, due to poor patient tolerance), oral acitretin at 25 to 35 mg once daily for 6 to 12 weeks has been reported as an alternative treatment.25

In the majority of cases of imatinib-induced LDE, it was undesirable to stop imatinib (eTable). Notably, in half the reported cases, imatinib was able to be continued and patients were treated symptomatically with either oral and/or topical steroids and/or acitretin with complete remission or tolerable recurrences. Dalmau et al9 reported 3 patients who responded poorly to topical and oral steroids and were subsequently treated with acitretin 25 mg once daily; 2 of 3 patients responded favorably to treatment and imatinib was able to be continued. In the current case imatinib initially helped, but because his rash was relatively asymptomatic, imatinib was restarted with control of rash with topical steroids. He developed some pancytopenia, which required intermittent stoppage of the imatinib.

Conclusion

We present a case of imatinib-induced cutaneous and oral LDE in a patient with GIST. Topical corticosteroids, oral acitretin, and oral steroids all may be reasonable treatment options if discontinuing imatinib is not possible in a symptomatic patient. If these therapies fail and the eruption is extensive or intolerable, dosage adjustment is another option to consider before discontinuation of imatinib.

Imatinib mesylate is a tyrosine kinase inhibitor initially approved by the US Food and Drug Administration in 2001 for chronic myeloid leukemia (CML). The indications for imatinib have expanded since its initial approval. It is increasingly important that dermatologists recognize adverse cutaneous manifestations associated with imatinib and are aware of their management and outcomes to avoid unnecessarily discontinuing a potentially lifesaving medication.

Adverse cutaneous manifestations in response to imatinib are not infrequent, accounting for 7% to 21% of all side effects.1 The most frequent cutaneous manifestations of imatinib are dry skin, alopecia, facial edema, and photosensitivity rash, respectively.1 Other less common manifestations include exfoliative dermatitis, nail disorders, psoriasis, folliculitis, hypotrichosis, urticaria, petechiae, Stevens-Johnson syndrome, erythema multiforme, Sweet syndrome, and leukocytoclastic vasculitis.

We report a case of imatinib-induced lichenoid drug eruption (LDE), a rare cutaneous side effect of imatinib use, along with a review of the literature.

Case Report

An 86-year-old man with a history of gastrointestinal stromal tumors (GISTs) and myelodysplastic syndrome presented with diffuse hyperpigmented skin lesions on the trunk, arms, legs, and lower lip of 2 weeks’ duration. He had been taking imatinib 400 mg once daily for 5 months for GIST. Although the oncologist stopped the medication 2 weeks prior, the lesions were persistent and gradually expanded to involve the trunk, arms, legs, and lower lip. He denied any pain or pruritus. Physical examination revealed multiple ill-defined, brown to violaceous, slightly scaly macules and patches on the trunk (Figures 1A and 1B), arms, and legs (Figure 1C), as well as violaceous to erythematous patches on the mucosal aspect of the lower lip (Figure 2). Two 4-mm punch biopsies were performed from the chest and back, which revealed an atrophic epidermis, lichenoid infiltration, and multiple melanophages in the upper dermis consistent with LDE (Figure 3). Direct immunofluorescence was negative. Therefore, based on the clinicopathologic correlation, the diagnosis of imatinib-induced LDE was made. He was treated with clobetasol ointment twice daily for 3 weeks with some improvement. His GIST was stable on follow-up computed tomography 3 months after presentation, and imatinib was resumed 1 month later with continued rash that was stable with topical corticosteroid treatment.

Figure 1. Widespread violaceous, hyperpigmented, slightly scaly macules and patches on the chest (A), back (B), and leg (C).

Figure 2. Lacy, violaceous to erythematous patches on the mucosal surface of the lower lip.

Figure 3. Atrophic epidermis, lichenoid infiltration of lymphocytes, and multiple melanophages in the upper dermis on histopathology (A and B)(H&E, original magnifications ×40 and ×100).

 

 

Comment

In addition to CML, imatinib has been approved for acute lymphoblastic leukemia, myelodysplastic syndromes, aggressive systemic mastocytosis, hypereosinophilic syndrome, chronic eosinophilic leukemia, dermatofibrosarcoma protuberans, and GIST. Moreover, off-label use of imatinib for various other tyrosine kinase–positive cancers and rheumatologic conditions have been documented.2,3 With the expanding use of imatinib, there will be more occasions for dermatologists to encounter cutaneous manifestations associated with its use.

According to a PubMed search of articles indexed for MEDLINE using the terms imatinib mesylate lichenoid drug, there have been few case reports of LDE associated with imatinib in the literature (eTable).4-24 Compared to classic LDE, imatinib-induced LDE has a few characteristic findings. Classic LDE frequently spares the oral mucosa and genitalia, but imatinib-induced LDE with manifestations on the oral mucosa and genitalia as well as cutaneous eruptions have been reported.4-9 In fact, the first known case of imatinib-induced LDE was an oral eruption in a patient with CML.4 In patients with oral involvement, lesions have been described as lacy reticular macules and violaceous papules, erosions, and ulcers.4,5,12 Interestingly, of those cases manifesting as concomitant oral and cutaneous LDE, the oral eruptions recurred more frequently, with 3 of 12 patients having recurrence of oral lesions after the cutaneous manifestations resolved.8,16 Genital manifestations of imatinib-induced LDE were much less common.9,11

To date, subsequent reports of imatinib-induced LDE have documented skin manifestations consistent with classic LDE occurring in a diffuse, bilateral, photodistributed pattern.10,15,16 One case presented with diffuse hyperpigmentation associated with LDE in a Japanese patient.20 The authors suggested this finding may be more prominent in patients with skin of color,20 which is consistent with the current case. Nail findings such as subungual hyperkeratosis and longitudinal ridging also have been reported.9,11

The latency period between initiation of imat-inib and onset of LDE generally ranges from 1 to 12 months, with onset most commonly occurring between 2 to 5 months or with dosage increase (eTable). Imatinib-induced LDE primarily has been documented with a 400-mg dose, with 1 case of a 600-mg dose and 1 case of an 800-mg dose, which suggests dose dependency. Furthermore, reports exist of several patients responding well to dose reduction with subsequent recurrence on dose reescalation.13,15

Historically, LDE resolves with discontinuation of the drug after a few weeks to months. When discontinuation of imatinib is unfavorable or patients report symptoms including severe pruritus or pain, treatment should be considered. Topical or oral corticosteroids can be used to treat imatinib-induced LDE, similar to lichen planus. When oral corticosteroids are contraindicated (eg, due to poor patient tolerance), oral acitretin at 25 to 35 mg once daily for 6 to 12 weeks has been reported as an alternative treatment.25

In the majority of cases of imatinib-induced LDE, it was undesirable to stop imatinib (eTable). Notably, in half the reported cases, imatinib was able to be continued and patients were treated symptomatically with either oral and/or topical steroids and/or acitretin with complete remission or tolerable recurrences. Dalmau et al9 reported 3 patients who responded poorly to topical and oral steroids and were subsequently treated with acitretin 25 mg once daily; 2 of 3 patients responded favorably to treatment and imatinib was able to be continued. In the current case imatinib initially helped, but because his rash was relatively asymptomatic, imatinib was restarted with control of rash with topical steroids. He developed some pancytopenia, which required intermittent stoppage of the imatinib.

Conclusion

We present a case of imatinib-induced cutaneous and oral LDE in a patient with GIST. Topical corticosteroids, oral acitretin, and oral steroids all may be reasonable treatment options if discontinuing imatinib is not possible in a symptomatic patient. If these therapies fail and the eruption is extensive or intolerable, dosage adjustment is another option to consider before discontinuation of imatinib.

References
  1. Scheinfeld N. Imatinib mesylate and dermatology part 2: a review of the cutaneous side effects of imatinib mesylate. J Drugs Dermatol. 2006;5:228-231.
  2. Kim H, Kim NH, Kang HJ, et al. Successful long-term use of imatinib mesylate in pediatric patients with sclerodermatous chronic GVHD. Pediatr Transplant. 2012;16:910-912.
  3. Prey S, Ezzedine K, Doussau A, et al. Imatinib mesylate in scleroderma-associated diffuse skin fibrosis: a phase II multicentre randomized double-blinded controlled trial. Br J Dermatol. 2012;167:1138-1144.
  4. Lim DS, Muir J. Oral lichenoid reaction to imatinib (STI 571, gleevec). Dermatology. 2002;205:169-171.
  5. Ena P, Chiarolini F, Siddi GM, et al. Oral lichenoid eruption secondary to imatinib (glivec). J Dermatolog Treat. 2004;15:253-255.
  6. Roux C, Boisseau-Garsaud AM, Saint-Cyr I, et al. Lichenoid cutaneous reaction to imatinib. Ann Dermatol Venereol. 2004;131:571-573.
  7. Prabhash K, Doval DC. Lichenoid eruption due to imat-inib. Indian J Dermatol Venereol Leprol. 2005;71:287-288.
  8. Pascual JC, Matarredona J, Miralles J, et al. Oral and cutaneous lichenoid reaction secondary to imatinib: report of two cases. Int J Dermatol. 2006;45:1471-1473.
  9. Dalmau J, Peramiquel L, Puig L, et al. Imatinib-associated lichenoid eruption: acitretin treatment allows maintained antineoplastic effect. Br J Dermatol. 2006;154:1213-1216.
  10. Chan CY, Browning J, Smith-Zagone MJ, et al. Cutaneous lichenoid dermatitis associated with imatinib mesylate. Dermatol Online J. 2007;13:29.
  11. Wahiduzzaman M, Pubalan M. Oral and cutaneous lichenoid reaction with nail changes secondary to imatinib: report of a case and literature review. Dermatol Online J. 2008;14:14.
  12. Basso FG, Boer CC, Correa ME, et al. Skin and oral lesions associated to imatinib mesylate therapy. Support Care Cancer. 2009;17:465-468.
  13. Kawakami T, Kawanabe T, Soma Y. Cutaneous lichenoid eruption caused by imatinib mesylate in a Japanese patient with chronic myeloid leukaemia. Acta Derm Venereol. 2009;89:325-326.
  14. Sendagorta E, Herranz P, Feito M, et al. Lichenoid drug eruption related to imatinib: report of a new case and review of the literature. Clin Exp Dermatol. 2009;34:E315-E316.
  15. Kuraishi N, Nagai Y, Hasegawa M, et al. Lichenoid drug eruption with palmoplantar hyperkeratosis due to imatinib mesylate: a case report and a review of the literature. Acta Derm Venereol. 2010;90:73-76.
  16. Brazzelli V, Muzio F, Manna G, et al. Photo-induced dermatitis and oral lichenoid reaction in a chronic myeloid leukemia patient treated with imatinib mesylate. Photodermatol Photoimmunol Photomed. 2012;28:2-5.
  17. Ghosh SK. Generalized lichenoid drug eruption associated with imatinib mesylate therapy. Indian J Dermatol. 2013;58:388-392.
  18. Lee J, Chung J, Jung M, et al. Lichenoid drug eruption after low-dose imatinib mesylate therapy. Ann Dermatol. 2013;25:500-502.
  19. Machaczka M, Gossart M. Multiple skin lesions caused by imatinib mesylate treatment of chronic myeloid leukemia. Pol Arch Med Wewn. 2013;123:251-252.
  20. Kagimoto Y, Mizuashi M, Kikuchi K, et al. Lichenoid drug eruption with hyperpigmentation caused by imatinib mesylate [published online June 20, 2013]. Int J Dermatol. 2014;53:E161-E162.
  21. Arshdeep, De D, Malhotra P, et al. Imatinib mesylate-induced severe lichenoid rash. Indian J Dermatol Venereol Leprol. 2014;80:93-95.
  22. Lau YM, Lam YK, Leung KH, et al. Trachyonychia in a patient with chronic myeloid leukaemia after imatinib mesylate. Hong Kong Med J. 2014;20:464.e2.
  23. Bhatia A, Kanish B, Chaudhary P. Lichenoid drug eruption due to imatinib mesylate. Int J Appl Basic Med Res. 2015;5:68-69.
  24. Luo JR, Xiang XJ, Xiong JP. Lichenoid drug eruption caused by imatinib mesylate in a Chinese patient with gastrointestinal stromal tumor. Int J Clin Pharmacol Ther. 2016;54:719-722.
  25. Laurberg G, Geiger JM, Hjorth N, et al. Treatment of lichen planus with acitretin. a double-blind, placebo-controlled study in 65 patients. J Am Acad Dermatol. 1991;24:434-437.
References
  1. Scheinfeld N. Imatinib mesylate and dermatology part 2: a review of the cutaneous side effects of imatinib mesylate. J Drugs Dermatol. 2006;5:228-231.
  2. Kim H, Kim NH, Kang HJ, et al. Successful long-term use of imatinib mesylate in pediatric patients with sclerodermatous chronic GVHD. Pediatr Transplant. 2012;16:910-912.
  3. Prey S, Ezzedine K, Doussau A, et al. Imatinib mesylate in scleroderma-associated diffuse skin fibrosis: a phase II multicentre randomized double-blinded controlled trial. Br J Dermatol. 2012;167:1138-1144.
  4. Lim DS, Muir J. Oral lichenoid reaction to imatinib (STI 571, gleevec). Dermatology. 2002;205:169-171.
  5. Ena P, Chiarolini F, Siddi GM, et al. Oral lichenoid eruption secondary to imatinib (glivec). J Dermatolog Treat. 2004;15:253-255.
  6. Roux C, Boisseau-Garsaud AM, Saint-Cyr I, et al. Lichenoid cutaneous reaction to imatinib. Ann Dermatol Venereol. 2004;131:571-573.
  7. Prabhash K, Doval DC. Lichenoid eruption due to imat-inib. Indian J Dermatol Venereol Leprol. 2005;71:287-288.
  8. Pascual JC, Matarredona J, Miralles J, et al. Oral and cutaneous lichenoid reaction secondary to imatinib: report of two cases. Int J Dermatol. 2006;45:1471-1473.
  9. Dalmau J, Peramiquel L, Puig L, et al. Imatinib-associated lichenoid eruption: acitretin treatment allows maintained antineoplastic effect. Br J Dermatol. 2006;154:1213-1216.
  10. Chan CY, Browning J, Smith-Zagone MJ, et al. Cutaneous lichenoid dermatitis associated with imatinib mesylate. Dermatol Online J. 2007;13:29.
  11. Wahiduzzaman M, Pubalan M. Oral and cutaneous lichenoid reaction with nail changes secondary to imatinib: report of a case and literature review. Dermatol Online J. 2008;14:14.
  12. Basso FG, Boer CC, Correa ME, et al. Skin and oral lesions associated to imatinib mesylate therapy. Support Care Cancer. 2009;17:465-468.
  13. Kawakami T, Kawanabe T, Soma Y. Cutaneous lichenoid eruption caused by imatinib mesylate in a Japanese patient with chronic myeloid leukaemia. Acta Derm Venereol. 2009;89:325-326.
  14. Sendagorta E, Herranz P, Feito M, et al. Lichenoid drug eruption related to imatinib: report of a new case and review of the literature. Clin Exp Dermatol. 2009;34:E315-E316.
  15. Kuraishi N, Nagai Y, Hasegawa M, et al. Lichenoid drug eruption with palmoplantar hyperkeratosis due to imatinib mesylate: a case report and a review of the literature. Acta Derm Venereol. 2010;90:73-76.
  16. Brazzelli V, Muzio F, Manna G, et al. Photo-induced dermatitis and oral lichenoid reaction in a chronic myeloid leukemia patient treated with imatinib mesylate. Photodermatol Photoimmunol Photomed. 2012;28:2-5.
  17. Ghosh SK. Generalized lichenoid drug eruption associated with imatinib mesylate therapy. Indian J Dermatol. 2013;58:388-392.
  18. Lee J, Chung J, Jung M, et al. Lichenoid drug eruption after low-dose imatinib mesylate therapy. Ann Dermatol. 2013;25:500-502.
  19. Machaczka M, Gossart M. Multiple skin lesions caused by imatinib mesylate treatment of chronic myeloid leukemia. Pol Arch Med Wewn. 2013;123:251-252.
  20. Kagimoto Y, Mizuashi M, Kikuchi K, et al. Lichenoid drug eruption with hyperpigmentation caused by imatinib mesylate [published online June 20, 2013]. Int J Dermatol. 2014;53:E161-E162.
  21. Arshdeep, De D, Malhotra P, et al. Imatinib mesylate-induced severe lichenoid rash. Indian J Dermatol Venereol Leprol. 2014;80:93-95.
  22. Lau YM, Lam YK, Leung KH, et al. Trachyonychia in a patient with chronic myeloid leukaemia after imatinib mesylate. Hong Kong Med J. 2014;20:464.e2.
  23. Bhatia A, Kanish B, Chaudhary P. Lichenoid drug eruption due to imatinib mesylate. Int J Appl Basic Med Res. 2015;5:68-69.
  24. Luo JR, Xiang XJ, Xiong JP. Lichenoid drug eruption caused by imatinib mesylate in a Chinese patient with gastrointestinal stromal tumor. Int J Clin Pharmacol Ther. 2016;54:719-722.
  25. Laurberg G, Geiger JM, Hjorth N, et al. Treatment of lichen planus with acitretin. a double-blind, placebo-controlled study in 65 patients. J Am Acad Dermatol. 1991;24:434-437.
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Practice Points

  • Imatinib mesylate can cause cutaneous adverse reactions including dry skin, alopecia, facial edema, photosensitivity rash, and lichenoid drug eruption (LDE).
  • Topical corticosteroids, oral acitretin, and oral steroids may be reasonable treatment options for imatinib-induced LDE if discontinuing imatinib is not possible in a symptomatic patient.
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Rupioid Psoriasis and Other Skin Diseases With Rupioid Manifestations

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Rupioid Psoriasis and Other Skin Diseases With Rupioid Manifestations

Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,1-3 reactive arthritis,4 disseminated histoplasmosis,5 keratotic scabies,6 secondary syphilis,7 and photosensitive skin lesions in association with aminoaciduria.8 To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.1 Although most cases of rupioid psoriasis were associated with psoriatic arthritis,3 our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.4 A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.5 Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.7

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.9 For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab3 have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.2

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

References

1. Christensen TE, Callis KP, Papenfuss J, et al. Observations of psoriasis in the absence of therapeutic intervention identifies two unappreciated morphologic variants, thin-plaque and thick-plaque psoriasis, and their associated phenotypes. J Invest Dermatol. 2006;126:2397-2403.

2. Feldman SR, Brown KL, Heald P. ‘Coral reef’ psoriasis: a marker of resistance to topical treatment. J Dermatolog Treat. 2008;19:257-258.

3. Necas M, Vasku V. Ustekinumab in the treatment of severe rupioid psoriasis: a case report. Acta Dermatovenerol Alp Panonica Adriat. 2010;19:23-27.

4. Sehgal VN, Koranne RV, Shyam Prasad AL. Unusual manifestations of Reiter’s disease in a child. Dermatologica. 1985;170:77-79.

5. Corti M, Villafañe MF, Palmieri O, et al. Rupioid histoplasmosis: first case reported in an AIDS patient in Argentina. Rev Inst Med Trop Sao Paulo. 2010;52:279-280.

6. Costa JB, Rocha de Sousa VL, da Trindade Neto PB, et al. Norwegian scabies mimicking rupioid psoriasis. An Bras Dermatol. 2012;87:910-913.

7. Bhagwat PV, Tophakhane RS, Rathod RM, et al. Rupioid syphilis in an HIV patient. Indian J Dermatol Venereol. 2009;75:201-202.

8. Haim S, Gilhar A, Cohen A. Cutaneous manifestations associated with aminoaciduria. report of two cases. Dermatologica. 1978;156:244-250.

9. Murakami T, Ohtsuki M, Nakagawa H. Rupioid psoriasis with arthropathy. Clin Exp Dermatol. 2000;25:409-412.

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Hye Jin Chung, MD; Daria Marley-Kemp, MEd, BS; Matthew Keller, MD

Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania. Ms. Marley-Kemp is from Jefferson Medical College, Philadelphia.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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rupioid manifestations, rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, photosensitive skin lesions, aminoaciduria, plaque psoriasis
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Hye Jin Chung, MD; Daria Marley-Kemp, MEd, BS; Matthew Keller, MD

Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania. Ms. Marley-Kemp is from Jefferson Medical College, Philadelphia.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

Author and Disclosure Information

Hye Jin Chung, MD; Daria Marley-Kemp, MEd, BS; Matthew Keller, MD

Drs. Chung and Keller are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, Pennsylvania. Ms. Marley-Kemp is from Jefferson Medical College, Philadelphia.

The authors report no conflict of interest.

Correspondence: Matthew Keller, MD, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,1-3 reactive arthritis,4 disseminated histoplasmosis,5 keratotic scabies,6 secondary syphilis,7 and photosensitive skin lesions in association with aminoaciduria.8 To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.1 Although most cases of rupioid psoriasis were associated with psoriatic arthritis,3 our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.4 A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.5 Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.7

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.9 For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab3 have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.2

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

Case Report

A 28-year-old man presented to the dermatology department with cone-shaped, oyster shell–like skin lesions on the scalp, trunk, arms, and legs of 1 month’s duration. He denied any fever, pruritus, pain, joint stiffness, or arthralgia. His family history was remarkable for psoriasis in his paternal grandfather and uncle.

A few years prior to the eruption, the patient developed a rash in the bilateral inguinal area but did not seek medical attention. One month prior to presentation, the rash began to spread to the scalp, trunk, arms, and legs. He was treated in the emergency department with a 5-day course of oral prednisone without any noticeable improvement. At the time of presentation to the dermatology clinic, he was found to have multiple well-demarcated erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crusts (Figure 1). Rapid plasma reagin testing was negative. A 4-mm punch biopsy specimen from the right upper arm demonstrated thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (Figure 2). In the stratum corneum, there was seroexudate with numerous red blood cells between the parakeratosis.

Figure 1. Multiple well-demarcated erythematous plaques with hyperkeratotic crust on the back (A). Closer view of erythematous plaques with conical, oyster shell–like, dirty-appearing, hyperkeratotic crust (B).

Figure 2. Thick parakeratosis with a remarkable Munro microabscess, regular psoriasiform acanthosis with thin suprapapillary epidermal plates, absent granular layer, and prominent papillary dermal edema (H&E, original magnification ×100).

The patient was diagnosed with rupioid psoriasis. The lesions dramatically improved with methotrexate 10 mg weekly and topical steroids. Two months following diagnosis the patient presented with persistent hyperkeratotic lesions on the back, as he had difficulty reaching the lesions to apply topical medications; intralesional steroid injections were added. This regimen resulted in near-complete resolution maintained at his most recent follow-up 2 years following diagnosis in our clinic.

Comment

Rupia is based on the Greek word rhupos, which means dirt or filth. The term rupioid has been used to describe well-demarcated, cone-shaped plaques with thick, dark, lamellate, and adherent crusts on the skin somewhat resembling oyster or limpet shells. Histologically, a serosanguineous exudate along with thick skin helps to impart a “dirty” appearance to rupioid lesions. Rupioid manifestations have been clinically observed in a variety of diseases, including rupioid psoriasis,1-3 reactive arthritis,4 disseminated histoplasmosis,5 keratotic scabies,6 secondary syphilis,7 and photosensitive skin lesions in association with aminoaciduria.8 To diagnose the underlying infectious or inflammatory diseases beneath the thick crusts, skin biopsy and a blood test for syphilis may be necessary.

Rupioid psoriasis is a morphologic subtype of plaque psoriasis with hyperkeratotic lesions that resemble an oyster or limpet shell. Patients with thick plaque psoriasis are more likely to be male with a higher incidence of nail disease and psoriatic arthritis as well as a greater body surface area affected than patients with thin plaque psoriasis.1 Although most cases of rupioid psoriasis were associated with psoriatic arthritis,3 our patient showed no evidence of psoriatic arthritis or nail changes.

Reactive arthritis may have a similar appearance to rupioid psoriasis but may be distinguished by a geographic relief map configuration with coalescing, keratotic and desquamating lesions, as well as associated urethritis, arthritis, and conjunctivitis.4 A rupioid eruption was reported as a manifestation of disseminated histoplasmosis with dirty-appearing, heaped-up, crusted lesions present on the cheeks, nose, and forehead on clinical examination and several intracellular and extracellular oval structures on histologic examination with periodic acid–Schiff and Gomori methenamine-silver stain.5 Malignant or rupioid syphilis refers to the stage in which papulopustules of pustular syphilis undergo central necrosis due to endarteritis obliterans and intravascular thrombosis.7

In our case, the patient’s psoriasis could have flared after discontinuation of the prednisone that was administered by the emergency department physician. Most cases have been treated with combined systemic and topical therapy.9 For systemic treatment, cyclosporine, intramuscular or oral methotrexate, adalimumab, and ustekinumab3 have been used with remarkable improvement. Hyperkeratotic types of psoriasis are generally thought to be resistant to topical therapy because of poor penetration of applied agents; however, a case of rupioid psoriasis without arthritis was successfully treated with topical steroids without concomitant systemic medications.2

Conclusion

Rupioid psoriasis is a morphological subtype of plaque psoriasis with hyperkeratotic lesions that resemble a limpet shell. Rupioid skin manifestations may be seen in a variety of diseases including rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria. Diagnosis of rupioid psoriasis often requires additional testing such as skin biopsy, skin scraping, and blood tests, and it typically requires systemic therapy for treatment.

References

1. Christensen TE, Callis KP, Papenfuss J, et al. Observations of psoriasis in the absence of therapeutic intervention identifies two unappreciated morphologic variants, thin-plaque and thick-plaque psoriasis, and their associated phenotypes. J Invest Dermatol. 2006;126:2397-2403.

2. Feldman SR, Brown KL, Heald P. ‘Coral reef’ psoriasis: a marker of resistance to topical treatment. J Dermatolog Treat. 2008;19:257-258.

3. Necas M, Vasku V. Ustekinumab in the treatment of severe rupioid psoriasis: a case report. Acta Dermatovenerol Alp Panonica Adriat. 2010;19:23-27.

4. Sehgal VN, Koranne RV, Shyam Prasad AL. Unusual manifestations of Reiter’s disease in a child. Dermatologica. 1985;170:77-79.

5. Corti M, Villafañe MF, Palmieri O, et al. Rupioid histoplasmosis: first case reported in an AIDS patient in Argentina. Rev Inst Med Trop Sao Paulo. 2010;52:279-280.

6. Costa JB, Rocha de Sousa VL, da Trindade Neto PB, et al. Norwegian scabies mimicking rupioid psoriasis. An Bras Dermatol. 2012;87:910-913.

7. Bhagwat PV, Tophakhane RS, Rathod RM, et al. Rupioid syphilis in an HIV patient. Indian J Dermatol Venereol. 2009;75:201-202.

8. Haim S, Gilhar A, Cohen A. Cutaneous manifestations associated with aminoaciduria. report of two cases. Dermatologica. 1978;156:244-250.

9. Murakami T, Ohtsuki M, Nakagawa H. Rupioid psoriasis with arthropathy. Clin Exp Dermatol. 2000;25:409-412.

References

1. Christensen TE, Callis KP, Papenfuss J, et al. Observations of psoriasis in the absence of therapeutic intervention identifies two unappreciated morphologic variants, thin-plaque and thick-plaque psoriasis, and their associated phenotypes. J Invest Dermatol. 2006;126:2397-2403.

2. Feldman SR, Brown KL, Heald P. ‘Coral reef’ psoriasis: a marker of resistance to topical treatment. J Dermatolog Treat. 2008;19:257-258.

3. Necas M, Vasku V. Ustekinumab in the treatment of severe rupioid psoriasis: a case report. Acta Dermatovenerol Alp Panonica Adriat. 2010;19:23-27.

4. Sehgal VN, Koranne RV, Shyam Prasad AL. Unusual manifestations of Reiter’s disease in a child. Dermatologica. 1985;170:77-79.

5. Corti M, Villafañe MF, Palmieri O, et al. Rupioid histoplasmosis: first case reported in an AIDS patient in Argentina. Rev Inst Med Trop Sao Paulo. 2010;52:279-280.

6. Costa JB, Rocha de Sousa VL, da Trindade Neto PB, et al. Norwegian scabies mimicking rupioid psoriasis. An Bras Dermatol. 2012;87:910-913.

7. Bhagwat PV, Tophakhane RS, Rathod RM, et al. Rupioid syphilis in an HIV patient. Indian J Dermatol Venereol. 2009;75:201-202.

8. Haim S, Gilhar A, Cohen A. Cutaneous manifestations associated with aminoaciduria. report of two cases. Dermatologica. 1978;156:244-250.

9. Murakami T, Ohtsuki M, Nakagawa H. Rupioid psoriasis with arthropathy. Clin Exp Dermatol. 2000;25:409-412.

Issue
Cutis - 94(3)
Issue
Cutis - 94(3)
Page Number
119-121
Page Number
119-121
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Rupioid Psoriasis and Other Skin Diseases With Rupioid Manifestations
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Rupioid Psoriasis and Other Skin Diseases With Rupioid Manifestations
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rupioid manifestations, rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, photosensitive skin lesions, aminoaciduria, plaque psoriasis
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rupioid manifestations, rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, photosensitive skin lesions, aminoaciduria, plaque psoriasis
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Practice Points

  • ­Diseases with rupioid manifestations include rupioid psoriasis, reactive arthritis, disseminated histoplasmosis, keratotic scabies, secondary syphilis, and photosensitive skin lesions associated with aminoaciduria.
  • ­Skin biopsy, skin scraping, and blood tests may be necessary to diagnose the underlying diseases beneath the thick crusts and to rule out other diagnoses within the differential.
  • ­Treatment of rupioid psoriasis is no different than typical plaque psoriasis, except for the need for systemic therapy in most cases due to the thick scale.
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