Characterization of Blood-borne Pathogen Exposures During Dermatologic Procedures: The Mayo Clinic Experience

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Characterization of Blood-borne Pathogen Exposures During Dermatologic Procedures: The Mayo Clinic Experience

Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.

To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.

Methods

Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as any percutaneous injury or mucosal exposure with foreign blood, tissue, or other bodily fluids that placed the health care worker at risk for communicable infections. Secondary aims included identification of the type of exposure, type of procedure associated with each exposure, common anatomic locations of exposures, and common instruments involved in each exposure.

Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).

Results

Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).

Incident Type by Occupational Group

Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.

Incident Details by Occupational Group

Incident Details by Occupational Group

Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.

 

 

The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.

Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).

Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.

Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).

Comment

In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1

Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.

The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.

Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.

Conclusion

This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.

References
  1. Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
  2. Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
  3. Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
  4. Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
  5. Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
  6. Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
  7. Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
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Author and Disclosure Information

Drs. Janeczek, Hoss, Fathi, and Ochoa are from the Department of Dermatology, Mayo Clinic, Scottsdale, Arizona. Ms. Shimshak is from the Mayo Clinic Alix School of Medicine, Scottsdale. Mr. Butterfield is from the Department of Health Sciences Research, Mayo Clinic, Scottsdale.

The authors report no conflict of interest.

The eTable is available in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Monica Janeczek, MD, Department of Dermatology, Mayo Clinic, 13400 East Shea Blvd, Scottsdale, AZ 85259 ([email protected]).

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Drs. Janeczek, Hoss, Fathi, and Ochoa are from the Department of Dermatology, Mayo Clinic, Scottsdale, Arizona. Ms. Shimshak is from the Mayo Clinic Alix School of Medicine, Scottsdale. Mr. Butterfield is from the Department of Health Sciences Research, Mayo Clinic, Scottsdale.

The authors report no conflict of interest.

The eTable is available in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Monica Janeczek, MD, Department of Dermatology, Mayo Clinic, 13400 East Shea Blvd, Scottsdale, AZ 85259 ([email protected]).

Author and Disclosure Information

Drs. Janeczek, Hoss, Fathi, and Ochoa are from the Department of Dermatology, Mayo Clinic, Scottsdale, Arizona. Ms. Shimshak is from the Mayo Clinic Alix School of Medicine, Scottsdale. Mr. Butterfield is from the Department of Health Sciences Research, Mayo Clinic, Scottsdale.

The authors report no conflict of interest.

The eTable is available in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Monica Janeczek, MD, Department of Dermatology, Mayo Clinic, 13400 East Shea Blvd, Scottsdale, AZ 85259 ([email protected]).

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Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.

To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.

Methods

Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as any percutaneous injury or mucosal exposure with foreign blood, tissue, or other bodily fluids that placed the health care worker at risk for communicable infections. Secondary aims included identification of the type of exposure, type of procedure associated with each exposure, common anatomic locations of exposures, and common instruments involved in each exposure.

Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).

Results

Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).

Incident Type by Occupational Group

Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.

Incident Details by Occupational Group

Incident Details by Occupational Group

Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.

 

 

The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.

Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).

Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.

Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).

Comment

In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1

Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.

The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.

Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.

Conclusion

This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.

Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.

To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.

Methods

Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as any percutaneous injury or mucosal exposure with foreign blood, tissue, or other bodily fluids that placed the health care worker at risk for communicable infections. Secondary aims included identification of the type of exposure, type of procedure associated with each exposure, common anatomic locations of exposures, and common instruments involved in each exposure.

Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).

Results

Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).

Incident Type by Occupational Group

Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.

Incident Details by Occupational Group

Incident Details by Occupational Group

Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.

 

 

The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.

Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).

Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.

Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).

Comment

In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1

Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.

The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.

Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.

Conclusion

This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.

References
  1. Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
  2. Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
  3. Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
  4. Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
  5. Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
  6. Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
  7. Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
References
  1. Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
  2. Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
  3. Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
  4. Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
  5. Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
  6. Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
  7. Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
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  • Most blood-borne pathogen (BBP) exposures in dermatologic staff occur due to medical sharps as opposed to splash incidents.
  • The most common implicated task in resident physicians and practicing dermatologists is suturing or assisting with suturing, and the most commonly associated instrument is the suture needle. In contrast, ancillary staff experience most BBP exposures during handling of sharps, wires, or instruments, and the injection syringe/needle is the most common instrument of injury.
  • Quality improvement measures are needed in prevention of BBP exposures and should focus on identified risk factors among occupational groups in the workplace.
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Flagellate Shiitake Mushroom Reaction With Histologic Features of Acute Generalized Exanthematous Pustulosis

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Flagellate Shiitake Mushroom Reaction With Histologic Features of Acute Generalized Exanthematous Pustulosis

To the Editor:

A 59-year-old man presented with a severely pruritic rash on the legs, arms, abdomen, groin, and buttocks of 3 days’ duration. He reported subjective fever and chills. Prior to the appearance of the rash, the patient and his family had eaten shiitake mushrooms daily for 3 days. He denied any new medications in the last several months or any recent upper respiratory or gastrointestinal tract illnesses. His medical history included type 2 diabetes mellitus and diabetes-induced end-stage renal disease requiring home peritoneal dialysis. His long-term medications for diabetes mellitus, hypertension, benign prostatic hyperplasia, hyperlipidemia, and insomnia included amlodipine, atorvastatin, finasteride, gabapentin, insulin glargine, linagliptin, metoprolol, and mirtazapine.

Physical examination revealed an afebrile man with medium brown skin tone and diffuse, bright red, erythematous patches on the lower legs, axillae, medial forearms, lateral trunk, lower abdomen, and groin. There were distinct flagellate, linear, red patches on the lower legs (Figure 1). In addition, small clusters of 1- to 2-mm superficial pustules were present on the right upper medial thigh and left forearm with micropapules grouped in the skin folds.

FIGURE 1. Linear, whiplike, red, crisscrossed patches on the lower legs consistent with flagellate dermatitis.

A shave biopsy specimen from a pustule on the right upper medial thigh revealed spongiotic dermatitis with neutrophilic subcorneal pustule formation and frequent eosinophils (Figure 2). The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (Figure 3). These histologic findings were consistent with acute generalized exanthematous pustulosis (AGEP). No biopsy was performed on the flagellate patches due to its clinically distinct presentation and well-established association with shiitake mushroom ingestion.

FIGURE 2. Bright red erythematous patch showing the location of biopsied pustule.

The patient was treated with triamcinolone ointment and systemic corticosteroids to reduce pruritus and quickly clear the lesions due to his comorbidities. He recovered completely within 1 week and had no evidence of postinflammatory hyperpigmentation from the flagellate dermatitis.

FIGURE 3. A shave biopsy of the right medial thigh showed spongiotic dermatitis with neutrophilic-predominant subcorneal pustule formation and frequent eosinophils. The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (H&E, original magnification ×10).

Flagellate dermatitis is an intensely pruritic dermatitis characterized by 1-mm, disseminated, erythematous papules in a linear grouped arrangement secondary to koebnerization due to the patient scratching. It was first described in 1977 by Nakamura.1 Although it rarely is seen outside of China and Japan, there are well-established associations of flagellate dermatitis with bleomycin and shiitake mushroom (Lentinula edodes) ingestion. One key clinical difference between the two causes is that postinflammatory hyperpigmentation changes usually are seen with bleomycin-induced flagellate dermatitis and typically are not present with shiitake mushroom–induced flagellate dermatitis.2 Following ingestion of shiitake mushrooms, the median time of onset of presentation typically is 24 hours but ranges from 12 hours to 5 days. Most patients completely recover by 3 weeks, with or without treatment.3 Although the pathogenesis of shiitake mushroom–induced flagellate dermatitis is not clear, the most common theory is a toxic reaction to lentinan, a polysaccharide isolated from shiitake mushrooms. However, type I and IV allergic hypersensitivities also have been supported by the time of onset, clearance, severe pruritus, benefit from steroids and antihistamines, and lack of grouped outbreaks in people exposed to shared meals containing shiitake mushrooms.3,4 Furthermore, there is a case of patch test–confirmed allergic contact dermatitis to shiitake mushrooms, demonstrating a 1+ reaction at 96 hours to the cap of a shiitake mushroom but a negative pin-prick test at 20 minutes, suggesting type IV hypersensitivity.5 An additional case revealed a positive skin-prick test with formation of a 4-mm wheal and subsequent pruritic papules and vesicles appearing 48 to 72 hours later at the prick site.6 Subsequent cases have been reported in association with consumption of raw shiitake mushrooms, but cases have been reported after consumption of fully cooked mushrooms, which does not support a toxin-mediated theory, as cooking the mushroom before consumption likely would denature or change the structure of the suspected toxin.2

Acute generalized exanthematous pustulosis is a rare eruption that occurs due to ingestion of a causative agent, usually an antibiotic, and is characterized by the presence of fever and disseminated, erythematous, pinpoint, sterile pustules on the skin and mucous membranes. It affects 1 to 5 persons per million per year, with more than 90% of cases attributed to drug ingestion.7 Spontaneous resolution can be expected within 15 days of its onset; however, there is a mortality rate of up to 5% that occurs most often in those with severe comorbidities or in older patients, for whom systemic corticosteroid therapy may be justified.7,8 A multinational case-control study conducted to evaluate the risk of AGEP associated with certain drugs revealed macrolides (namely pristinamycin); β-lactam antibiotics including penicillin, aminopenicillin, and cephalosporin; quinolones; hydroxychloroquine; anti-infective sulfonamides; terbinafine; and diltiazem as the most strongly associated culprits.9 Our patient’s flagellate dermatitis was unique in that it also showed histologic features of AGEP. The pathogenesis of drug-induced AGEP has been partially elucidated and involves activation of drug-specific CD4+ and CD8+ T cells that migrate to the skin and participate in apoptotic signaling of keratinocytes and recruitment of neutrophils and eosinophils, which form subcorneal sterile pustules.7 In a study of severe cutaneous adverse drug reactions, 50% (7/14) of patients with AGEP had positive patch tests to the causative agent.10 This T cell–dependent response explains why the condition responds to systemic corticosteroids. Additionally, our case report of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP suggests that the pathogenesis of flagellate dermatitis may be a T cell–mediated type IV hypersensitivity reaction. The time of onset, lack of grouped outbreaks in those sharing shiitake mushroom–containing meals, severe pruritus, lack of cases demonstrating an anaphylactic or wheal and flare response, benefit of steroids, and a case with histologic features of AGEP all lend support to this theory.

We report a case of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP. The time course, histologic features of AGEP, absence of new medications, and resolution with discontinuation of shiitake mushrooms lends support of the hypothesis that the pathogenesis of shiitake mushroom–induced flagellate dermatitis is similar to AGEP’s type IV hypersensitivity reaction. To further elucidate its pathogenesis, skin prick testing and patch testing with shiitake mushrooms in patients exhibiting shiitake mushroom–induced flagellate dermatitis may prove to be beneficial.

References
  1. Nakamura T. Toxicoderma caused by shiitake (Lentinus edodes)[in Japanese]. Jpn J Clin Dermatol. 1977;31:65-68.
  2. Chu EY, Anand D, Dawn A, et al. Shiitake dermatitis: a report of 3 cases and review of the literature. Cutis. 2013;91:287-290.
  3. Boels D, Landreau A, Bruneau C, et al. Shiitake dermatitis recorded by French Poison Control Centers—new case series with clinical observations. Clin Toxicol (Phila). 2014;52:625-628.
  4. Nakamura T. Shiitake (Lentinus edodes) dermatitis. Contact Dermatitis. 1992;27:65-70.
  5. Curnow P, Tam M. Contact dermatitis to shiitake mushroom. Australas J Dermatol. 2003;44:155-157.
  6. Lippert U, Martin V, Schwertfeger C, et al. Shiitake dermatitis. Br J Dermatol. 2003;148:178-179.
  7. Fernando SL. Acute generalised exanthematous pustulosis. Australas J Dermatol. 2012;53:87-92.
  8. Sidoroff A, Halevy S, Bavinck JN, et al. Acute generalized exanthematous pustulosis (AGEP)—a clinical reaction pattern. J Cutan Pathol. 2001;28:113-119.
  9. Sidoroff A, Dunant A, Viboud C, et al. Risk factors for acute generalized exanthematous pustulosis (AGEP)—results of a multinational case-control study (EuroSCAR). Br J Dermatol. 2007;157:989-996.
  10. Wolkenstein P, Chosidow O, Flechet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
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Dr. Browning is from Presbyterian St. Luke’s Medical Center, Denver, Colorado. Drs. Fathi, Smith, and Alkousakis are from the Department of Dermatology, University of Colorado Denver School of Medicine, Aurora.

The authors report no conflict of interest.

Correspondence: Richard J. Browning, MD, UCHealth Medical Group, 100 Cook St, Denver, CO 80203 ([email protected]).

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Correspondence: Richard J. Browning, MD, UCHealth Medical Group, 100 Cook St, Denver, CO 80203 ([email protected]).

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Correspondence: Richard J. Browning, MD, UCHealth Medical Group, 100 Cook St, Denver, CO 80203 ([email protected]).

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To the Editor:

A 59-year-old man presented with a severely pruritic rash on the legs, arms, abdomen, groin, and buttocks of 3 days’ duration. He reported subjective fever and chills. Prior to the appearance of the rash, the patient and his family had eaten shiitake mushrooms daily for 3 days. He denied any new medications in the last several months or any recent upper respiratory or gastrointestinal tract illnesses. His medical history included type 2 diabetes mellitus and diabetes-induced end-stage renal disease requiring home peritoneal dialysis. His long-term medications for diabetes mellitus, hypertension, benign prostatic hyperplasia, hyperlipidemia, and insomnia included amlodipine, atorvastatin, finasteride, gabapentin, insulin glargine, linagliptin, metoprolol, and mirtazapine.

Physical examination revealed an afebrile man with medium brown skin tone and diffuse, bright red, erythematous patches on the lower legs, axillae, medial forearms, lateral trunk, lower abdomen, and groin. There were distinct flagellate, linear, red patches on the lower legs (Figure 1). In addition, small clusters of 1- to 2-mm superficial pustules were present on the right upper medial thigh and left forearm with micropapules grouped in the skin folds.

FIGURE 1. Linear, whiplike, red, crisscrossed patches on the lower legs consistent with flagellate dermatitis.

A shave biopsy specimen from a pustule on the right upper medial thigh revealed spongiotic dermatitis with neutrophilic subcorneal pustule formation and frequent eosinophils (Figure 2). The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (Figure 3). These histologic findings were consistent with acute generalized exanthematous pustulosis (AGEP). No biopsy was performed on the flagellate patches due to its clinically distinct presentation and well-established association with shiitake mushroom ingestion.

FIGURE 2. Bright red erythematous patch showing the location of biopsied pustule.

The patient was treated with triamcinolone ointment and systemic corticosteroids to reduce pruritus and quickly clear the lesions due to his comorbidities. He recovered completely within 1 week and had no evidence of postinflammatory hyperpigmentation from the flagellate dermatitis.

FIGURE 3. A shave biopsy of the right medial thigh showed spongiotic dermatitis with neutrophilic-predominant subcorneal pustule formation and frequent eosinophils. The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (H&E, original magnification ×10).

Flagellate dermatitis is an intensely pruritic dermatitis characterized by 1-mm, disseminated, erythematous papules in a linear grouped arrangement secondary to koebnerization due to the patient scratching. It was first described in 1977 by Nakamura.1 Although it rarely is seen outside of China and Japan, there are well-established associations of flagellate dermatitis with bleomycin and shiitake mushroom (Lentinula edodes) ingestion. One key clinical difference between the two causes is that postinflammatory hyperpigmentation changes usually are seen with bleomycin-induced flagellate dermatitis and typically are not present with shiitake mushroom–induced flagellate dermatitis.2 Following ingestion of shiitake mushrooms, the median time of onset of presentation typically is 24 hours but ranges from 12 hours to 5 days. Most patients completely recover by 3 weeks, with or without treatment.3 Although the pathogenesis of shiitake mushroom–induced flagellate dermatitis is not clear, the most common theory is a toxic reaction to lentinan, a polysaccharide isolated from shiitake mushrooms. However, type I and IV allergic hypersensitivities also have been supported by the time of onset, clearance, severe pruritus, benefit from steroids and antihistamines, and lack of grouped outbreaks in people exposed to shared meals containing shiitake mushrooms.3,4 Furthermore, there is a case of patch test–confirmed allergic contact dermatitis to shiitake mushrooms, demonstrating a 1+ reaction at 96 hours to the cap of a shiitake mushroom but a negative pin-prick test at 20 minutes, suggesting type IV hypersensitivity.5 An additional case revealed a positive skin-prick test with formation of a 4-mm wheal and subsequent pruritic papules and vesicles appearing 48 to 72 hours later at the prick site.6 Subsequent cases have been reported in association with consumption of raw shiitake mushrooms, but cases have been reported after consumption of fully cooked mushrooms, which does not support a toxin-mediated theory, as cooking the mushroom before consumption likely would denature or change the structure of the suspected toxin.2

Acute generalized exanthematous pustulosis is a rare eruption that occurs due to ingestion of a causative agent, usually an antibiotic, and is characterized by the presence of fever and disseminated, erythematous, pinpoint, sterile pustules on the skin and mucous membranes. It affects 1 to 5 persons per million per year, with more than 90% of cases attributed to drug ingestion.7 Spontaneous resolution can be expected within 15 days of its onset; however, there is a mortality rate of up to 5% that occurs most often in those with severe comorbidities or in older patients, for whom systemic corticosteroid therapy may be justified.7,8 A multinational case-control study conducted to evaluate the risk of AGEP associated with certain drugs revealed macrolides (namely pristinamycin); β-lactam antibiotics including penicillin, aminopenicillin, and cephalosporin; quinolones; hydroxychloroquine; anti-infective sulfonamides; terbinafine; and diltiazem as the most strongly associated culprits.9 Our patient’s flagellate dermatitis was unique in that it also showed histologic features of AGEP. The pathogenesis of drug-induced AGEP has been partially elucidated and involves activation of drug-specific CD4+ and CD8+ T cells that migrate to the skin and participate in apoptotic signaling of keratinocytes and recruitment of neutrophils and eosinophils, which form subcorneal sterile pustules.7 In a study of severe cutaneous adverse drug reactions, 50% (7/14) of patients with AGEP had positive patch tests to the causative agent.10 This T cell–dependent response explains why the condition responds to systemic corticosteroids. Additionally, our case report of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP suggests that the pathogenesis of flagellate dermatitis may be a T cell–mediated type IV hypersensitivity reaction. The time of onset, lack of grouped outbreaks in those sharing shiitake mushroom–containing meals, severe pruritus, lack of cases demonstrating an anaphylactic or wheal and flare response, benefit of steroids, and a case with histologic features of AGEP all lend support to this theory.

We report a case of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP. The time course, histologic features of AGEP, absence of new medications, and resolution with discontinuation of shiitake mushrooms lends support of the hypothesis that the pathogenesis of shiitake mushroom–induced flagellate dermatitis is similar to AGEP’s type IV hypersensitivity reaction. To further elucidate its pathogenesis, skin prick testing and patch testing with shiitake mushrooms in patients exhibiting shiitake mushroom–induced flagellate dermatitis may prove to be beneficial.

To the Editor:

A 59-year-old man presented with a severely pruritic rash on the legs, arms, abdomen, groin, and buttocks of 3 days’ duration. He reported subjective fever and chills. Prior to the appearance of the rash, the patient and his family had eaten shiitake mushrooms daily for 3 days. He denied any new medications in the last several months or any recent upper respiratory or gastrointestinal tract illnesses. His medical history included type 2 diabetes mellitus and diabetes-induced end-stage renal disease requiring home peritoneal dialysis. His long-term medications for diabetes mellitus, hypertension, benign prostatic hyperplasia, hyperlipidemia, and insomnia included amlodipine, atorvastatin, finasteride, gabapentin, insulin glargine, linagliptin, metoprolol, and mirtazapine.

Physical examination revealed an afebrile man with medium brown skin tone and diffuse, bright red, erythematous patches on the lower legs, axillae, medial forearms, lateral trunk, lower abdomen, and groin. There were distinct flagellate, linear, red patches on the lower legs (Figure 1). In addition, small clusters of 1- to 2-mm superficial pustules were present on the right upper medial thigh and left forearm with micropapules grouped in the skin folds.

FIGURE 1. Linear, whiplike, red, crisscrossed patches on the lower legs consistent with flagellate dermatitis.

A shave biopsy specimen from a pustule on the right upper medial thigh revealed spongiotic dermatitis with neutrophilic subcorneal pustule formation and frequent eosinophils (Figure 2). The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (Figure 3). These histologic findings were consistent with acute generalized exanthematous pustulosis (AGEP). No biopsy was performed on the flagellate patches due to its clinically distinct presentation and well-established association with shiitake mushroom ingestion.

FIGURE 2. Bright red erythematous patch showing the location of biopsied pustule.

The patient was treated with triamcinolone ointment and systemic corticosteroids to reduce pruritus and quickly clear the lesions due to his comorbidities. He recovered completely within 1 week and had no evidence of postinflammatory hyperpigmentation from the flagellate dermatitis.

FIGURE 3. A shave biopsy of the right medial thigh showed spongiotic dermatitis with neutrophilic-predominant subcorneal pustule formation and frequent eosinophils. The dermis contained scattered mixed inflammatory cells including neutrophils, eosinophils, lymphocytes, and histiocytes (H&E, original magnification ×10).

Flagellate dermatitis is an intensely pruritic dermatitis characterized by 1-mm, disseminated, erythematous papules in a linear grouped arrangement secondary to koebnerization due to the patient scratching. It was first described in 1977 by Nakamura.1 Although it rarely is seen outside of China and Japan, there are well-established associations of flagellate dermatitis with bleomycin and shiitake mushroom (Lentinula edodes) ingestion. One key clinical difference between the two causes is that postinflammatory hyperpigmentation changes usually are seen with bleomycin-induced flagellate dermatitis and typically are not present with shiitake mushroom–induced flagellate dermatitis.2 Following ingestion of shiitake mushrooms, the median time of onset of presentation typically is 24 hours but ranges from 12 hours to 5 days. Most patients completely recover by 3 weeks, with or without treatment.3 Although the pathogenesis of shiitake mushroom–induced flagellate dermatitis is not clear, the most common theory is a toxic reaction to lentinan, a polysaccharide isolated from shiitake mushrooms. However, type I and IV allergic hypersensitivities also have been supported by the time of onset, clearance, severe pruritus, benefit from steroids and antihistamines, and lack of grouped outbreaks in people exposed to shared meals containing shiitake mushrooms.3,4 Furthermore, there is a case of patch test–confirmed allergic contact dermatitis to shiitake mushrooms, demonstrating a 1+ reaction at 96 hours to the cap of a shiitake mushroom but a negative pin-prick test at 20 minutes, suggesting type IV hypersensitivity.5 An additional case revealed a positive skin-prick test with formation of a 4-mm wheal and subsequent pruritic papules and vesicles appearing 48 to 72 hours later at the prick site.6 Subsequent cases have been reported in association with consumption of raw shiitake mushrooms, but cases have been reported after consumption of fully cooked mushrooms, which does not support a toxin-mediated theory, as cooking the mushroom before consumption likely would denature or change the structure of the suspected toxin.2

Acute generalized exanthematous pustulosis is a rare eruption that occurs due to ingestion of a causative agent, usually an antibiotic, and is characterized by the presence of fever and disseminated, erythematous, pinpoint, sterile pustules on the skin and mucous membranes. It affects 1 to 5 persons per million per year, with more than 90% of cases attributed to drug ingestion.7 Spontaneous resolution can be expected within 15 days of its onset; however, there is a mortality rate of up to 5% that occurs most often in those with severe comorbidities or in older patients, for whom systemic corticosteroid therapy may be justified.7,8 A multinational case-control study conducted to evaluate the risk of AGEP associated with certain drugs revealed macrolides (namely pristinamycin); β-lactam antibiotics including penicillin, aminopenicillin, and cephalosporin; quinolones; hydroxychloroquine; anti-infective sulfonamides; terbinafine; and diltiazem as the most strongly associated culprits.9 Our patient’s flagellate dermatitis was unique in that it also showed histologic features of AGEP. The pathogenesis of drug-induced AGEP has been partially elucidated and involves activation of drug-specific CD4+ and CD8+ T cells that migrate to the skin and participate in apoptotic signaling of keratinocytes and recruitment of neutrophils and eosinophils, which form subcorneal sterile pustules.7 In a study of severe cutaneous adverse drug reactions, 50% (7/14) of patients with AGEP had positive patch tests to the causative agent.10 This T cell–dependent response explains why the condition responds to systemic corticosteroids. Additionally, our case report of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP suggests that the pathogenesis of flagellate dermatitis may be a T cell–mediated type IV hypersensitivity reaction. The time of onset, lack of grouped outbreaks in those sharing shiitake mushroom–containing meals, severe pruritus, lack of cases demonstrating an anaphylactic or wheal and flare response, benefit of steroids, and a case with histologic features of AGEP all lend support to this theory.

We report a case of shiitake mushroom–induced flagellate dermatitis with histologic features of AGEP. The time course, histologic features of AGEP, absence of new medications, and resolution with discontinuation of shiitake mushrooms lends support of the hypothesis that the pathogenesis of shiitake mushroom–induced flagellate dermatitis is similar to AGEP’s type IV hypersensitivity reaction. To further elucidate its pathogenesis, skin prick testing and patch testing with shiitake mushrooms in patients exhibiting shiitake mushroom–induced flagellate dermatitis may prove to be beneficial.

References
  1. Nakamura T. Toxicoderma caused by shiitake (Lentinus edodes)[in Japanese]. Jpn J Clin Dermatol. 1977;31:65-68.
  2. Chu EY, Anand D, Dawn A, et al. Shiitake dermatitis: a report of 3 cases and review of the literature. Cutis. 2013;91:287-290.
  3. Boels D, Landreau A, Bruneau C, et al. Shiitake dermatitis recorded by French Poison Control Centers—new case series with clinical observations. Clin Toxicol (Phila). 2014;52:625-628.
  4. Nakamura T. Shiitake (Lentinus edodes) dermatitis. Contact Dermatitis. 1992;27:65-70.
  5. Curnow P, Tam M. Contact dermatitis to shiitake mushroom. Australas J Dermatol. 2003;44:155-157.
  6. Lippert U, Martin V, Schwertfeger C, et al. Shiitake dermatitis. Br J Dermatol. 2003;148:178-179.
  7. Fernando SL. Acute generalised exanthematous pustulosis. Australas J Dermatol. 2012;53:87-92.
  8. Sidoroff A, Halevy S, Bavinck JN, et al. Acute generalized exanthematous pustulosis (AGEP)—a clinical reaction pattern. J Cutan Pathol. 2001;28:113-119.
  9. Sidoroff A, Dunant A, Viboud C, et al. Risk factors for acute generalized exanthematous pustulosis (AGEP)—results of a multinational case-control study (EuroSCAR). Br J Dermatol. 2007;157:989-996.
  10. Wolkenstein P, Chosidow O, Flechet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
References
  1. Nakamura T. Toxicoderma caused by shiitake (Lentinus edodes)[in Japanese]. Jpn J Clin Dermatol. 1977;31:65-68.
  2. Chu EY, Anand D, Dawn A, et al. Shiitake dermatitis: a report of 3 cases and review of the literature. Cutis. 2013;91:287-290.
  3. Boels D, Landreau A, Bruneau C, et al. Shiitake dermatitis recorded by French Poison Control Centers—new case series with clinical observations. Clin Toxicol (Phila). 2014;52:625-628.
  4. Nakamura T. Shiitake (Lentinus edodes) dermatitis. Contact Dermatitis. 1992;27:65-70.
  5. Curnow P, Tam M. Contact dermatitis to shiitake mushroom. Australas J Dermatol. 2003;44:155-157.
  6. Lippert U, Martin V, Schwertfeger C, et al. Shiitake dermatitis. Br J Dermatol. 2003;148:178-179.
  7. Fernando SL. Acute generalised exanthematous pustulosis. Australas J Dermatol. 2012;53:87-92.
  8. Sidoroff A, Halevy S, Bavinck JN, et al. Acute generalized exanthematous pustulosis (AGEP)—a clinical reaction pattern. J Cutan Pathol. 2001;28:113-119.
  9. Sidoroff A, Dunant A, Viboud C, et al. Risk factors for acute generalized exanthematous pustulosis (AGEP)—results of a multinational case-control study (EuroSCAR). Br J Dermatol. 2007;157:989-996.
  10. Wolkenstein P, Chosidow O, Flechet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
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Practice Points

  • Ingestion of shiitake mushrooms and bleomycin is associated with flagellate dermatitis.
  • Acute generalized exanthematous pustulosis (AGEP) is a rare condition associated with certain drug ingestion.
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Cartilage Sutures for a Large Nasal Defect

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Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Figure 1. A and B, Surgical defect.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.1

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.2 An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Figure 2. Simple interrupted sutures placed into the nasal cartilage to narrow the nose.

Figure 3. Immediate postoperative appearance.

At 4-month follow-up, intralesional triamcinolone was injected into the slight induration at the right nasal tip. At 7-month follow-up, the patient was pleased with the cosmetic and functional result (Figure 4).

Figure 4. A and B, Postoperative follow-up at 7 months

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.5 Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).5 The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

References
  1. Smith JM, Orseth ML, Nijhawan RI. Reconstruction of large nasal dorsum defects. Dermatol Surg. 2018;44:1607-1610.
  2. Snow SN. Rotation flaps to reconstruct nasal tip defects following Mohs surgery. Dermatol Surg. 1997;23:916-919.
  3. Malone CH, Hays JP, Tausend WE, et al. Interdomal sutures for nasal tip refinement and reduced wound size. J Am Acad Dermatol. 2017;77:E107-E108.
  4. Pelster MW, Behshad R, Maher IA. Large nasal tip defects-utilization of interdomal sutures before Burow’s graft for optimization of nasal contour. Dermatol Surg. 2019;45:743-746.
  5. Gruber RP, Chang E, Buchanan E. Suture techniques in rhinoplasty. Clin Plast Surg. 2010;37:231-243.
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The authors report no conflict of interest.

Correspondence: Daniel Condie, MD, The Center for Dermatology and Plastic Surgery, 3530 S Val Vista Dr, Ste B-109, Gilbert, AZ 85297 ([email protected]).

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The authors report no conflict of interest.

Correspondence: Daniel Condie, MD, The Center for Dermatology and Plastic Surgery, 3530 S Val Vista Dr, Ste B-109, Gilbert, AZ 85297 ([email protected]).

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Dr. Condie is from The Center for Dermatology and Plastic Surgery, Gilbert, Arizona. Dr. Fathi is from Southwest Skin Specialists, Scottsdale, Arizona. Dr. Nijhawan is from the Department of Dermatology, University of Texas Southwestern Medical Center, Dallas.

The authors report no conflict of interest.

Correspondence: Daniel Condie, MD, The Center for Dermatology and Plastic Surgery, 3530 S Val Vista Dr, Ste B-109, Gilbert, AZ 85297 ([email protected]).

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Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Figure 1. A and B, Surgical defect.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.1

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.2 An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Figure 2. Simple interrupted sutures placed into the nasal cartilage to narrow the nose.

Figure 3. Immediate postoperative appearance.

At 4-month follow-up, intralesional triamcinolone was injected into the slight induration at the right nasal tip. At 7-month follow-up, the patient was pleased with the cosmetic and functional result (Figure 4).

Figure 4. A and B, Postoperative follow-up at 7 months

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.5 Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).5 The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

 

Practice Gap

A 69-year-old man underwent staged excision for an invasive melanoma (0.4-mm Breslow depth; stage Ia) of the right dorsal nose. Two stages were required to achieve clear margins, leaving a 3.0×2.5-cm defect involving the nasal dorsum, right nasal sidewall, and nasal supratip (Figure 1). He declined any multistage repair and preferred a full-thickness skin graft (FTSG) over any interpolation flap.

Figure 1. A and B, Surgical defect.

Given the size of our patient’s defect, primary repair was not possible and second intention healing may have resulted in a suboptimal cosmetic outcome, potential alar distortion, and prolonged healing. No single local flap, such as the dorsal nasal rotation flap, crescentic advancement flap, bilobed flap, and Rintala flap, would have provided adequate coverage. A FTSG of the entire defect would not have been an ideal tissue match, and given the limited surrounding laxity, a Burow FTSG would have required the linear repair to extend well into the forehead with a questionable cosmetic outcome.

The Technique

We opted to repair the defect using a combination of local flaps for a single-stage repair. Using the right cheek reservoir, a crescentic advancement flap was performed to restore the right nasal sidewall as best as possible with a standing cone taken superiorly. To execute this flap, an incision was made extending from the alar sulcus into the nasolabial fold while preserving the apical triangle of the upper cutaneous lip. The flap was elevated submuscularly on the nose, and broad undermining was performed in the subcutaneous plane of the medial cheek. A crescentic redundancy above the alar sulcus was excised, and periosteal tacking sutures were placed to both help advance the flap and to recreate the nasofacial sulcus.1

Next, a nasal tip spiral/rotation flap was designed to restore the remaining nasal defect.2 An incision was made at the right inferiormost aspect of the defect and extended along the inferior border of the nasal tip as it crossed the midline to the left side of the nose. After incising and elevating the flap in the submuscular plane, there was not enough of a tissue reservoir to cover the entire remaining nasal defect.

To resolve this intraoperative conundrum, simple interrupted sutures were placed into the nasal cartilage at midline to narrow the structure of the nose (Figure 2). Three 4-0 polyglactin 910 sutures were placed beginning with the upper lateral cartilages and extending inferiorly to the lower lateral cartilages. Narrowing the nasal cartilages allowed for a smaller residual defect. The nasal tip rotation flap was then spiraled into place with adequate coverage. Some of the flap tip was trimmed after the superior aspect of the rotation flap was sutured to the inferior edge of the crescentic advancement flap. The immediate postoperative appearance is shown in Figure 3.

Figure 2. Simple interrupted sutures placed into the nasal cartilage to narrow the nose.

Figure 3. Immediate postoperative appearance.

At 4-month follow-up, intralesional triamcinolone was injected into the slight induration at the right nasal tip. At 7-month follow-up, the patient was pleased with the cosmetic and functional result (Figure 4).

Figure 4. A and B, Postoperative follow-up at 7 months

Practice Implications

Cartilage sutures highlight an underutilized technique in nasal reconstruction, with few cases reported in the dermatologic surgery literature.3,4 The interdomal suture is placed through the left and right lower lateral cartilages to help narrow and redefine the nasal tip.5 Reported techniques include simple interrupted suture or horizontal mattress suture. Suture material for nasal cartilage may be permanent (nylon or polypropylene) or long-lasting (polydioxanone or polyglactin 910).5 The use of interdomal sutures has been reported to narrow and decrease the volume of nasal tip defects prior to repair with local flaps and FTSG.3,4 In addition to the interdomal suture of the lower lateral nasal cartilage, simple interrupted sutures were placed in the upper lateral cartilages that created an even smaller residual defect. Sutures of the nasal cartilage may be a good option for select patients in dermatologic reconstruction, allowing for a simple repair with the added benefit of improved cosmetic result.

A combination of local flaps may be used to repair large nasal defects involving multiple subunits, especially in patients who decline multistage reconstruction. A nasal tip rotation/spiral flap can be considered for the appropriate nasal tip defect. Suturing the nasal cartilage with either permanent or long-lasting suture can narrow the cartilage and facilitate flap coverage for nasal defects while also improving the appearance of patients with wide prominent lower noses.

References
  1. Smith JM, Orseth ML, Nijhawan RI. Reconstruction of large nasal dorsum defects. Dermatol Surg. 2018;44:1607-1610.
  2. Snow SN. Rotation flaps to reconstruct nasal tip defects following Mohs surgery. Dermatol Surg. 1997;23:916-919.
  3. Malone CH, Hays JP, Tausend WE, et al. Interdomal sutures for nasal tip refinement and reduced wound size. J Am Acad Dermatol. 2017;77:E107-E108.
  4. Pelster MW, Behshad R, Maher IA. Large nasal tip defects-utilization of interdomal sutures before Burow’s graft for optimization of nasal contour. Dermatol Surg. 2019;45:743-746.
  5. Gruber RP, Chang E, Buchanan E. Suture techniques in rhinoplasty. Clin Plast Surg. 2010;37:231-243.
References
  1. Smith JM, Orseth ML, Nijhawan RI. Reconstruction of large nasal dorsum defects. Dermatol Surg. 2018;44:1607-1610.
  2. Snow SN. Rotation flaps to reconstruct nasal tip defects following Mohs surgery. Dermatol Surg. 1997;23:916-919.
  3. Malone CH, Hays JP, Tausend WE, et al. Interdomal sutures for nasal tip refinement and reduced wound size. J Am Acad Dermatol. 2017;77:E107-E108.
  4. Pelster MW, Behshad R, Maher IA. Large nasal tip defects-utilization of interdomal sutures before Burow’s graft for optimization of nasal contour. Dermatol Surg. 2019;45:743-746.
  5. Gruber RP, Chang E, Buchanan E. Suture techniques in rhinoplasty. Clin Plast Surg. 2010;37:231-243.
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Scurvy Masquerading as Reactive Arthritis

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Scurvy Masquerading as Reactive Arthritis

To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
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The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

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The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

Author and Disclosure Information

Drs. Christopher and Fathi are from and Dr. Menachof was from the University of Colorado, Denver. Dr. Christopher is from the Department of Ophthalmology and Dr. Fathi is from the Department of Dermatology. Dr. Menachof currently is from The Indian Health Service, Rockville, Maryland.

The authors report no conflict of interest.

Correspondence: Karen L. Christopher, MD, 1675 Aurora Ct, F731, Aurora, CO 80045 ([email protected]).

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To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

To the Editor:

A 28-year-old recently homeless white man with a history of heroin abuse was admitted with a worsening rash and left ankle pain of 1 week’s duration, as well as subjective fever after 3 weeks of a productive cough, sore throat, hoarse voice, and general malaise. Six days prior to presentation, he developed redness and swelling of the dorsal aspects of both hands with accompanying rash, and 2 days prior to presentation he developed a similar rash on the legs with associated left ankle pain, redness, and swelling. He also reported eye redness, pain, photophobia, crusty eye discharge, and a pins and needles sensation on the soles of both feet. Additionally, he had noted difficulty with urination over several days. He had been homeless for less than 1 month prior to admission.

On physical examination, the patient appeared to be well nourished. Skin examination was notable for scattered perifollicular hemorrhagic and hyperkeratotic papules ranging in size from 3 to 6 mm with associated nummular alopecia of the bilateral medial thighs (Figure); well-demarcated desquamated patches on the weight-bearing aspects of the plantar feet; and a 2.0-cm, well-demarcated, thinly raised erythematous patch of the inferolateral penile shaft. Oral examination was notable for multiple discrete areas of ulceration on the lateral aspects of the tongue. Ophthalmic examination revealed conjunctival injection and photophobia. The ankles were edematous and tender (the left ankle more than the right), and range of passive motion was limited by pain.

A and B, Scattered perifollicular hemorrhagic and hyperkeratotic papules with associated alopecia on the thighs.


Laboratory values were remarkable for a hemoglobin count of 13.1 g/dL (reference range, 14.2–18 g/dL), erythrocyte sedimentation rate of 31 mm/h (reference range, 0–10 mm/h), and C-reactive protein level of 5.4 mg/dL (reference range, 0–0.8 mg/dL). Urinalysis was unremarkable, blood cultures were negative, and a chest radiograph was normal. Human immunodeficiency virus and rapid plasma reagin tests were negative, with normal levels of IgG, IgA, and IgM. IgE was elevated at 572 IU/mL (reference range, 0–100 IU/mL). Ultrasonography of the leg was negative for deep vein thrombosis, and a left ankle radiograph was negative for fracture. The patient previously was found to have antinuclear antibodies of 1:40 and negative antineutrophil cytoplasmic antibodies, anti–double-stranded DNA, anti–Sjögren syndrome antigens A and B, and cryoglobulins, as well as normal complement levels. The constellation of rash, arthritis, conjunctivitis, and difficulty with urination raised a high suspicion for reactive arthritis; however, the patient was found to be HLA-B27 negative with a negative urine chlamydia test.

The patient was mildly hypokalemic at 2.9 mmol/L (reference range, 3.5–5.0 mmol/L) and hypoalbuminemic at 3.6 g/dL (reference range, 3.9–5.0 g/dL). He had a slightly elevated international normalized ratio of 1.4 (reference range, 0.9–1.2). Further questioning revealed that his diet consisted mostly of soda and energy drinks; his vitamin C level was subsequently checked and found to be 0 mg/dL (reference range, 0.2–2.0 mg/dL). A diagnosis of scurvy was made, and his symptoms improved at the hospital while maintaining a diet with normal levels of vitamin C. His rash had markedly improved by hospital day 2, joint swelling decreased, and the conjunctival injection and eye pain had resolved. Upon outpatient follow-up, his rash and joint swelling continued to improve, and he had not experienced any further areas of hair loss.

Scurvy, a condition caused by vitamin C deficiency, is a disease of historical importance, as it ravaged ships full of sailors in days past; however, its incidence has decreased drastically since Lind1 first described its treatment using citrus fruits in 1753. Nonetheless, even with modern day access to foods rich in vitamin C, scurvy is far more common than expected in the developed world.



Vitamin C (ascorbic acid) plays a crucial role in human biochemistry. Although many plants and animals can synthesize ascorbic acid, humans and other animals such as guinea pigs lack the required enzyme, making vitamin C an essential nutrient required in dietary intake.­2-4 Hypovitaminosis C leads to scurvy when collagen production becomes impaired due to lack of ascorbic acid as a required cofactor for its synthesis, which leads to tissue and capillary fragility, causing hemorrhage and perivascular edema.4 The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency (<11 μmol/L or <0.2 mg/dL) with rapid resolution upon vitamin C supplementation.5

 

 

Important sources of vitamin C include citrus fruits, strawberries, broccoli, spinach, and potatoes. Recommended daily intake is 75 to 90 mg, with smokers requiring 110 to 125 mg daily because of increased oxidative stress.6-9 Although access to these foods in the modern United States is high, as many as 10% of males and 6.9% of females are vitamin C deficient, and in the subset of generally healthy middle-class Americans, as many as 6% are deficient.8,10 The highest risk groups tend to be smokers and individuals with low incomes.8 Although vitamin C deficiency does not automatically equate to scurvy, early studies on experimentally induced scurvy in prisoners showed that signs of scurvy may begin to develop in as few as 29 days of complete vitamin C deprivation, with overt scurvy developing after approximately 40 to 90 days.11,12

Patients with scurvy often pose a diagnostic dilemma for physicians because their presenting symptoms, such as fatigue, anemia, and rash, are nonspecific and can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups to determine the cause of the symptoms. Increased awareness of the current prevalence of hypovitaminosis C may help to decrease these unnecessary costs by putting scurvy higher on the differential for patients with this spectrum of symptoms.



Scurvy has been called the eternal masquerader because its nonspecific signs and symptoms have often led to misdiagnosis.13 Cases of scurvy mimicking diseases ranging from bone tumors14 to spondyloarthritis15 and vasculitis16 have been reported. The typical patient at risk for scurvy tends to fall in one of the following categories: psychiatric illness, gastrointestinal disorders, malnourishment, chronic alcoholism, drug use, elderly age, infants, restrictive dietary habits or food allergies, or those in developing countries.17-20 Our patient did not fit particularly well into any of the aforementioned high-risk categories; he had only recently become homeless and had a history of intravenous drug use but had not been using drugs in the months prior to the development of scurvy. Additionally, his salient symptoms were more consistent with reactive arthritis than with classic scurvy.

Although he had many symptoms consistent with scurvy such as generalized malaise, perifollicular hemorrhage and hyperkeratosis, spongy edema of the joints, and mild anemia on laboratory testing, he was missing several classic scurvy symptoms. Unlike many patients with scurvy, our patient did not describe any history of bruising easily or dental concerns, and examination was notably absent of ecchymoses as well as spongy or bleeding gums. He did, however, present with eye irritation and photophobia. These symptoms, consistent with keratoconjunctivitis sicca, are lesser known because ocular findings are rarely found in scurvy.21 Patients with scurvy can report eye burning and irritation, redness, blurry vision, and sensitivity to bright light secondary to increased dryness of the corneal surfaces. Horrobin et al22 postulated that this symptom may be mediated by regulation of prostaglandin E1 by vitamin C.

Another less common sign of scurvy found in our patient was patchy alopecia. Alopecia most often is seen in association with concomitant Sjögren syndrome.11,23 The etiology of the hair loss stems from the role of ascorbic acid in disulfide bonding during hair formation. The hair may fracture, coil into a corkscrew hair, or bend in several places, leading to a swan-neck deformity. Although a skin biopsy was not performed in our patient, results typically demonstrate a coiled hair in its follicle.24,25

We present the case of an otherwise generally healthy patient who developed vitamin C deficiency due to a diet consisting mostly of soda and energy drinks. His case presented a diagnostic dilemma, as his symptoms at first seemed most consistent with reactive arthritis and he was missing several of the risk factors and symptoms that would have led to an early diagnosis of scurvy. Vitamin C deficiency is not as uncommon as expected in the developed world; practitioners must be aware of the common as well as the unusual signs of scurvy.

References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
References
  1. Lind J. A Treatise of the Scurvy. Edinburgh, Scotland: Sands, Murray, and Cochran; 1753.
  2. Levine M, Rumsey SC, Daruwala R, et al. Criteria and recommendations for vitamin C intake. JAMA. 1999;281:1415-1423.
  3. Jacob RA. Vitamin C. In: Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease. Baltimore, MD: William & Wilkins; 1999:467-483.
  4. Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902.
  5. Hirschman JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906.
  6. Bardnard ND, Weissinger R, Jaster BJ, et al, eds. Nutrition Guide for Clinicians. 2nd ed. Washington, DC: Physician’s Committee For Responsible Medicine; 2009:33.
  7. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington DC: National Academic Press; 2000.
  8. Schleicher RL, Carroll MD, Ford ES, et al. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am J Clin Nutr. 2009;90:1252-1263.
  9. Schectman G, Byrd JC, Gruchow HW. The influence of smoking on vitamin C status in adults. Am J Public Health. 1989;79:158-162.
  10. Johnston CS, Thompson LL. Vitamin C status of an outpatient population. J Am Coll Nutr. 1998;17:366-370.
  11. Hodges RE, Baker EM, Hood J, et al. Experimental scurvy in man. Am J Clin Nutr. 1969;22:535-548.
  12. Hodges RE, Hood J, Canham JE, et al. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr. 1971;24:432-443.
  13. Gupta P, Taneja K, Iyer PU, et al. Scurvy—the eternal masquerader. Ann Trop Paediatr. 1989;9:118-121.
  14. Haq RU, Dhammi IK, Jain AK, et al. Infantile scurvy masquerading as bone tumour. Ann Acad Med Singapore. 2013;42:363-365.
  15. Pazzola G, Possemato N, Germanò G, et al. Scurvy mimicking spondyloarthritis in a young man. Clin Exp Rheumatol. 2013;31:795.
  16. Friesgaard Christensen A, Clemmensen O, Junker P. Palpable purpura with an unexpected outcome. Case Rep Rheumatol. 2013;2013:678427.
  17. Des Roches A, Paradis L, Paradis J, et al. Food allergy as a new risk factor for scurvy. Allergy. 2006;61:1487-1488.
  18. Pimentel L. Scurvy: historical review and current diagnostic approach. Am J Emerg Med. 2003;21:328-332.
  19. Codreanu F, Jarlot S, Astier C, et al. An apple a day...chronic glossitis in a 4-year-old boy. Eur Ann Allergy Clin Immunol. 2012;44:86-88.
  20. Stephen R, Utecht T. Scurvy identified in the emergency department: a case report. J Emerg Med. 2001;21:235-237.
  21. Hood J, Hodges RE. Ocular lesions in scurvy. Am J Clin Nutr. 1969;22:559-567.
  22. Horrobin DF, Oka M, Manku MS. The regulation of prostaglandin E1 formation: a candidate for one of the fundamental mechanisms involved in the actions of vitamin C. Med Hypotheses. 1979;5:849-858.
  23. Hood J, Burns CA, Hodges RE. Sjogren’s syndrome in scurvy. N Engl J Med. 1970;282:1120-1124.
  24. Walter JF. Scurvy resulting from a self-imposed diet. West J Med. 1979;130:177-179.
  25. Velandia B, Centor RM, McConnell V, et al. Scurvy is still present in developed countries. J Gen Intern Med. 2008;23:1281-1284.
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  • Patients with scurvy often pose a diagnostic dilemma because their presenting symptoms can lead physicians down a laborious and costly road of unnecessary tests including vasculitic, infectious, and rheumatologic workups.
  • The diagnosis of scurvy is clinical and typically is based on signs such as perivascular hemorrhage, bleeding gums, anemia, impaired wound healing, and ecchymoses in the setting of vitamin C deficiency with rapid resolution upon vitamin C supplementation.
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